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  • 37

    Загружено:

    Carlos Hernández
    112 просмотров190 страниц

    Оригинальное название

    37.txt

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    © © All Rights Reserved

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    112 просмотров190 страниц

    37

    Загружено:

    Carlos Hernández

    Авторское право:

    © All Rights Reserved
    Скачайте в формате TXT, PDF, TXT или читайте онлайн в Scribd
    Отметить как неприемлемый контент
    из 190

    var title_f0_37_592="Diaphragm";

    var content_f0_37_592=[" <div id=\"graphicsToolbar\">",


    " <div id=\"graphicsCopy\">",
    " &copy;2013 UpToDate",
    " <sup>",
    " &reg;",
    " </sup>",
    " </div>",
    " <div id=\"graphicsLinks\">",
    " <a href=\"?imageKey=OBGYN%2F54756%7EOBGYN
    %2F69595&amp;source=image_view&amp;view=print&amp;elapsedTimeMs=2\" onclick=\"\">",
    " <img alt=\"Print this page\" src=\"./../images/icn_print.myextg\"
    title=\"Print this page\"/>",
    " </a>",
    " <a class=\"icontxt textLink\" href=\"?imageKey=OBGYN%2F54756%7EOBGYN
    %2F69595&amp;source=image_view&amp;view=print&amp;elapsedTimeMs=2\" onclick=\"\"
    title=\"Print this page\">",
    " Print",
    " </a>",
    " <a class=\"etacLink\" href=\"#\">",
    " <img alt=\"Email graphic(s)\" src=\"./../images/icn_email.myextg\"
    title=\"Email graphic(s)\"/>",
    " </a>",
    " <a class=\"icontxt textLink etacLink\" href=\"#\" title=\"Email graphic(s)\">",
    " Email",
    " </a>",
    " </div>",
    " </div>",
    " <div class=\"graphic\">",
    " <div class=\"figure\" style=\"width: 470px\">",
    " <div class=\"ttl\">",
    " Diaphragm",
    " </div>",
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    " </div>",
    " <div class=\"lgnd\">",
    " <div class=\"footnotes\">",
    " </div>",
    " <div class=\"reference\">",
    " </div>",
    " </div>",
    " </div>",
    " </div>",
    " <div class=\"graphic\">",
    " <div class=\"figure\" style=\"width: 470px\">",
    " <div class=\"ttl\">",
    " Diaphragm fitting kit",
    " </div>",
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    " </div>",
    " <div class=\"lgnd\">",
    " <div class=\"footnotes\">",
    " </div>",
    " <div class=\"reference\">",
    " </div>",
    " </div>",
    " </div>",
    " </div>",
    "</div>"].join("\n");
    var script_f0_37_592=[""].join("\n");
    var outline_f0_37_592=null;
    var title_f0_37_593="Chondro histology";
    var content_f0_37_593=[" <div id=\"graphicsToolbar\">",
    " <div id=\"graphicsCopy\">",
    " &copy;2013 UpToDate",
    " <sup>",
    " &reg;",
    " </sup>",
    " </div>",
    " <div id=\"graphicsLinks\">",
    " <a href=\"?imageKey=ONC
    %2F74562&amp;source=image_view&amp;view=print&amp;elapsedTimeMs=1\" onclick=\"\">",
    " <img alt=\"Print this page\" src=\"./../images/icn_print.myextg\"
    title=\"Print this page\"/>",
    " </a>",
    " <a class=\"icontxt textLink\" href=\"?imageKey=ONC
    %2F74562&amp;source=image_view&amp;view=print&amp;elapsedTimeMs=1\" onclick=\"\"
    title=\"Print this page\">",
    " Print",
    " </a>",
    " <a class=\"etacLink\" href=\"#\">",
    " <img alt=\"Email graphic(s)\" src=\"./../images/icn_email.myextg\"
    title=\"Email graphic(s)\"/>",
    " </a>",
    " <a class=\"icontxt textLink etacLink\" href=\"#\" title=\"Email graphic(s)\">",
    " Email",
    " </a>",
    " </div>",
    " </div>",
    " <div class=\"graphic\">",
    " <div class=\"figure\" style=\"width: 536px\">",
    " <div class=\"ttl\">",
    " Histology of grade 1, 2, and 3 chondrosarcoma",
    " </div>",
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    jUbF2iiisyj/2Q==);\">",
    " </div>",
    " <div class=\"lgnd\">",
    " While cellularity is low in grade 1 chondrosarcoma (A) with chondroid matrix
    and absent mitoses, in grade 2 chondrosarcoma (B) mitoses are found (inset). In
    grade 3 chondrosarcoma (C), a high cellularity with muco-myxoid matrix changes is
    seen with cytonuclear atypia (hematoxylin and eosin staining, &sim;500X).",
    " <div class=\"footnotes\">",
    " </div>",
    " <div class=\"reference\">",
    " Reproduced with permission from: Gelderblom H, Hogendoorn PCW, Dijkstra SD,
    et al. The clinical approach towards chondrosarcoma. Oncologist 2008; 13:320.
    Copyright &copy;2008 AlphaMed Press.",
    " </div>",
    " <div class=\"contractual\">",
    " <br/>",
    " <a href=\"file://www.TheOncologist.com\">",
    " file://www.TheOncologist.com",
    " </a>",
    " </div>",
    " </div>",
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    var outline_f0_37_593=null;
    var title_f0_37_594="Echocardiogram D-TGA";
    var content_f0_37_594=[" <div id=\"graphicsToolbar\">",
    " <div id=\"graphicsCopy\">",
    " &copy;2013 UpToDate",
    " <sup>",
    " &reg;",
    " </sup>",
    " </div>",
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    " <a href=\"?imageKey=PEDS
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    " </a>",
    " <a class=\"icontxt textLink\" href=\"?imageKey=PEDS
    %2F64927&amp;source=image_view&amp;view=print&amp;elapsedTimeMs=2\" onclick=\"\"
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    " Print",
    " </a>",
    " <a class=\"etacLink\" href=\"#\">",
    " <img alt=\"Email graphic(s)\" src=\"./../images/icn_email.myextg\"
    title=\"Email graphic(s)\"/>",
    " </a>",
    " <a class=\"icontxt textLink etacLink\" href=\"#\" title=\"Email graphic(s)\">",
    " Email",
    " </a>",
    " </div>",
    " </div>",
    " <div class=\"graphic\">",
    " <div class=\"figure\" style=\"width: 470px\">",
    " <div class=\"ttl\">",
    " Echocardiogram of D-transposition of the great arteries",
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    " </div>",
    " <div class=\"lgnd\">",
    " Echocardiogram of D-transposition of the great arteries. Subcostal short axis
    view demonstrates the anteriorly positioned right ventricle (RV) giving rise to the
    aorta (Ao). The pulmonary artery (PA) is posteriorly related to the aorta and
    arises from the left ventricle. The aorta is identified as the vessel that gives
    rise to the head and neck vessels as well as the coronary arteries, while the
    pulmonary artery branches into the right and left pulmonary arteries. Mixing of
    blood between the two parallel circuits occurs through the patent ductus arteriosus
    (PDA).",
    " <div class=\"footnotes\">",
    " </div>",
    " <div class=\"reference\">",
    " </div>",
    " </div>",
    " </div>",
    " </div>",
    "</div>"].join("\n");
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    var title_f0_37_595="Patient information: Secondhand smoke: Risks to children (The
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    " <img src=\"file://www.uptodate.com/images/basics-more-title.png\"/>",
    " </h4>",
    " <dl>",
    " <dt class=\"basics\">",
    " The Basics",
    " </dt>",
    " <dd>",
    " <a href=\"UTD.htm?23/28/24002\">",
    " Patient information: Acute bronchitis (The Basics)",
    " </a>",
    " </dd>",
    " <dd>",
    " <a href=\"UTD.htm?16/58/17315\">",
    " Patient information: Asthma in children (The Basics)",
    " </a>",
    " </dd>",
    " <dd>",
    " <a href=\"UTD.htm?13/7/13427\">",
    " Patient information: Cough in children (The Basics)",
    " </a>",
    " </dd>",
    " <dd>",
    " <a href=\"UTD.htm?43/38/44642\">",
    " Patient information: Ear infections (otitis media) (The Basics)",
    " </a>",
    " </dd>",
    " <dd>",
    " <a href=\"UTD.htm?37/1/37907\">",
    " Patient information: How to plan and prepare for a healthy pregnancy (The
    Basics)",
    " </a>",
    " </dd>",
    " <dd>",
    " <a href=\"UTD.htm?14/17/14611\">",
    " Patient information: Pneumonia in children (The Basics)",
    " </a>",
    " </dd>",
    " <dd>",
    " <a href=\"UTD.htm?17/46/18146\">",
    " Patient information: Quitting smoking (The Basics)",
    " </a>",
    " </dd>",
    " <dd>",
    " <a href=\"UTD.htm?37/38/38497\">",
    " Patient information: Sudden infant death syndrome (SIDS) (The Basics)",
    " </a>",
    " </dd>",
    " <dt class=\"beyondthebasics\">",
    " Beyond the Basics",
    " </dt>",
    " <dd>",
    " <a href=\"UTD.htm?37/0/37892\">",
    " Patient information: Asthma symptoms and diagnosis in children (Beyond
    the Basics)",
    " </a>",
    " </dd>",
    " <dd>",
    " <a href=\"UTD.htm?15/16/15619\">",
    " Patient information: Ear infections (otitis media) in children (Beyond
    the Basics)",
    " </a>",
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    " <dd>",
    " <a href=\"UTD.htm?19/13/19670\">",
    " Patient information: Quitting smoking (Beyond the Basics)",
    " </a>",
    " </dd>",
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    " <a href=\"UTD.htm?7/40/7811\">",
    " Patient information: Sudden infant death syndrome (SIDS) (Beyond the
    Basics)",
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    " <div id=\"tooltipper\">",
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    " <div id=\"basicsTopicLeft\">",
    " <div id=\"topicTitle\">",
    " Patient information: Secondhand smoke: Risks to children (The Basics)",
    " </div>",
    " <a class=\"contributor contributor_credentials\" href=\"./authors-and-
    editors/patient-information\">",
    " Written by the doctors and editors at UpToDate",
    " </a>",
    " <div id=\"topicText\">",
    " <p class=\"headingAnchor\" id=\"H287369052\">",
    " <span class=\"h1\">",
    " What is secondhand smoke?",
    " </span>",
    " &nbsp;&mdash;&nbsp;Secondhand smoke is the term doctors use for the smoke
    that people (who do not smoke) breathe in from other people&rsquo;s smoking.
    Another term for secondhand smoke is &ldquo;environmental tobacco smoke.&rdquo;",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H287369067\">",
    " <span class=\"h1\">",
    " Does secondhand smoke cause health problems in children?",
    " </span>",
    " &nbsp;&mdash;&nbsp;Yes. Studies have shown that secondhand smoke from people
    smoking in the home can cause health problems in children. These problems are worse
    if both parents smoke.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H287369082\">",
    " <span class=\"h1\">",
    " What health problems can secondhand smoke cause in children?",
    " </span>",
    " &nbsp;&mdash;&nbsp;Secondhand smoke increases the chance of children having
    the following health problems:",
    " </p>",
    " <p>",
    " <ul class=\"bulletCompact-block\">",
    " <li>",
    " Breathing symptoms, such as coughing, coughing up mucus, or wheezing
    (noisy breathing)",
    " </li>",
    " <li>",
    " Lung infections, such as bronchitis and pneumonia &ndash; These infections
    can be especially serious in babies and young children.",
    " </li>",
    " <li>",
    " Asthma &ndash; Asthma is a lung condition that makes it hard to breathe.
    It doesn&rsquo;t cause symptoms all the time. But when symptoms flare up, children
    wheeze, cough, or get a tight feeling in their chest.",
    " </li>",
    " <li>",
    " The lungs not growing normally during childhood",
    " </li>",
    " <li>",
    " Ear infections",
    " </li>",
    " <li>",
    " Hearing loss (later in childhood)",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " Later on as adults, children who grew up with secondhand smoke are more
    likely to get:",
    " </p>",
    " <p>",
    " <ul class=\"bulletCompact-block\">",
    " <li>",
    " Asthma",
    " </li>",
    " <li>",
    " Lung cancer",
    " </li>",
    " <li>",
    " Other types of cancers",
    " </li>",
    " <li>",
    " Heart disease",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " Also, children who grow up with parents who smoke are more likely to take up
    smoking themselves.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H287369097\">",
    " <span class=\"h1\">",
    " What if my child already has asthma?",
    " </span>",
    " &nbsp;&mdash;&nbsp;If your child already has asthma, secondhand smoke can
    make his or her symptoms worse or severe. Also, secondhand smoke causes children
    with asthma to need their asthma medicines or go to the hospital more often.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H287369112\">",
    " <span class=\"h1\">",
    " Can secondhand smoke affect an unborn baby?",
    " </span>",
    " &nbsp;&mdash;&nbsp;Yes. If a woman (who doesn&rsquo;t smoke) lives in a home
    with secondhand smoke, her baby has a higher chance of weighing less than normal at
    birth.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H287369127\">",
    " <span class=\"h1\">",
    " What problems can happen if a woman smokes during pregnancy?",
    " </span>",
    " &nbsp;&mdash;&nbsp;Women who smoke during pregnancy have a higher chance of
    having a miscarriage, which is when a pregnancy ends on its own.",
    " </p>",
    " <p>",
    " When a woman smokes during pregnancy, her baby has a higher chance of:",
    " </p>",
    " <p>",
    " <ul class=\"bulletCompact-block\">",
    " <li>",
    " Being born too early",
    " </li>",
    " <li>",
    " Not growing as much as normal in the uterus (womb)",
    " </li>",
    " <li>",
    " Being born with a birth defect",
    " </li>",
    " <li>",
    " Dying from sudden infant death syndrome (called &ldquo;SIDS&rdquo;) later
    on &ndash; SIDS is when a baby dies suddenly during sleep for no known reason.",
    " </li>",
    " </ul>",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H287369142\">",
    " <span class=\"h1\">",
    " Is it enough to just make a smoke-free room in my home?",
    " </span>",
    " &nbsp;&mdash;&nbsp;No. If you want to help your child&rsquo;s health, you
    need to make your whole home smoke-free. You also need to make your car smoke-free.
    It will not help enough to make a smoke-free room, smoke at home only when your
    child is not there, or use an air cleaner.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H287369157\">",
    " <span class=\"h1\">",
    " What should I do if I want to quit smoking?",
    " </span>",
    " &nbsp;&mdash;&nbsp;If you want to quit smoking, think of the letters in the
    word &ldquo;START.&rdquo; They can help you remember the steps to take:",
    " </p>",
    " <p>",
    " S = Set a quit date.",
    " </p>",
    " <p>",
    " T = Tell family, friends, and the people around you that you plan to quit.",
    " </p>",
    " <p>",
    " A = Anticipate or plan ahead for the tough times you&rsquo;ll face while
    quitting.",
    " </p>",
    " <p>",
    " R = Remove cigarettes and other tobacco products from your home, car, and
    work.",
    " </p>",
    " <p>",
    " T = Talk to your doctor or nurse about getting help to quit.",
    " </p>",
    " <p>",
    " Your doctor or nurse can help you in different ways. He or she can:",
    " </p>",
    " <p>",
    " <ul class=\"bulletCompact-block\">",
    " <li>",
    " Put you in touch with a counselor &ndash; A counselor can help you figure
    out what triggers your smoking and what you can do instead.",
    " </li>",
    " <li>",
    " Prescribe medicines to help you quit smoking &ndash; Some medicines reduce
    your craving for cigarettes. Others reduce unpleasant symptoms (called
    &ldquo;withdrawal symptoms&rdquo;) that happen when you stop smoking.",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " You can also get help from a free phone line (1-800-QUIT-NOW) or the Web
    site",
    " <a class=\"external\" href=\"file://www.smokefree.gov/\">",
    " www.smokefree.gov",
    " </a>",
    " .",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H287369172\">",
    " <span class=\"h1\">",
    " More on this topic",
    " </span>",
    " </p>",
    " <p>",
    " <a class=\"medical medical_basics\" href=\"UTD.htm?17/46/18146?
    source=see_link\">",
    " Patient information: Quitting smoking (The Basics)",
    " </a>",
    " <br/>",
    " <a class=\"medical medical_basics\" href=\"UTD.htm?37/1/37907?
    source=see_link\">",
    " Patient information: How to plan and prepare for a healthy pregnancy (The
    Basics)",
    " </a>",
    " <br/>",
    " <a class=\"medical medical_basics\" href=\"UTD.htm?16/58/17315?
    source=see_link\">",
    " Patient information: Asthma in children (The Basics)",
    " </a>",
    " <br/>",
    " <a class=\"medical medical_basics\" href=\"UTD.htm?13/7/13427?
    source=see_link\">",
    " Patient information: Cough in children (The Basics)",
    " </a>",
    " <br/>",
    " <a class=\"medical medical_basics\" href=\"UTD.htm?14/17/14611?
    source=see_link\">",
    " Patient information: Pneumonia in children (The Basics)",
    " </a>",
    " <br/>",
    " <a class=\"medical medical_basics\" href=\"UTD.htm?23/28/24002?
    source=see_link\">",
    " Patient information: Acute bronchitis (The Basics)",
    " </a>",
    " <br/>",
    " <a class=\"medical medical_basics\" href=\"UTD.htm?43/38/44642?
    source=see_link\">",
    " Patient information: Ear infections (otitis media) (The Basics)",
    " </a>",
    " <br/>",
    " <a class=\"medical medical_basics\" href=\"UTD.htm?37/38/38497?
    source=see_link\">",
    " Patient information: Sudden infant death syndrome (SIDS) (The Basics)",
    " </a>",
    " </p>",
    " <p>",
    " <a class=\"medical medical_patient\" href=\"UTD.htm?19/13/19670?
    source=see_link\">",
    " Patient information: Quitting smoking (Beyond the Basics)",
    " </a>",
    " <br/>",
    " <a class=\"medical medical_patient\" href=\"UTD.htm?15/16/15619?
    source=see_link\">",
    " Patient information: Ear infections (otitis media) in children (Beyond the
    Basics)",
    " </a>",
    " <br/>",
    " <a class=\"medical medical_patient\" href=\"UTD.htm?37/0/37892?
    source=see_link\">",
    " Patient information: Asthma symptoms and diagnosis in children (Beyond the
    Basics)",
    " </a>",
    " <br/>",
    " <a class=\"medical medical_patient\" href=\"UTD.htm?7/40/7811?
    source=see_link\">",
    " Patient information: Sudden infant death syndrome (SIDS) (Beyond the
    Basics)",
    " </a>",
    " </p>",
    " </div>",
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    " This topic retrieved from UpToDate on:",
    " </span>",
    " Apr 20, 2013.",
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    " <h1>",
    " TOPIC OUTLINE",
    " </h1>",
    " <div id=\"outline\">",
    " <ul>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H287369052\">",
    " What is secondhand smoke?",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H287369067\">",
    " Does secondhand smoke cause health problems in children?",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H287369082\">",
    " What health problems can secondhand smoke cause in children?",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H287369097\">",
    " What if my child already has asthma?",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H287369112\">",
    " Can secondhand smoke affect an unborn baby?",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H287369127\">",
    " What problems can happen if a woman smokes during pregnancy?",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H287369142\">",
    " Is it enough to just make a smoke-free room in my home?",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H287369157\">",
    " What should I do if I want to quit smoking?",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H287369172\">",
    " More on this topic",
    " </a>",
    " </li>",
    " </ul>",
    " </div>",
    " <h1>",
    " RELATED TOPICS",
    " </h1>",
    " <div id=\"relatedTopics\">",
    " <ul>",
    " <li class=\"plainItem\">",
    " <a class=\"medical medical_basics\" href=\"UTD.htm?23/28/24002?
    source=related_link\">",
    " Patient information: Acute bronchitis (The Basics)",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"medical medical_basics\" href=\"UTD.htm?16/58/17315?
    source=related_link\">",
    " Patient information: Asthma in children (The Basics)",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"medical medical_patient\" href=\"UTD.htm?37/0/37892?
    source=related_link\">",
    " Patient information: Asthma symptoms and diagnosis in children (Beyond the
    Basics)",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"medical medical_basics\" href=\"UTD.htm?13/7/13427?
    source=related_link\">",
    " Patient information: Cough in children (The Basics)",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"medical medical_basics\" href=\"UTD.htm?43/38/44642?
    source=related_link\">",
    " Patient information: Ear infections (otitis media) (The Basics)",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"medical medical_patient\" href=\"UTD.htm?15/16/15619?
    source=related_link\">",
    " Patient information: Ear infections (otitis media) in children (Beyond the
    Basics)",
    " </a>",
    " </li>",
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    " <a class=\"medical medical_basics\" href=\"UTD.htm?37/1/37907?
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    " Patient information: How to plan and prepare for a healthy pregnancy (The
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    " </a>",
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    " <li class=\"plainItem\">",
    " <a class=\"medical medical_basics\" href=\"UTD.htm?14/17/14611?
    source=related_link\">",
    " Patient information: Pneumonia in children (The Basics)",
    " </a>",
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    " <a class=\"medical medical_patient\" href=\"UTD.htm?19/13/19670?
    source=related_link\">",
    " Patient information: Quitting smoking (Beyond the Basics)",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"medical medical_basics\" href=\"UTD.htm?17/46/18146?
    source=related_link\">",
    " Patient information: Quitting smoking (The Basics)",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"medical medical_patient\" href=\"UTD.htm?7/40/7811?
    source=related_link\">",
    " Patient information: Sudden infant death syndrome (SIDS) (Beyond the
    Basics)",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"medical medical_basics\" href=\"UTD.htm?37/38/38497?
    source=related_link\">",
    " Patient information: Sudden infant death syndrome (SIDS) (The Basics)",
    " </a>",
    " </li>",
    " </ul>",
    " </div>",
    " </div>"].join("\n");
    var title_f0_37_596="Edrophonium: Pediatric drug information";
    var content_f0_37_596=[" <noscript>",
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    " <!-- TC:TOPIC_PAGE -->",
    " <div id=\"topicContent\">",
    " <div id=\"drugTitle\">",
    " Edrophonium: Pediatric drug information",
    " </div>",
    " <div id=\"lexiTitleImg\">",
    " <img height=\"17\" src=\"./../images/lexiComp/Lexicomp_2012_71x17.myextg\"
    width=\"71\"/>",
    " </div>",
    " <div class=\"clear\">",
    " </div>",
    " <div id=\"drugCopy\">",
    " Copyright 1978-2013 Lexicomp, Inc. All rights reserved.",
    " </div>",
    " <div id=\"topicText\">",
    " (For additional information",
    " <a class=\"drug drug_general\" href=\"UTD.htm?34/21/35156?source=see_link\">",
    " see \"Edrophonium: Drug information\"",
    " </a>",
    " )",
    " <br/>",
    " For abbreviations and symbols that may be used in Lexicomp (",
    " <a class=\"graphic graphic_table\" href=\"UTD.htm?23/39/24183\">",
    " show table",
    " </a>",
    " )",
    " <div class=\"list ubnlist drugH1Div drugBrandNames\" id=\"F164242\"
    xmlns=\"file://www.w3.org/1999/xhtml\">",
    " <span class=\"drugH1\">",
    " Brand Names: U.S.",
    " </span>",
    " <ul>",
    " <li>",
    " Enlon&reg;",
    " </li>",
    " </ul>",
    " </div>",
    " <div class=\"list cbnlist drugH1Div drugBrandNames\" id=\"F164243\"
    xmlns=\"file://www.w3.org/1999/xhtml\">",
    " <span class=\"drugH1\">",
    " Brand Names: Canada",
    " </span>",
    " <ul>",
    " <li>",
    " Enlon&reg;;",
    " </li>",
    " <li>",
    " Tensilon&reg;",
    " </li>",
    " </ul>",
    " </div>",
    " <div class=\"list_set htclist drugH1Div drugBrandNames\" id=\"F1058297\"
    xmlns=\"file://www.w3.org/1999/xhtml\">",
    " <span class=\"drugH1\">",
    " Therapeutic Category",
    " </span>",
    " <ul>",
    " <li>",
    " <span class=\"list-set-name\">",
    " Antidote, Neuromuscular Blocking Agent",
    " </span>",
    " </li>",
    " <li>",
    " <span class=\"list-set-name\">",
    " Cholinergic Agent",
    " </span>",
    " </li>",
    " <li>",
    " <span class=\"list-set-name\">",
    " Diagnostic Agent, Myasthenia Gravis",
    " </span>",
    " </li>",
    " </ul>",
    " </div>",
    " <div class=\"block dos drugH1Div\" id=\"F1058292\"
    xmlns=\"file://www.w3.org/1999/xhtml\">",
    " <span class=\"drugH1\">",
    " Dosing: Usual",
    " </span>",
    " <p>",
    " (For additional information",
    " <a class=\"drug drug_general\" href=\"UTD.htm?34/21/35156?
    source=see_link\">",
    " see \"Edrophonium: Drug information\"",
    " </a>",
    " )",
    " </p>",
    " <p style=\"text-indent:0em;display:inline\">",
    " Usually administered I.V., however, if not possible, I.M. or SubQ may be
    used",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:2em;margin-top:2em;text-
    align:justify;\">",
    " Infants: Diagnosis of myasthenia gravis: Initial:",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
    " I.M., SubQ: 0.5-1 mg",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
    " I.V.: Initial: 0.1 mg, followed by 0.4 mg (if no response); total dose = 0.5
    mg",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
    " Children:",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
    " Diagnosis of myasthenia gravis: Initial:",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:6em;text-align:justify;\">",
    " I.M., SubQ: &le;34 kg: 2 mg; &gt;34 kg: 5 mg",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:6em;text-align:justify;\">",
    " I.V.: 0.04 mg/kg given over 1 minute followed by 0.16 mg/kg given within 45
    seconds (if no response) (maximum dose: 10 mg total)",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:8em;text-align:justify;\">",
    " <b>",
    " or",
    " </b>",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:8em;text-align:justify;\">",
    " Alternative (manufacturer's recommendations):",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:10em;text-align:justify;\">",
    " &le;34 kg: 1 mg; if no response after 45 seconds, it may be repeated in 1 mg
    increments every 30-45 seconds to a total of 5 mg",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:10em;text-align:justify;\">",
    " &gt;34 kg: 2 mg; if no response after 45 seconds, it may be repeated in 1 mg
    increments every 30-45 seconds to a total of 10 mg",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
    " Titration of oral anticholinesterase therapy: I.V.: 0.04 mg/kg once given 1
    hour after oral intake of the drug being used in treatment; if strength improves,
    an increase in neostigmine or pyridostigmine dose is indicated",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
    " Adults:",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
    " Diagnosis of myasthenia gravis: Initial:",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:6em;text-align:justify;\">",
    " I.M., SubQ: Initial: 10 mg; if no cholinergic reaction occurs, administer 2
    mg 30 minutes later to rule out false-negative reaction",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:6em;text-align:justify;\">",
    " I.V.: 2 mg test dose administered over 15-30 seconds; 8 mg given 45 seconds
    later (if no response is seen); test dose may be repeated after 30 minutes.",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
    " Titration of oral anticholinesterase therapy: I.V.: 1-2 mg given 1 hour after
    oral dose of anticholinesterase; if strength improves, an increase in neostigmine
    or pyridostigmine dose is indicated",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
    " Differentiation of cholinergic from myasthenic crisis: I.V.: 1 mg, may repeat
    after 1 minute (",
    " <b>",
    " Note:",
    " </b>",
    " Intubation and controlled ventilation may be required if patient has
    cholinergic crises.)",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
    " Reversal of nondepolarizing neuromuscular blocking agents (neostigmine with
    atropine usually preferred): I.V.: 10 mg over 30-45 seconds, may repeat every 5-10
    minutes up to 40 mg total dose",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
    " Termination of paroxysmal atrial tachycardia: I.V.: 5-10 mg",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
    " <b>",
    " Dosing adjustment in renal impairment:",
    " </b>",
    " Dose may need to be reduced in patients with chronic renal failure",
    " </p>",
    " </div>",
    " <div class=\"block foc drugH1Div\" id=\"F164225\"
    xmlns=\"file://www.w3.org/1999/xhtml\">",
    " <span class=\"drugH1\">",
    " Dosage Forms: U.S.",
    " </span>",
    " <p style=\"text-indent:0em;text-align:justify;display:inline\">",
    " Excipient information presented when available (limited, particularly for
    generics); consult specific product labeling.",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
    " Injection, solution, as chloride:",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
    " Enlon&reg;: 10 mg/mL (15 mL) [contains natural rubber/natural latex in
    packaging, sodium sulfite]",
    " </p>",
    " </div>",
    " <div class=\"block geq drugH1Div\" id=\"F164211\"
    xmlns=\"file://www.w3.org/1999/xhtml\">",
    " <span class=\"drugH1\">",
    " Generic Equivalent Available: U.S.",
    " </span>",
    " <p style=\"text-indent:0em;display:inline\">",
    " No",
    " </p>",
    " </div>",
    " <div class=\"block adm drugH1Div\" id=\"F1058301\"
    xmlns=\"file://www.w3.org/1999/xhtml\">",
    " <span class=\"drugH1\">",
    " Administration",
    " </span>",
    " <p style=\"text-indent:0em;display:inline\">",
    " Parenteral: Edrophonium is administered by direct I.V. or I.M. injection",
    " </p>",
    " </div>",
    " <div class=\"block scp drugH1Div\" id=\"F164267\"
    xmlns=\"file://www.w3.org/1999/xhtml\">",
    " <span class=\"drugH1\">",
    " Compatibility",
    " </span>",
    " <p style=\"text-indent:0em;display:inline\">",
    " <b>",
    " Y-site administration: Compatible:",
    " </b>",
    " Heparin, hydrocortisone sodium succinate, potassium chloride, vitamin B
    complex with C.",
    " </p>",
    " </div>",
    " <div class=\"block use drugH1Div\" id=\"F1058300\"
    xmlns=\"file://www.w3.org/1999/xhtml\">",
    " <span class=\"drugH1\">",
    " Use",
    " </span>",
    " <p style=\"text-indent:0em;display:inline\">",
    " Diagnosis of myasthenia gravis; differentiation of cholinergic crises from
    myasthenia crises; reversal of nondepolarizing neuromuscular blockers; treatment of
    paroxysmal atrial tachycardia",
    " </p>",
    " </div>",
    " <div class=\"block arm drugH1Div\" id=\"F164266\"
    xmlns=\"file://www.w3.org/1999/xhtml\">",
    " <span class=\"drugH1\">",
    " Adverse Reactions",
    " </span>",
    " <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
    " Cardiovascular: Arrhythmias (especially bradycardia), AV block, carbon
    monoxide decreased, cardiac arrest, ECG changes (nonspecific), flushing,
    hypotension, nodal rhythm, syncope, tachycardia",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
    " Central nervous system: Convulsions, dizziness, drowsiness, dysarthria,
    dysphonia, headache, loss of consciousness",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
    " Dermatologic: Skin rash, thrombophlebitis (I.V.), urticaria",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
    " Gastrointestinal: Diarrhea, dysphagia, flatulence, hyperperistalsis, nausea,
    salivation, stomach cramps, vomiting",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
    " Genitourinary: Urinary urgency",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
    " Neuromuscular &amp; skeletal: Arthralgias, fasciculations, muscle cramps,
    spasms, weakness",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
    " Ocular: Lacrimation, small pupils",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
    " Respiratory: Bronchiolar constriction, bronchospasm, dyspnea, bronchial
    secretions increased, laryngospasm, respiratory arrest, respiratory depression,
    respiratory muscle paralysis",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
    " Miscellaneous: Allergic reactions, anaphylaxis, diaphoresis increased",
    " </p>",
    " </div>",
    " <div class=\"block coi drugH1Div\" id=\"F1058305\"
    xmlns=\"file://www.w3.org/1999/xhtml\">",
    " <span class=\"drugH1\">",
    " Contraindications",
    " </span>",
    " <p style=\"text-indent:0em;display:inline\">",
    " Hypersensitivity to edrophonium or any component; GI or GU mechanical
    obstruction",
    " </p>",
    " </div>",
    " <div class=\"block pre drugH1Div\" id=\"F1058291\"
    xmlns=\"file://www.w3.org/1999/xhtml\">",
    " <span class=\"drugH1\">",
    " Precautions",
    " </span>",
    " <p style=\"text-indent:0em;display:inline\">",
    " Use with caution in asthmatic patients, patients with cardiac dysrhythmias,
    and those receiving a cardiac glycoside",
    " </p>",
    " </div>",
    " <div class=\"block war drugH1Div\" id=\"F1058290\"
    xmlns=\"file://www.w3.org/1999/xhtml\">",
    " <span class=\"drugH1\">",
    " Warnings",
    " </span>",
    " <p style=\"text-indent:0em;display:inline\">",
    " Overdosage can cause cholinergic crisis which may be fatal; I.V. atropine
    should be readily available for treatment of cholinergic reactions; injection
    contains sulfites which may cause allergic reactions in susceptible individuals",
    " </p>",
    " </div>",
    " <div class=\"block cyt drugH1Div\" id=\"F13299253\"
    xmlns=\"file://www.w3.org/1999/xhtml\">",
    " <span class=\"drugH1\">",
    " Metabolism/Transport Effects",
    " </span>",
    " <p style=\"text-indent:0em;display:inline\">",
    " None known.",
    " </p>",
    " </div>",
    " <div class=\"block dri drugH1Div\" id=\"F164219\"
    xmlns=\"file://www.w3.org/1999/xhtml\">",
    " <span class=\"drugH1\">",
    " Drug Interactions",
    " </span>",
    " <br/>",
    " <br/>",
    " <div class=\"lexi\" id=\"lexiInteractAddInfo\">",
    " (For additional information:",
    " <a class=\"dip\" href=\"./drug-interaction\" target=\"_blank\">",
    " Launch Lexi-Interact&trade; Drug Interactions Program",
    " </a>",
    " )",
    " </div>",
    " <div class=\"lexi\" id=\"lexiInteractImgB\">",
    " <img border=\"0\" height=\"17\"
    src=\"./../images/lexiComp/Lexicomp_2012_71x17.myextg\" width=\"71\"/>",
    " </div>",
    " <div class=\"clear\">",
    " </div>",
    " <p style=\"text-indent:-2em;margin-left:2em;\">",
    " Beta-Blockers: Acetylcholinesterase Inhibitors may enhance the bradycardic
    effect of Beta-Blockers.",
    " <b>",
    " Exceptions:",
    " </b>",
    " Levobunolol; Metipranolol.",
    " <i>",
    " Risk C: Monitor therapy",
    " </i>",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:2em;\">",
    " Cholinergic Agonists: Acetylcholinesterase Inhibitors may enhance the
    adverse/toxic effect of Cholinergic Agonists.",
    " <i>",
    " Risk C: Monitor therapy",
    " </i>",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:2em;\">",
    " Corticosteroids (Systemic): May enhance the adverse/toxic effect of
    Acetylcholinesterase Inhibitors. Increased muscular weakness may occur.",
    " <i>",
    " Risk C: Monitor therapy",
    " </i>",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:2em;\">",
    " Dipyridamole: May diminish the therapeutic effect of Acetylcholinesterase
    Inhibitors.",
    " <i>",
    " Risk C: Monitor therapy",
    " </i>",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:2em;\">",
    " Neuromuscular-Blocking Agents (Nondepolarizing): Acetylcholinesterase
    Inhibitors may diminish the neuromuscular-blocking effect of Neuromuscular-Blocking
    Agents (Nondepolarizing).",
    " <i>",
    " Risk C: Monitor therapy",
    " </i>",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:2em;\">",
    " Succinylcholine: Acetylcholinesterase Inhibitors may increase the serum
    concentration of Succinylcholine. Management: Consider alternatives to this
    combination due to a risk of prolonged neuromuscular blockade.",
    " <i>",
    " Risk D: Consider therapy modification",
    " </i>",
    " </p>",
    " </div>",
    " <div class=\"block mop drugH1Div\" id=\"F1058296\"
    xmlns=\"file://www.w3.org/1999/xhtml\">",
    " <span class=\"drugH1\">",
    " Monitoring Parameters",
    " </span>",
    " <p style=\"text-indent:0em;display:inline\">",
    " Pre- and postinjection strength (cranial musculature is most useful); heart
    rate, respiratory rate, blood pressure, changes in fasciculations",
    " </p>",
    " </div>",
    " <div class=\"block pha drugH1Div\" id=\"F1058289\"
    xmlns=\"file://www.w3.org/1999/xhtml\">",
    " <span class=\"drugH1\">",
    " Mechanism of Action",
    " </span>",
    " <p style=\"text-indent:0em;display:inline\">",
    " Inhibits destruction of acetylcholine by acetylcholinesterase. This
    facilitates transmission of impulses across myoneural junction and results in
    increased cholinergic responses such as miosis, increased tonus of intestinal and
    skeletal muscles, bronchial and ureteral constriction, bradycardia, and increased
    salivary and sweat gland secretions",
    " </p>",
    " </div>",
    " <div class=\"block phd drugH1Div\" id=\"F1058303\"
    xmlns=\"file://www.w3.org/1999/xhtml\">",
    " <span class=\"drugH1\">",
    " Pharmacodynamics",
    " </span>",
    " <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
    " Onset of action:",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
    " I.M.: 2-10 minutes",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
    " I.V.: 30-60 seconds",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:2em;text-align:justify;\">",
    " Duration:",
    " </p>",
    " <p style=\"text-indent:-2em;margin-left:4em;text-align:justify;\">",
    " I.M.: 5-30 minutes",
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    " </div>",
    " <div class=\"lgnd\">",
    " Chest CT scan shows multiple necrobiotic nodules (biopsy-proven) in a patient
    with Crohn's disease.",
    " <div class=\"footnotes\">",
    " </div>",
    " <div class=\"reference\">",
    " Courtesy of Steven E Weinberger, MD.",
    " </div>",
    " </div>",
    " </div>",
    " </div>",
    "</div>"].join("\n");
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    var outline_f0_37_597=null;
    var title_f0_37_598="Primary TB in an infant PA";
    var content_f0_37_598=[" <div id=\"graphicsToolbar\">",
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    " &copy;2013 UpToDate",
    " <sup>",
    " &reg;",
    " </sup>",
    " </div>",
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    " <a class=\"etacLink\" href=\"#\">",
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    " </div>",
    " <div class=\"graphic2\" style=\"width: 1040px;\">",
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    cdoycdAK8vkPBHbHNFFAH/9k=);\">",
    " </div>",
    " <div class=\"lgnd\">",
    " Large left sided pleural effusion produces complete opacification of the left
    hemithorax with cardiomediastinal shift to the right.",
    " <div class=\"footnotes\">",
    " </div>",
    " <div class=\"reference\">",
    " Courtesy of Paul Stark, MD.",
    " </div>",
    " </div>",
    " </div>",
    " <div class=\"figure\" style=\"width: 450px\">",
    " <div class=\"ttl\">",
    " Normal chest radiograph",
    " </div>",
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    " </div>",
    " <div class=\"lgnd\">",
    " Posteroanterior view of a normal chest radiograph.",
    " <div class=\"footnotes\">",
    " </div>",
    " <div class=\"reference\">",
    " Courtesy of Carol M Black, MD.",
    " </div>",
    " </div>",
    " </div>",
    " </div>",
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    " </div>",
    " <div class=\"lgnd\">",
    " <div class=\"footnotes\">",
    " </div>",
    " <div class=\"reference\">",
    " Reproduced with permission from: Leeson CR, Leeson TS, Paparo AA. Textbook of
    Histology, 5th ed, WB Saunders, Philadelphia, 1985, p.318.",
    " </div>",
    " </div>",
    " </div>",
    " </div>",
    "</div>"].join("\n");
    var script_f0_37_599=[""].join("\n");
    var outline_f0_37_599=null;
    var title_f0_37_600="Treatment regimens for chronic hepatitis C virus genotypes 2,
    3, and 4";
    var content_f0_37_600=[" <noscript>",
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    " <!-- TC:TOPIC_PAGE -->",
    " <div id=\"topicContent\">",
    " <div id=\"topicTitle\">",
    " Treatment regimens for chronic hepatitis C virus genotypes 2, 3, and 4",
    " </div>",
    " <div id=\"topicContributors\">",
    " <div>",
    " <a id=\"authors\">",
    " </a>",
    " <a class=\"contributor contributor_credentials contributorType\"
    href=\"UTD.htm?0/37/600/contributors\">",
    " Author",
    " </a>",
    " <br/>",
    " <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
    0/37/600/contributors\">",
    " Sanjiv Chopra, MD",
    " </a>",
    " <br/>",
    " </div>",
    " <div>",
    " <a class=\"contributor contributor_credentials contributorType\"
    href=\"UTD.htm?0/37/600/contributors\">",
    " Section Editor",
    " </a>",
    " <br/>",
    " <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
    0/37/600/contributors\">",
    " Adrian M Di Bisceglie, MD",
    " </a>",
    " <br/>",
    " </div>",
    " <div>",
    " <a class=\"contributor contributor_credentials contributorType\"
    href=\"UTD.htm?0/37/600/contributors\">",
    " Deputy Editor",
    " </a>",
    " <br/>",
    " <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
    0/37/600/contributors\">",
    " Allyson Bloom, MD",
    " </a>",
    " <br/>",
    " </div>",
    " </div>",
    " <div id=\"disclosures\">",
    " <a href=\"UTD.htm?0/37/600/contributor-disclosure\" target=\"_blank\">",
    " Disclosures",
    " </a>",
    " </div>",
    " <div id=\"reviewProcess\">",
    " <span>",
    " All topics are updated as new evidence becomes available and our",
    " </span>",
    " <a href=\"/home/editorial-policy\" target=\"_blank\">",
    " peer review process",
    " </a>",
    " <span>",
    " is complete.",
    " </span>",
    " </div>",
    " <div id=\"literatureReviewDate\">",
    " <span class=\"emphasis\">",
    " Literature review current through:",
    " </span>",
    " Oct 2013.",
    " <span class=\"pipeSpace\">",
    " |",
    " </span>",
    " <span class=\"emphasis\">",
    " This topic last updated:",
    " </span>",
    " Mar 8, 2013.",
    " </div>",
    " <div id=\"topicText\">",
    " <p class=\"headingAnchor\" id=\"H12153729\">",
    " <span class=\"h1\">",
    " INTRODUCTION",
    " </span>",
    " &nbsp;&mdash;&nbsp;Hepatitis C virus (HCV) can cause both acute and chronic
    hepatitis. The acute process is self-limited, rarely causes hepatic failure, and
    usually leads to chronic infection. Chronic HCV infection often follows a
    progressive course over many years and can ultimately result in cirrhosis,
    hepatocellular carcinoma, and the need for liver transplantation. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?30/50/31530?
    source=see_link\">",
    " \"Clinical manifestations and natural history of chronic hepatitis C virus
    infection\"",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " The goal of treatment is to eradicate HCV RNA, which is predicted by the
    achievement of a sustained virologic response (SVR) as defined by the absence of
    HCV RNA by polymerase chain reaction six months after stopping treatment. An SVR is
    associated with a 99 percent chance of being HCV RNA negative during long-term
    follow-up [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/600/abstract/1\">",
    " 1",
    " </a>",
    " ]. Achievement of an SVR has also been associated with improved clinical
    outcomes. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?34/59/35768?
    source=see_link&amp;anchor=H9#H9\">",
    " \"Mechanism of action and efficacy of standard interferon alfa for the
    treatment of chronic hepatitis C virus infection\", section on 'Long-term
    efficacy'",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?42/45/43735?
    source=see_link&amp;anchor=H9643992#H9643992\">",
    " \"Overview of the management of chronic hepatitis C virus infection\",
    section on 'Goal of antiviral therapy'",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " This topic will review the treatment of patients with chronic HCV genotypes 2,
    3, and 4. Treatment of patients with genotype 1, data regarding the efficacy of
    various treatment regimens, experimental agents for the treatment of HCV, the
    treatment of acute HCV, the selection of patients for treatment, the management of
    treatment-induced side effects, and factors that predict a response to treatment
    are discussed elsewhere:",
    " </p>",
    " <p>",
    " <ul class=\"bulletCompact-block\">",
    " <li>",
    " (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?42/45/43735?
    source=see_link\">",
    " \"Overview of the management of chronic hepatitis C virus infection\"",
    " </a>",
    " .)",
    " </li>",
    " <li>",
    " (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?23/47/24314?
    source=see_link\">",
    " \"Treatment regimens for chronic hepatitis C virus genotype 1\"",
    " </a>",
    " .)",
    " </li>",
    " <li>",
    " (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?40/23/41337?
    source=see_link\">",
    " \"Mechanism of action and efficacy of peginterferon for the treatment of
    chronic hepatitis C virus infection\"",
    " </a>",
    " .)",
    " </li>",
    " <li>",
    " (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?15/26/15785?
    source=see_link\">",
    " \"Studies of telaprevir and boceprevir in the treatment of chronic
    hepatitis C virus genotype 1\"",
    " </a>",
    " .)",
    " </li>",
    " <li>",
    " (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?37/30/38378?
    source=see_link\">",
    " \"Investigational therapies for hepatitis C virus infection\"",
    " </a>",
    " .)",
    " </li>",
    " <li>",
    " (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?18/7/18554?
    source=see_link\">",
    " \"Clinical manifestations, diagnosis, and treatment of acute hepatitis C in
    adults\"",
    " </a>",
    " .)",
    " </li>",
    " <li>",
    " (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?16/9/16538?
    source=see_link\">",
    " \"Management of the side effects of peginterferon and ribavirin being used
    for treatment of chronic hepatitis C virus infection\"",
    " </a>",
    " .)",
    " </li>",
    " <li>",
    " (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?14/8/14474?
    source=see_link\">",
    " \"Predictors of a sustained virologic response following treatment with
    peginterferon and ribavirin for chronic hepatitis C virus infection\"",
    " </a>",
    " .)",
    " </li>",
    " </ul>",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H19315213\">",
    " <span class=\"h1\">",
    " GUIDELINES",
    " </span>",
    " &nbsp;&mdash;&nbsp;Treatment guidelines for chronic hepatitis C virus (HCV)
    infection were published in 2009 by the American Association for the Study of Liver
    Diseases (AASLD) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/600/abstract/2\">",
    " 2",
    " </a>",
    " ] and can be accessed at",
    " <a class=\"external\"
    href=\"file://www.aasld.org/practiceguidelines/Pages/default.aspx\">",
    " www.aasld.org/practiceguidelines/Pages/default.aspx",
    " </a>",
    " . The discussion that follows is consistent with the AASLD guidelines.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H488642015\">",
    " <span class=\"h1\">",
    " FACTORS ASSOCIATED WITH A RESPONSE TO TREATMENT",
    " </span>",
    " &nbsp;&mdash;&nbsp;Several host and viral characteristics have been associated
    with a response to antiviral therapy and are discussed in detail elsewhere. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?14/8/14474?
    source=see_link\">",
    " \"Predictors of a sustained virologic response following treatment with
    peginterferon and ribavirin for chronic hepatitis C virus infection\"",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H488642863\">",
    " <span class=\"h1\">",
    " SELECTION OF PATIENTS FOR TREATMENT",
    " </span>",
    " &nbsp;&mdash;&nbsp;How to determine which patients are candidates for
    treatment is discussed elsewhere. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?37/59/38841?
    source=see_link\">",
    " \"Patient selection for antiviral therapy for chronic hepatitis C virus
    infection\"",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H488641848\">",
    " <span class=\"h1\">",
    " MONITORING VIRAL LOAD DURING THERAPY",
    " </span>",
    " &nbsp;&mdash;&nbsp;Once therapy has been started, the likelihood that a
    patient will fail to achieve a sustained virologic response (SVR) can be predicted
    by the virologic response at 12 weeks of therapy, and probably even earlier. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?14/8/14474?
    source=see_link&amp;anchor=H32984769#H32984769\">",
    " \"Predictors of a sustained virologic response following treatment with
    peginterferon and ribavirin for chronic hepatitis C virus infection\", section on
    'Changes in viral load during treatment'",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " A rapid virologic response is the strongest on-treatment predictor of
    achieving an SVR. Some but not all data suggest that shorter courses of therapy
    (eg, 24 weeks) may not adversely affect patients who achieve a rapid virologic
    response (negative HCV RNA after four weeks of treatment). (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?27/21/27990?
    source=see_link&amp;anchor=H15546553#H15546553\">",
    " \"Response-guided therapy for chronic hepatitis C virus infection\", section
    on 'Shortening therapy for patients who achieve an RVR'",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " An early virologic response (EVR) is defined as at least a 2 log",
    " <sub>",
    " 10",
    " </sub>",
    " reduction in HCV RNA or HCV RNA negativity by week 12. A patient with
    a \"complete EVR\" has attained complete viral suppression by week 12; a patient
    with a \"partial EVR\" has achieved greater than a 2 log",
    " <sub>",
    " 10",
    " </sub>",
    " decline in viremia but continues to have detectable HCV RNA. An SVR is
    unlikely in patients who lack an EVR, and it is generally recommended that
    treatment be stopped in patients who fail to achieve an EVR. Patients who
    are \"partial responders\" have lower overall SVR rates compared with complete
    responders (ie, no detectable viremia at 12 weeks). Studies are ongoing to
    determine if there are patients, such as patients who have a slow decline in HCV
    RNA, who would benefit from extended courses of therapy. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?27/21/27990?
    source=see_link&amp;anchor=H15546859#H15546859\">",
    " \"Response-guided therapy for chronic hepatitis C virus infection\", section
    on 'Lengthening therapy for those who fail to achieve a complete EVR'",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " We suggest that patients have their viral loads checked at baseline and at
    weeks 4, 12, and 24 of therapy to assess for a treatment response and to make
    decisions about continuing treatment or possibly altering the duration of
    treatment. Patients with an end of treatment response (negative HCV RNA at the
    completion of treatment) should also have a viral load checked 24 weeks after
    therapy is completed to assess for an SVR. An SVR is associated with a 99 percent
    chance of being HCV RNA negative during long-term follow-up [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/600/abstract/1\">",
    " 1",
    " </a>",
    " ].",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H19310924\">",
    " <span class=\"h1\">",
    " CHOICE OF PEGINTERFERON",
    " </span>",
    " &nbsp;&mdash;&nbsp;Peginterferon alfa-2a (Pegasys, Roche Pharmaceuticals) and
    peginterferon alfa-2b (Peg-Intron, Schering-Plough Corporation) differ in their
    pharmacokinetics. Studies comparing the two peginterferons in combination with",
    " <a class=\"drug drug_general\" href=\"UTD.htm?26/25/27033?source=see_link\">",
    " ribavirin",
    " </a>",
    " have had variable results [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/600/abstract/3-9\">",
    " 3-9",
    " </a>",
    " ]. While the largest randomized trial (IDEAL) showed that peginterferon alfa-
    2a and peginterferon alfa-2b appeared to have comparable efficacies in the
    treatment of chronic hepatitis C [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/600/abstract/4\">",
    " 4",
    " </a>",
    " ], meta-analyses suggest a slight advantage for peginterferon alfa-2a [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/600/abstract/10,11\">",
    " 10,11",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " One meta-analysis compared sustained virologic response (SVR) rates and
    adverse event rates between patients treated with peginterferon alfa-2a and alfa-2b
    [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/600/abstract/10\">",
    " 10",
    " </a>",
    " ]. The analysis included only randomized controlled trials. Eight trials with
    4335 patients were included in the analysis of SVR rates. The analysis found that
    peginterferon alfa-2a was superior to peginterferon alfa-2b (SVR rates of 47 versus
    41 percent; relative risk [RR] 1.11, 95% confidence interval [CI] 1.04-1.19).",
    " </p>",
    " <p>",
    " When patients with genotypes 1 and 4 were examined, the results continued to
    favor peginterferon alfa-2a (RR 1.21, 95% CI 1.03-1.24). Similar results were noted
    for patients with genotypes 2 and 3 (RR 1.11, 95% CI 1.02-1.22). There was no
    difference between the treatments with regard to adverse events, though the number
    of patients included in the meta-analysis was too small to draw definitive
    conclusions. We suggest treatment with peginterferon alfa-2a in patients with
    chronic HCV genotype 2, 3, or 4 rather than treatment with peginterferon alfa-2b.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H488644295\">",
    " <span class=\"h1\">",
    " DOSES OF PEGINTERFERON AND RIBAVIRIN",
    " </span>",
    " &nbsp;&mdash;&nbsp;There are two peginterferon preparations used in the
    treatment of HCV (peginterferon alfa-2a and peginterferon alfa-2b). The doses of
    peginterferon differ for the two preparations:",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " For peginterferon alfa-2a, the dose is 180 micrograms subcutaneously per
    week",
    " </li>",
    " <li>",
    " For peginterferon alfa-2b, the dose is 1.5",
    " <span class=\"nowrap\">",
    " microgram/kg",
    " </span>",
    " subcutaneously per week",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " Depending on the genotype being treated,",
    " <a class=\"drug drug_general\" href=\"UTD.htm?26/25/27033?source=see_link\">",
    " ribavirin",
    " </a>",
    " dosing may or may not be weight-based. Ribavirin is given in divided daily
    doses (typically twice per day). For genotypes 2 and 3, ribavirin dosing is not
    weight-based. Patients instead receive a standard dose of 800 mg (typically 400 mg
    twice daily).",
    " </p>",
    " <p>",
    " For genotype 4,",
    " <a class=\"drug drug_general\" href=\"UTD.htm?26/25/27033?source=see_link\">",
    " ribavirin",
    " </a>",
    " is weight-based:",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " For patients receiving peginterferon alfa-2a, the",
    " <a class=\"drug drug_general\" href=\"UTD.htm?26/25/27033?
    source=see_link\">",
    " ribavirin",
    " </a>",
    " dose is 1000 mg for patients who weigh 75 kg or less, or 1200 mg for those
    who weigh more than 75 kg.",
    " </li>",
    " <li>",
    " For patients receiving peginterferon alfa-2b, the",
    " <a class=\"drug drug_general\" href=\"UTD.htm?26/25/27033?
    source=see_link\">",
    " ribavirin",
    " </a>",
    " dose is 800 mg for patients weighing &lt;65 kg, 1000 mg for 65 to 85 kg,
    1200 mg for &gt;85 to 105 kg, and 1400 mg for &gt;105 kg.",
    " </li>",
    " </ul>",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H488642654\">",
    " <span class=\"h1\">",
    " TREATMENT REGIMENS",
    " </span>",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H488640991\">",
    " <span class=\"h2\">",
    " Treatment-naive patients",
    " </span>",
    " &nbsp;&mdash;&nbsp;Patients with genotype 2, 3, or 4 should receive dual
    therapy with peginterferon and",
    " <a class=\"drug drug_general\" href=\"UTD.htm?26/25/27033?source=see_link\">",
    " ribavirin",
    " </a>",
    " . Protease inhibitors are",
    " <strong>",
    " not",
    " </strong>",
    " used in the treatment of patients with genotype 2, 3, or 4.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H488642640\">",
    " <span class=\"h3\">",
    " Genotype 2 or 3",
    " </span>",
    " &nbsp;&mdash;&nbsp;Patients with genotype 2 or 3 should receive treatment with
    peginterferon and",
    " <a class=\"drug drug_general\" href=\"UTD.htm?26/25/27033?source=see_link\">",
    " ribavirin",
    " </a>",
    " . Ribavirin is not weight-based for the treatment of genotypes 2 or 3. All
    patients receive 800 mg in daily divided doses (typically 400 mg twice daily).
    Treatment with peginterferon plus ribavirin should be administered for 24 weeks in
    patients with genotype 2 or 3. These patients generally have a better response to
    peginterferon and ribavirin than those with genotype 1 or 4. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?14/8/14474?
    source=see_link&amp;anchor=H16092652#H16092652\">",
    " \"Predictors of a sustained virologic response following treatment with
    peginterferon and ribavirin for chronic hepatitis C virus infection\", section on
    'Viral factors'",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H488642647\">",
    " <span class=\"h3\">",
    " Genotype 4",
    " </span>",
    " &nbsp;&mdash;&nbsp;Patients with genotype 4 should received treatment with
    peginterferon and weight-based",
    " <a class=\"drug drug_general\" href=\"UTD.htm?26/25/27033?source=see_link\">",
    " ribavirin",
    " </a>",
    " . Treatment with peginterferon plus weight-based ribavirin should be planned
    for 48 weeks, but the actual duration of therapy will be determined in part by the
    viral response. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?27/21/27990?
    source=see_link\">",
    " \"Response-guided therapy for chronic hepatitis C virus infection\"",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " Treatment should be discontinued in patients who do not achieve at least a 2
    log",
    " <sub>",
    " 10",
    " </sub>",
    " reduction in HCV RNA at week 12 (ie, early virologic response). (See",
    " <a class=\"local\" href=\"#H488641848\">",
    " 'Monitoring viral load during therapy'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " Patients who have at least a 2 log",
    " <sub>",
    " 10",
    " </sub>",
    " reduction in HCV RNA but still have detectable HCV RNA at week 12 should be
    retested at week 24. Treatment should be discontinued if HCV RNA continues to be
    positive.",
    " </li>",
    " </ul>",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H12154514\">",
    " <span class=\"h2\">",
    " Relapsers and nonresponders",
    " </span>",
    " &nbsp;&mdash;&nbsp;Recommendations from the National Institutes of Health and
    the American Association for the Study of Liver Diseases suggest that retreatment
    of patients who did not achieve a sustained virologic response (SVR) with prior
    interferon-based therapy should be based upon:",
    " </p>",
    " <p>",
    " <ul class=\"bulletCompact-block\">",
    " <li>",
    " The previous type of response",
    " </li>",
    " <li>",
    " The previous therapy and the difference in the potency of the new therapy",
    " </li>",
    " <li>",
    " The severity of the underlying liver disease",
    " </li>",
    " <li>",
    " Viral genotype and other predictive factors of response",
    " </li>",
    " <li>",
    " Tolerance and compliance with previous therapy",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?42/45/43735?
    source=see_link\">",
    " \"Overview of the management of chronic hepatitis C virus infection\"",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?40/23/41337?
    source=see_link&amp;anchor=H12156576#H12156576\">",
    " \"Mechanism of action and efficacy of peginterferon for the treatment of
    chronic hepatitis C virus infection\", section on 'Retreatment of prior
    nonresponders'",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H12154102\">",
    " <span class=\"h3\">",
    " Prior treatment with standard interferon monotherapy",
    " </span>",
    " &nbsp;&mdash;&nbsp;In patients who relapse after an initial response to
    interferon monotherapy, we recommend combination therapy with peginterferon plus
    weight-based",
    " <a class=\"drug drug_general\" href=\"UTD.htm?26/25/27033?source=see_link\">",
    " ribavirin",
    " </a>",
    " .",
    " </p>",
    " <p>",
    " Patients who are nonresponders to interferon monotherapy are less likely to
    respond to combination therapy compared with those who relapsed [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/600/abstract/12\">",
    " 12",
    " </a>",
    " ]. In prior nonresponders, we suggest a trial of combination therapy with
    peginterferon and",
    " <a class=\"drug drug_general\" href=\"UTD.htm?26/25/27033?source=see_link\">",
    " ribavirin",
    " </a>",
    " in patients who tolerated interferon monotherapy and have moderate to advanced
    histologic features on liver biopsy.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H12154109\">",
    " <span class=\"h3\">",
    " Prior treatment with standard interferon and ribavirin",
    " </span>",
    " &nbsp;&mdash;&nbsp;Options for nonresponders or relapsers following
    combination therapy with standard interferon and",
    " <a class=\"drug drug_general\" href=\"UTD.htm?26/25/27033?source=see_link\">",
    " ribavirin",
    " </a>",
    " include observation, enrollment in a clinical trial, or a course of
    peginterferon plus ribavirin.",
    " </p>",
    " <p>",
    " Data suggest that the response to peginterferon plus",
    " <a class=\"drug drug_general\" href=\"UTD.htm?26/25/27033?source=see_link\">",
    " ribavirin",
    " </a>",
    " in these patients is in the range of 10 to 20 percent overall, though the
    studies also included patients with genotype 1 [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/600/abstract/13\">",
    " 13",
    " </a>",
    " ]. Higher response rates are seen in patients infected with genotype 2 or 3,
    in relapsers, and in patients who do not have cirrhosis. If treatment is to be
    given, we suggest it be administered for 24 weeks for patients with genotype 2 or 3
    or for 48 weeks for patients with genotype 4.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H12154116\">",
    " <span class=\"h3\">",
    " Prior treatment with peginterferon and ribavirin",
    " </span>",
    " &nbsp;&mdash;&nbsp;The treatment of patients who are nonresponders to
    peginterferon and",
    " <a class=\"drug drug_general\" href=\"UTD.htm?26/25/27033?source=see_link\">",
    " ribavirin",
    " </a>",
    " is unsettled. For those who failed treatment with a full course of
    peginterferon alfa-2a or alfa-2b plus ribavirin, we generally do not suggest
    retreatment with peginterferon and ribavirin.",
    " </p>",
    " <p>",
    " Retreatment can be considered in selected patients who had a partial response
    to previous therapy or had an interrupted or inadequate course of therapy. The
    results of the patient's liver biopsy help guide the decision to retreat. If the
    biopsy was performed within five years and there was minimal or no fibrosis, we do
    not retreat. If the biopsy showed moderate or severe fibrosis and the patient
    tolerated therapy well, we will offer the patient retreatment. For patients who did
    not tolerate the treatment, the decision to offer retreatment is less clear and
    will depend in large part on the patient's preferences. For patients who have not
    had a liver biopsy within the last five years, we repeat the liver biopsy prior to
    making retreatment decisions.",
    " </p>",
    " <p>",
    " There is some evidence supporting the use of a different form of peginterferon
    for patients who are being retreated. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?40/23/41337?
    source=see_link&amp;anchor=H12156576#H12156576\">",
    " \"Mechanism of action and efficacy of peginterferon for the treatment of
    chronic hepatitis C virus infection\", section on 'Retreatment of prior
    nonresponders'",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H12158458\">",
    " <span class=\"h1\">",
    " MAINTENANCE THERAPY IN NONRESPONDERS",
    " </span>",
    " &nbsp;&mdash;&nbsp;Several studies had suggested that interferon-based
    treatments may be associated with clinical improvement, even in patients who do not
    achieve an SVR. However, final results of the HALT-C trial (evaluating low-dose
    peginterferon alfa-2a) were negative; long-term maintenance therapy did not halt
    liver disease progression [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/600/abstract/14\">",
    " 14",
    " </a>",
    " ]. Currently, maintenance therapy is not recommended for nonresponders. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?40/23/41337?
    source=see_link&amp;anchor=H6411393#H6411393\">",
    " \"Mechanism of action and efficacy of peginterferon for the treatment of
    chronic hepatitis C virus infection\", section on 'Maintenance therapy in
    nonresponders'",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H12154559\">",
    " <span class=\"h1\">",
    " TREATMENT IN SPECIAL POPULATIONS",
    " </span>",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H12154826\">",
    " <span class=\"h2\">",
    " Recurrence after liver transplantation",
    " </span>",
    " &nbsp;&mdash;&nbsp;Recurrence of HCV occurs in more than 95 percent of
    patients after liver transplantation. However, the therapeutic options are limited
    in this population, and rigorous clinical trials are difficult to conduct. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?16/5/16474?
    source=see_link&amp;anchor=H15#H15\">",
    " \"Liver transplantation for hepatitis C virus infection\", section on
    'Treatment of recurrence'",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H12154772\">",
    " <span class=\"h2\">",
    " Coinfection with HIV",
    " </span>",
    " &nbsp;&mdash;&nbsp;All human immunodeficiency virus (HIV) infected patients
    should undergo screening for HCV. Treatment should be considered in these patients
    because coinfection is associated with an accelerated course of HCV. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?17/38/18026?
    source=see_link\">",
    " \"Treatment of hepatitis C virus infection in the HIV-infected patient\"",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H12154615\">",
    " <span class=\"h2\">",
    " Thalassemia",
    " </span>",
    " &nbsp;&mdash;&nbsp;HCV infection in patients with thalassemia is common, with
    reported prevalences of anti-HCV antibodies in such patients of 4 to 85 percent [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/600/abstract/15\">",
    " 15",
    " </a>",
    " ]. Treatment in these patients may be complicated by the hemolysis associated
    with",
    " <a class=\"drug drug_general\" href=\"UTD.htm?26/25/27033?source=see_link\">",
    " ribavirin",
    " </a>",
    " , leading to worsening iron overload. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?16/9/16538?
    source=see_link&amp;anchor=H3#H3\">",
    " \"Management of the side effects of peginterferon and ribavirin being used
    for treatment of chronic hepatitis C virus infection\", section on 'Anemia'",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " Guidelines from the American Society of Hematology recommend the following [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/600/abstract/15\">",
    " 15",
    " </a>",
    " ]:",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " Combination therapy with peginterferon plus",
    " <a class=\"drug drug_general\" href=\"UTD.htm?26/25/27033?
    source=see_link\">",
    " ribavirin",
    " </a>",
    " should be suggested to patients with HCV chronic hepatitis or compensated
    cirrhosis.",
    " </li>",
    " <li>",
    " Therapy should be administered for 48 weeks to patients infected by genotype
    4 and for 24 weeks for patients infected by genotype 2 or 3.",
    " </li>",
    " <li>",
    " In patients infected with genotype 4, antiviral therapy should be withdrawn
    after 12 weeks if serum HCV RNA levels have not decreased by at least 2 log",
    " <sub>",
    " 10",
    " </sub>",
    " compared with baseline.",
    " </li>",
    " <li>",
    " An increase in the number of blood transfusions during antiviral therapy may
    be required to maintain a hemoglobin level of more than 9",
    " <span class=\"nowrap\">",
    " g/dL.",
    " </span>",
    " The guidelines do not recommend the use of growth factors such as
    erythropoietin (which is already elevated in these patients).",
    " </li>",
    " <li>",
    " Intensification of chelation treatment before starting antiviral treatment
    should be considered in patients with severe iron burden. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?7/39/7802?
    source=see_link&amp;anchor=H19#H19\">",
    " \"Treatment of beta thalassemia\", section on 'Iron chelation therapy'",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?24/49/25370?
    source=see_link\">",
    " \"Chelation therapy for iron overload states\"",
    " </a>",
    " .)",
    " </li>",
    " <li>",
    " Clinical monitoring of liver disease is necessary in thalassemia patients
    with HCV chronic hepatitis or cirrhosis who have contraindications to antiviral
    therapy or have failed previous antiviral therapy.",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " There are no guidelines about whether patients with a drop in hemoglobin
    during treatment with",
    " <a class=\"drug drug_general\" href=\"UTD.htm?26/25/27033?source=see_link\">",
    " ribavirin",
    " </a>",
    " should have their ribavirin dose reduced. In one study of patients with
    thalassemia undergoing treatment for HCV, the dose of ribavirin was reduced if the
    patient's blood transfusion requirement doubled [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/600/abstract/16\">",
    " 16",
    " </a>",
    " ]. Until additional data become available, we believe that it is reasonable to
    decrease the dose of ribavirin by 200",
    " <span class=\"nowrap\">",
    " mg/day",
    " </span>",
    " in patients whose transfusion requirements double.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H12153764\">",
    " <span class=\"h1\">",
    " SIDE EFFECTS OF TREATMENT",
    " </span>",
    " &nbsp;&mdash;&nbsp;The side effects of interferon (standard or pegylated)
    and",
    " <a class=\"drug drug_general\" href=\"UTD.htm?26/25/27033?source=see_link\">",
    " ribavirin",
    " </a>",
    " , as well as their management, are discussed elsewhere. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?16/9/16538?
    source=see_link\">",
    " \"Management of the side effects of peginterferon and ribavirin being used
    for treatment of chronic hepatitis C virus infection\"",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H60837661\">",
    " <span class=\"h1\">",
    " FOLLOW-UP AFTER TREATMENT",
    " </span>",
    " &nbsp;&mdash;&nbsp;Patients who achieve an SVR who do not have cirrhosis do
    not require any specific follow-up for their HCV, though some will check an HCV
    viral load one year after the completion of treatment to confirm that the patient
    has achieved an SVR. Patients who fail to achieve an SVR should be followed for
    signs of progression of their liver disease. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?30/50/31530?
    source=see_link\">",
    " \"Clinical manifestations and natural history of chronic hepatitis C virus
    infection\"",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?22/41/23194?
    source=see_link&amp;anchor=H2#H2\">",
    " \"Diagnostic approach to the patient with cirrhosis\", section on 'Clinical
    manifestations'",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?42/45/43735?
    source=see_link&amp;anchor=H3#H3\">",
    " \"Overview of the management of chronic hepatitis C virus infection\",
    section on 'General management'",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " Patients with cirrhosis, regardless of whether they attain an SVR, require
    ongoing monitoring because they continue to be at risk of hepatocellular
    carcinoma&nbsp;and require ongoing surveillance. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?16/59/17337?
    source=see_link&amp;anchor=H15#H15\">",
    " \"Overview of the complications, prognosis, and management of cirrhosis\",
    section on 'Treatment'",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"PATIENT_INFORMATION\">",
    " <span class=\"h1\">",
    " INFORMATION FOR PATIENTS",
    " </span>",
    " &nbsp;&mdash;&nbsp;UpToDate offers two types of patient education
    materials, \"The Basics\" and \"Beyond the Basics.\" The Basics patient education
    pieces are written in plain language, at the 5",
    " <sup>",
    " th",
    " </sup>",
    " to 6",
    " <sup>",
    " th",
    " </sup>",
    " grade reading level, and they answer the four or five key questions a patient
    might have about a given condition. These articles are best for patients who want a
    general overview and who prefer short, easy-to-read materials. Beyond the Basics
    patient education pieces are longer, more sophisticated, and more detailed. These
    articles are written at the 10",
    " <sup>",
    " th",
    " </sup>",
    " to 12",
    " <sup>",
    " th",
    " </sup>",
    " grade reading level and are best for patients who want in-depth information
    and are comfortable with some medical jargon.",
    " </p>",
    " <p>",
    " Here are the patient education articles that are relevant to this topic. We
    encourage you to print or e-mail these topics to your patients. (You can also
    locate patient education articles on a variety of subjects by searching
    on \"patient info\" and the keyword(s) of interest.)",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " Basics topics (see",
    " <a class=\"medical medical_basics\" href=\"UTD.htm?4/22/4451?
    source=see_link\">",
    " \"Patient information: Latest medicines for hepatitis C (The Basics)\"",
    " </a>",
    " and",
    " <a class=\"medical medical_basics\" href=\"UTD.htm?29/35/30258?
    source=see_link\">",
    " \"Patient information: Treatment for hepatitis C (The Basics)\"",
    " </a>",
    " )",
    " </li>",
    " </ul>",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H12156966\">",
    " <span class=\"h1\">",
    " SUMMARY AND RECOMMENDATIONS",
    " </span>",
    " &nbsp;&mdash;&nbsp;The decision to treat a patient with chronic hepatitis C
    virus (HCV) infection is based upon several factors, including the natural history
    of the disease, the stage of fibrosis, and the efficacy and adverse effects related
    to therapy. In general, patients being considered for treatment should have
    histologic and virologic evidence of chronic HCV infection. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?42/45/43735?
    source=see_link\">",
    " \"Overview of the management of chronic hepatitis C virus infection\"",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?37/59/38841?
    source=see_link\">",
    " \"Patient selection for antiviral therapy for chronic hepatitis C virus
    infection\"",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " <strong>",
    " Genotype 2 or 3:",
    " </strong>",
    " For patients with genotype 2 or 3 who are candidates for therapy, we
    recommend treatment with peginterferon and",
    " <a class=\"drug drug_general\" href=\"UTD.htm?26/25/27033?
    source=see_link\">",
    " ribavirin",
    " </a>",
    " (not weight-based) rather than treating with standard interferon and
    ribavirin or peginterferon monotherapy (",
    " <a class=\"grade\" href=\"._grade_1?title=Grade 1A\">",
    " Grade 1A",
    " </a>",
    " ). Treatment with peginterferon plus ribavirin should be administered for 24
    weeks in patients with genotype 2 or 3. (See",
    " <a class=\"local\" href=\"#H488640991\">",
    " 'Treatment-naive patients'",
    " </a>",
    " above and",
    " <a class=\"local\" href=\"#H12154514\">",
    " 'Relapsers and nonresponders'",
    " </a>",
    " above and",
    " <a class=\"local\" href=\"#H488644295\">",
    " 'Doses of peginterferon and ribavirin'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " <strong>",
    " Genotype 4:",
    " </strong>",
    " For patients with genotype 4 who are candidates for therapy, we recommend
    treatment with peginterferon and weight-based",
    " <a class=\"drug drug_general\" href=\"UTD.htm?26/25/27033?
    source=see_link\">",
    " ribavirin",
    " </a>",
    " rather than treating with standard interferon and ribavirin or peginterferon
    monotherapy (",
    " <a class=\"grade\" href=\"._grade_1?title=Grade 1A\">",
    " Grade 1A",
    " </a>",
    " ). Treatment with peginterferon plus weight-based ribavirin should be
    planned for 48 weeks, but the actual duration of therapy will be determined in part
    by the viral response. (See",
    " <a class=\"local\" href=\"#H488640991\">",
    " 'Treatment-naive patients'",
    " </a>",
    " above and",
    " <a class=\"local\" href=\"#H12154514\">",
    " 'Relapsers and nonresponders'",
    " </a>",
    " above and",
    " <a class=\"local\" href=\"#H488641848\">",
    " 'Monitoring viral load during therapy'",
    " </a>",
    " above and",
    " <a class=\"local\" href=\"#H488644295\">",
    " 'Doses of peginterferon and ribavirin'",
    " </a>",
    " above.)",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " <ul class=\"hyphen-block\">",
    " <li>",
    " Treatment should be discontinued in patients who do not achieve at least a 2
    log",
    " <sub>",
    " 10",
    " </sub>",
    " reduction in HCV RNA at week 12 (ie, early virologic response).",
    " </li>",
    " <li>",
    " Patients who have at least a 2 log",
    " <sub>",
    " 10",
    " </sub>",
    " reduction in HCV RNA but still have detectable HCV RNA at week 12 should be
    retested at week 24. Treatment should be discontinued if HCV RNA continues to be
    positive at week 24.",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " For patients with chronic hepatitis C genotype 2, 3, or 4, we suggest
    treatment with peginterferon alfa-2a rather than peginterferon alfa-2b (",
    " <a class=\"grade\" href=\"._grade_5?title=Grade 2B\">",
    " Grade 2B",
    " </a>",
    " ). (See",
    " <a class=\"local\" href=\"#H19310924\">",
    " 'Choice of peginterferon'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " We suggest that patients have their viral loads checked at baseline and at
    weeks 4, 12, and 24 of therapy to assess for a treatment response and to make
    decisions about continuing treatment or possibly altering the duration of
    treatment. Patients should also have a viral load checked 24 weeks after therapy is
    completed to assess for an SVR. (See",
    " <a class=\"local\" href=\"#H488641848\">",
    " 'Monitoring viral load during therapy'",
    " </a>",
    " above.)",
    " </li>",
    " </ul>",
    " </p>",
    " </div>",
    " <div id=\"topicAgreement\">",
    " Use of UpToDate is subject to the",
    " <a class=\"licenseLink\" href=\"./license\" id=\"sla_in_page\"
    target=\"_blank\">",
    " Subscription and License Agreement",
    " </a>",
    " .",
    " </div>",
    " <div class=\"headingAnchor\" id=\"references\">",
    " <h1>",
    " REFERENCES",
    " </h1>",
    " <ol id=\"reference\">",
    " <li>",
    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/600/abstract/1\">",
    " Swain MG, Lai MY, Shiffman ML, et al. A sustained virologic response is
    durable in patients with chronic hepatitis C treated with peginterferon alfa-2a and
    ribavirin. Gastroenterology 2010; 139:1593.",
    " </a>",
    " </li>",
    " <li>",
    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/600/abstract/2\">",
    " Ghany MG, Strader DB, Thomas DL, et al. Diagnosis, management, and treatment
    of hepatitis C: an update. Hepatology 2009; 49:1335.",
    " </a>",
    " </li>",
    " <li>",
    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/600/abstract/3\">",
    " Silva M, Poo J, Wagner F, et al. A randomised trial to compare the
    pharmacokinetic, pharmacodynamic, and antiviral effects of peginterferon alfa-2b
    and peginterferon alfa-2a in patients with chronic hepatitis C (COMPARE). J Hepatol
    2006; 45:204.",
    " </a>",
    " </li>",
    " <li>",
    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/600/abstract/4\">",
    " McHutchison JG, Lawitz EJ, Shiffman ML, et al. Peginterferon alfa-2b or
    alfa-2a with ribavirin for treatment of hepatitis C infection. N Engl J Med 2009;
    361:580.",
    " </a>",
    " </li>",
    " <li>",
    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/600/abstract/5\">",
    " Di Bisceglie AM, Ghalib RH, Hamzeh FM, Rustgi VK. Early virologic response
    after peginterferon alpha-2a plus ribavirin or peginterferon alpha-2b plus
    ribavirin treatment in patients with chronic hepatitis C. J Viral Hepat 2007;
    14:721.",
    " </a>",
    " </li>",
    " <li>",
    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/600/abstract/6\">",
    " Laguno M, Cifuentes C, Murillas J, et al. Randomized trial comparing
    pegylated interferon alpha-2b versus pegylated interferon alpha-2a, both plus
    ribavirin, to treat chronic hepatitis C in human immunodeficiency virus patients.
    Hepatology 2009; 49:22.",
    " </a>",
    " </li>",
    " <li>",
    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/600/abstract/7\">",
    " Rumi MG, Aghemo A, Prati GM, et al. Randomized study of peginterferon-
    alpha2a plus ribavirin vs peginterferon-alpha2b plus ribavirin in chronic hepatitis
    C. Gastroenterology 2010; 138:108.",
    " </a>",
    " </li>",
    " <li>",
    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/600/abstract/8\">",
    " Ascione A, De Luca M, Tartaglione MT, et al. Peginterferon alfa-2a plus
    ribavirin is more effective than peginterferon alfa-2b plus ribavirin for treating
    chronic hepatitis C virus infection. Gastroenterology 2010; 138:116.",
    " </a>",
    " </li>",
    " <li>",
    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/600/abstract/9\">",
    " Awad T, Thorlund K, Hauser G, et al; Cochrane Hepato-Biliary Group.
    Peginterferon alpha-2a may achieve higher sustained virological response than
    peginteferon alpha-2b in chronic hepatitis C: a Cochrane systematic review of
    randomized clinical trials. Hepatology 2009; 50(Suppl):707A.",
    " </a>",
    " </li>",
    " <li>",
    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/600/abstract/10\">",
    " Awad T, Thorlund K, Hauser G, et al. Peginterferon alpha-2a is associated
    with higher sustained virological response than peginterferon alfa-2b in chronic
    hepatitis C: systematic review of randomized trials. Hepatology 2010; 51:1176.",
    " </a>",
    " </li>",
    " <li>",
    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/600/abstract/11\">",
    " Flori N, Funakoshi N, Duny Y, et al. Pegylated Interferon-&alpha;2a and
    Ribavirin versus Pegylated Interferon-&alpha;2b and Ribavirin in Chronic Hepatitis
    C : A Meta-Analysis. Drugs 2013; 73:263.",
    " </a>",
    " </li>",
    " <li>",
    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/600/abstract/12\">",
    " Cheng SJ, Bonis PA, Lau J, et al. Interferon and ribavirin for patients with
    chronic hepatitis C who did not respond to previous interferon therapy: a meta-
    analysis of controlled and uncontrolled trials. Hepatology 2001; 33:231.",
    " </a>",
    " </li>",
    " <li>",
    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/600/abstract/13\">",
    " Singal AG, Waljee AK, Shiffman M, et al. Meta-analysis: re-treatment of
    genotype I hepatitis C nonresponders and relapsers after failing interferon and
    ribavirin combination therapy. Aliment Pharmacol Ther 2010; 32:969.",
    " </a>",
    " </li>",
    " <li>",
    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/600/abstract/14\">",
    " Di Bisceglie AM, Shiffman ML, Everson GT, et al. Prolonged therapy of
    advanced chronic hepatitis C with low-dose peginterferon. N Engl J Med 2008;
    359:2429.",
    " </a>",
    " </li>",
    " <li>",
    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/600/abstract/15\">",
    " Di Marco V, Capra M, Angelucci E, et al. Management of chronic viral
    hepatitis in patients with thalassemia: recommendations from an international
    panel. Blood 2010; 116:2875.",
    " </a>",
    " </li>",
    " <li>",
    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/600/abstract/16\">",
    " Sood A, Sobti P, Midha V, et al. Efficacy and safety of pegylated IFN alfa
    2b alone or in combination with ribavirin in thalassemia major with chronic
    hepatitis C. Indian J Gastroenterol 2010; 29:62.",
    " </a>",
    " </li>",
    " </ol>",
    " </div>",
    " <div id=\"topicVersionRevision\">",
    " Topic 15795 Version 16.0",
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    " <a href=\"#\" title=\"Collapse Topic Outline\">",
    " <img alt=\"\" src=\"./../images/orange_arrow_left.myextg\"/>",
    " </a>",
    " </div>",
    " <div id=\"innerOutline\">",
    " <h1>",
    " TOPIC OUTLINE",
    " </h1>",
    " <div id=\"outline\">",
    " <ul>",
    " <li>",
    " <a class=\"sr_button\" href=\"#H12156966\" id=\"summRecButton\">",
    " <span>",
    " SUMMARY &amp; RECOMMENDATIONS",
    " </span>",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H12153729\">",
    " INTRODUCTION",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H19315213\">",
    " GUIDELINES",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H488642015\">",
    " FACTORS ASSOCIATED WITH A RESPONSE TO TREATMENT",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H488642863\">",
    " SELECTION OF PATIENTS FOR TREATMENT",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H488641848\">",
    " MONITORING VIRAL LOAD DURING THERAPY",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H19310924\">",
    " CHOICE OF PEGINTERFERON",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H488644295\">",
    " DOSES OF PEGINTERFERON AND RIBAVIRIN",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H488642654\">",
    " TREATMENT REGIMENS",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H488640991\">",
    " Treatment-naive patients",
    " </a>",
    " </li>",
    " <li class=\"dashItem\">",
    " <a class=\"outlineLink\" href=\"#H488642640\">",
    " - Genotype 2 or 3",
    " </a>",
    " </li>",
    " <li class=\"dashItem\">",
    " <a class=\"outlineLink\" href=\"#H488642647\">",
    " - Genotype 4",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H12154514\">",
    " Relapsers and nonresponders",
    " </a>",
    " </li>",
    " <li class=\"dashItem\">",
    " <a class=\"outlineLink\" href=\"#H12154102\">",
    " - Prior treatment with standard interferon monotherapy",
    " </a>",
    " </li>",
    " <li class=\"dashItem\">",
    " <a class=\"outlineLink\" href=\"#H12154109\">",
    " - Prior treatment with standard interferon and ribavirin",
    " </a>",
    " </li>",
    " <li class=\"dashItem\">",
    " <a class=\"outlineLink\" href=\"#H12154116\">",
    " - Prior treatment with peginterferon and ribavirin",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H12158458\">",
    " MAINTENANCE THERAPY IN NONRESPONDERS",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H12154559\">",
    " TREATMENT IN SPECIAL POPULATIONS",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H12154826\">",
    " Recurrence after liver transplantation",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H12154772\">",
    " Coinfection with HIV",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H12154615\">",
    " Thalassemia",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H12153764\">",
    " SIDE EFFECTS OF TREATMENT",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H60837661\">",
    " FOLLOW-UP AFTER TREATMENT",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#PATIENT_INFORMATION\">",
    " INFORMATION FOR PATIENTS",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H12156966\">",
    " SUMMARY AND RECOMMENDATIONS",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a href=\"#references\">",
    " REFERENCES",
    " </a>",
    " </li>",
    " </ul>",
    " </div>",
    " <h1>",
    " RELATED TOPICS",
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    " </div>",
    " </div>"].join("\n");
    var title_f0_37_601="Impact of universal infant immunization with pneumococcal
    (Streptococcus pneumoniae) conjugate vaccines in the United States";
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    " <div id=\"topicContent\">",
    " <div id=\"topicTitle\">",
    " Impact of universal infant immunization with pneumococcal (Streptococcus
    pneumoniae) conjugate vaccines in the United States",
    " </div>",
    " <div id=\"topicContributors\">",
    " <div>",
    " <a id=\"authors\">",
    " </a>",
    " <a class=\"contributor contributor_credentials contributorType\"
    href=\"UTD.htm?0/37/601/contributors\">",
    " Author",
    " </a>",
    " <br/>",
    " <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
    0/37/601/contributors\">",
    " Elaine I Tuomanen, MD",
    " </a>",
    " <br/>",
    " </div>",
    " <div>",
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    href=\"UTD.htm?0/37/601/contributors\">",
    " Section Editor",
    " </a>",
    " <br/>",
    " <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
    0/37/601/contributors\">",
    " Sheldon L Kaplan, MD",
    " </a>",
    " <br/>",
    " </div>",
    " <div>",
    " <a class=\"contributor contributor_credentials contributorType\"
    href=\"UTD.htm?0/37/601/contributors\">",
    " Deputy Editor",
    " </a>",
    " <br/>",
    " <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
    0/37/601/contributors\">",
    " Mary M Torchia, MD",
    " </a>",
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    " Literature review current through:",
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    " Oct 2013.",
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    " This topic last updated:",
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    " Feb 28, 2013.",
    " </div>",
    " <div id=\"topicText\">",
    " <p class=\"headingAnchor\" id=\"H1\">",
    " <span class=\"h1\">",
    " INTRODUCTION",
    " </span>",
    " &nbsp;&mdash;&nbsp;",
    " <em>",
    " Streptococcus pneumoniae",
    " </em>",
    " (",
    " <em>",
    " pneumococcus",
    " </em>",
    " ) is a leading cause of serious illness among children worldwide [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/1\">",
    " 1",
    " </a>",
    " ]. Before universal infant immunization with pneumococcal conjugate vaccine in
    the United States,",
    " <em>",
    " S. pneumoniae",
    " </em>",
    " caused approximately 17,000 cases of invasive disease each year among children
    younger than five years of age, including 700 cases of meningitis and 200 deaths
    [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/1\">",
    " 1",
    " </a>",
    " ]. It was the most frequent cause of bacteremia, bacterial pneumonia,
    bacterial meningitis, sinusitis, and acute otitis media [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/1\">",
    " 1",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " The 7-valent pneumococcal conjugate vaccine (PCV7) was added to the schedule
    of recommended vaccines for children younger than two years of age in the United
    States in 2000 [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/1,2\">",
    " 1,2",
    " </a>",
    " ]. PCV7 contains serotypes 4, 6B, 9V, 14, 18C, 19F, and 23F conjugated to a
    mutant of diphtheria toxoid (",
    " <a class=\"graphic graphic_table graphicRef77274 \" href=\"UTD.htm?
    14/59/15293\">",
    " table 1",
    " </a>",
    " ). The routine use of PCV7 resulted in a decreased incidence of invasive
    pneumococcal disease in children. However, there were increasing data to suggest
    that universal infant immunization with PCV7 changed the serotype patterns of
    invasive disease, nasopharyngeal (NP) colonization, and antibiotic resistance
    patterns. In 2010, a 13-valent pneumococcal conjugate vaccine replaced PCV7 in the
    routine childhood immunization schedule [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/3\">",
    " 3",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " The impact of universal infant immunization with PCV7 and PCV13 on invasive
    serotypes, nasopharyngeal flora, and antibiotic resistance in children in the
    United States will be reviewed here. The impact in adults is discussed separately.
    (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?7/29/7642?
    source=see_link&amp;anchor=H3#H3\">",
    " \"Invasive pneumococcal (Streptococcus pneumoniae) infections and
    bacteremia\", section on 'Impact of childhood vaccination'",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " Pneumococcal conjugate and polysaccharide vaccines also are discussed
    separately. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?7/14/7402?
    source=see_link\">",
    " \"Pneumococcal (Streptococcus pneumoniae) conjugate vaccines in children\"",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?13/38/13926?
    source=see_link\">",
    " \"Pneumococcal (Streptococcus pneumoniae) polysaccharide vaccines in
    children\"",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?21/12/21705?
    source=see_link\">",
    " \"Pneumococcal vaccination in adults\"",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H2\">",
    " <span class=\"h1\">",
    " EFFICACY",
    " </span>",
    " &nbsp;&mdash;&nbsp;Surveillance after the introduction of the 7-valent
    pneumococcal conjugate vaccine (PCV7) to the standard childhood immunization
    schedule has shown that the vaccine is effective in preventing invasive
    pneumococcal disease (IPD) and providing herd immunity (",
    " <a class=\"graphic graphic_figure graphicRef64834 \" href=\"UTD.htm?
    10/26/10658\">",
    " figure 1",
    " </a>",
    " ). In 2003, it was estimated that 29,599 cases of vaccine serotype IPD were
    prevented through routine immunization. Approximately two-thirds of these cases
    were prevented through herd immunity [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/4\">",
    " 4",
    " </a>",
    " ]. The greatest decline has been noted in pneumococcal bacteremia without a
    focus.",
    " </p>",
    " <p>",
    " The efficacy of universal infant immunization with PCV7 in the United States
    on the incidence of IPD in children and adults is discussed in detail separately.
    (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?7/14/7402?
    source=see_link&amp;anchor=H8#H8\">",
    " \"Pneumococcal (Streptococcus pneumoniae) conjugate vaccines in children\",
    section on 'Efficacy and effectiveness'",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?7/29/7642?
    source=see_link&amp;anchor=H3#H3\">",
    " \"Invasive pneumococcal (Streptococcus pneumoniae) infections and
    bacteremia\", section on 'Impact of childhood vaccination'",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H9889776\">",
    " <span class=\"h1\">",
    " INVASIVE DISEASE CAUSED BY NON-VACCINE SEROTYPES",
    " </span>",
    " &nbsp;&mdash;&nbsp;Surveillance of pneumococcal isolates in children with
    invasive pneumococcal disease (IPD) indicates that, after the introduction of the
    7-valent pneumococcal conjugate vaccine (PCV7) to the routine childhood
    immunization schedule, there was an increase in the proportion of cases of IPD
    caused by nonvaccine serotypes (eg, replacement serotypes), including serotypes
    19A, 6C, and 22F, and serogroups 15 and 33 (",
    " <a class=\"graphic graphic_figure graphicRef64834 \" href=\"UTD.htm?
    10/26/10658\">",
    " figure 1",
    " </a>",
    " ) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/4-22\">",
    " 4-22",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " However, the increase in IPD caused by nonvaccine serotypes was small compared
    with the overall decline in IPD [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/4\">",
    " 4",
    " </a>",
    " ]. Data from the CDC Active Bacterial Core (ABC) surveillance indicate that in
    2003, there was an estimated increase of IPD caused by nonvaccine serotypes of 4721
    cases, whereas there was an estimated decrease in IPD caused by vaccine serotypes
    of 29,599 cases: a net decline of 24,878 cases [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/4\">",
    " 4",
    " </a>",
    " ]. An increase in the proportion of IPD due to nonvaccine serotypes was noted
    in a number of other studies [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/5-20\">",
    " 5-20",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " Surveillance from eight children&rsquo;s hospitals in the United States
    following introduction of PCV13 in 2010 indicates that the most common non-PCV13
    serotypes isolated from children hospitalized with IPD were 33F, 22F, 12, 15B, 15C,
    23A, and 11 [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/23\">",
    " 23",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " These reports highlight the ability of pneumococcus to adapt to vaccine
    selective pressure and the need to remain vigilant for the invasive disease caused
    by nonvaccine serotypes. Factors other than the use of pneumococcal conjugate
    vaccines (eg, patterns of antibiotic use) may contribute to IPD epidemiology [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/24-26\">",
    " 24-26",
    " </a>",
    " ].",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H4\">",
    " <span class=\"h2\">",
    " Serotype 19A",
    " </span>",
    " &nbsp;&mdash;&nbsp;Among children, serotype 19A emerged as an important cause
    of IPD by replacement serotypes after the introduction of the 7-valent pneumococcal
    conjugate vaccine [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/16,22,27-29\">",
    " 16,22,27-29",
    " </a>",
    " ]. Serotype 19A also emerged as an important cause of multidrug-resistant
    acute otitis media, coalescent mastoiditis, and chronic sinusitis [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/30-33\">",
    " 30-33",
    " </a>",
    " ]. Serotype 19A is included in the 13-valent pneumococcal conjugate vaccine
    that was licensed in 2010. Surveillance from eight children&rsquo;s hospitals in
    the United States following introduction of PCV13 in 2010 demonstrated a 58 percent
    decline in IPD due to serotype 19A among hospitalized children; but 19A remained
    the most frequently isolated serotype [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/23\">",
    " 23",
    " </a>",
    " ]. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?28/60/29642?
    source=see_link&amp;anchor=H16#H16\">",
    " \"Acute otitis media in children: Epidemiology, microbiology, clinical
    manifestations, and complications\", section on 'Microbiology'",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?7/14/7402?
    source=see_link&amp;anchor=H6#H6\">",
    " \"Pneumococcal (Streptococcus pneumoniae) conjugate vaccines in children\",
    section on 'Other vaccines'",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H5\">",
    " <span class=\"h1\">",
    " NASOPHARYNGEAL FLORA",
    " </span>",
    " &nbsp;&mdash;&nbsp;Studies evaluating the effects of universal immunization
    with the 7-valent pneumococcal conjugate vaccine (PCV7) on nasopharyngeal (NP)
    carriage have shown that vaccination does not change the overall rate of
    pneumococcal carriage [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/20,34-38\">",
    " 20,34-38",
    " </a>",
    " ]. However, it does reduce the acquisition of vaccine serotypes and increases
    the acquisition of nonvaccine serotypes [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/7,20,35-48\">",
    " 7,20,35-48",
    " </a>",
    " ].",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H6\">",
    " <span class=\"h2\">",
    " PCV7 serotypes",
    " </span>",
    " &nbsp;&mdash;&nbsp;Conjugate vaccines reduce NP carriage of the serotypes
    included in the vaccine (",
    " <a class=\"graphic graphic_table graphicRef77274 \" href=\"UTD.htm?
    14/59/15293\">",
    " table 1",
    " </a>",
    " ) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/35-37,39-43,47,48\">",
    " 35-37,39-43,47,48",
    " </a>",
    " ]. This was demonstrated in several pre-licensure investigations of small
    cohorts of children [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/39,40\">",
    " 39,40",
    " </a>",
    " ], and in post-licensure surveillance of children in Massachusetts:",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " In one study, 275 children (2 to 24 months of age) underwent NP cultures at
    well-child and acute-care visits for acute otitis media between 2000 and 2003 [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/42\">",
    " 42",
    " </a>",
    " ]. During this time period, NP colonization with PCV7 vaccine serotypes
    decreased from 22 to 2 percent.",
    " </li>",
    " <li>",
    " In another report, NP cultures were obtained from children &lt;7 years of
    age at well-child and acute-care visits in primary care practices in Massachusetts
    communities between 2001 and 2009 [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/35,38,48\">",
    " 35,38,48",
    " </a>",
    " ]. NP colonization with PCV7 vaccine serotypes decreased from 36 to 2
    percent.",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " Immunization of preschool children with conjugate vaccines also may provide
    herd immunity to their younger siblings. In a randomized trial, 262 toddlers (aged
    12 to 35 months of age) attending day care centers were assigned to receive a 9-
    valent pneumococcal conjugate vaccine (PCV9) (",
    " <a class=\"graphic graphic_table graphicRef77274 \" href=\"UTD.htm?
    14/59/15293\">",
    " table 1",
    " </a>",
    " ) or meningococcal conjugate vaccine [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/41\">",
    " 41",
    " </a>",
    " ]. NP cultures were assessed at monthly or bimonthly intervals for the first
    two years of the study. NP cultures also were assessed at monthly intervals in 46
    of the subjects' younger siblings who were not attending day care. Fewer siblings
    of PCV9 recipients had NP cultures positive for vaccine serotypes than siblings of
    controls (21 versus 34 percent).",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H7\">",
    " <span class=\"h2\">",
    " Non-PCV7 serotypes",
    " </span>",
    " &nbsp;&mdash;&nbsp;In contrast to the inhibitory effect on vaccine serotypes,
    pneumococcal vaccination in children is associated with increases in the nasal
    carriage of nonvaccine serotypes [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/20,35-38,40-47\">",
    " 20,35-38,40-47",
    " </a>",
    " ]. In the Massachusetts surveillance studies described above, NP carriage of
    nonvaccine serotypes increased from 7 to 16 percent in children 2 to 24 months of
    age between 2000 and 2003 [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/42\">",
    " 42",
    " </a>",
    " ] and from 15 to 29 percent in children &lt;7 years of age between 2001 and
    2007, with significant increases in serotypes 19A, 35B, 23A, and 7F [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/38\">",
    " 38",
    " </a>",
    " ]. The most common nonvaccine serotypes colonizing the NP of the older
    children were 11, 15, and 29.",
    " </p>",
    " <p>",
    " Post-hoc analysis of a large randomized trial on the effect of PCV7 on
    pneumococcal carriage indicated that nasopharyngeal acquisition of serotype 19A was
    increased among children who received PCV7 at 2, 4, and 11 months compared with
    those who were unvaccinated (16.2 versus 9.2 percent, relative risk 1.75, 95% CI
    1.14-2.7) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/49\">",
    " 49",
    " </a>",
    " ]. The proportion of children who had used antibiotics in the six months
    before nasopharyngeal culture was similar between groups. The clonal distribution
    of the nasopharyngeal isolates was similar to that of serotype 19A invasive
    isolates.",
    " </p>",
    " <p>",
    " A similar increase in colonization with nonvaccine serotypes has been noted
    among the younger siblings of PCV9 recipients. In the day care trial described
    above, a greater proportion of siblings of PCV9 recipients than siblings of control
    vaccine recipients had NP cultures positive for nonvaccine serotypes (19 versus 13
    percent) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/41\">",
    " 41",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " The clinical implications of these changes in NP colonization remain to be
    determined. The effect of colonization with nonvaccine serotypes, some of which are
    penicillin-resistant, will depend upon the ability of the new serotypes to cause
    local (eg, otitis media) or invasive disease [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/44,50\">",
    " 44,50",
    " </a>",
    " ].",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H8\">",
    " <span class=\"h2\">",
    " Staphylococcus aureus",
    " </span>",
    " &nbsp;&mdash;&nbsp;Nasal carriage of",
    " <em>",
    " Staphylococcus aureus",
    " </em>",
    " in children appears to be inversely related to NP carriage of pneumococcal
    vaccine serotypes [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/51,52\">",
    " 51,52",
    " </a>",
    " ]. A potential concern with",
    " <em>",
    " S. aureus",
    " </em>",
    " carriage is the increasing frequency of community-associated methicillin-
    resistant",
    " <em>",
    " S. aureus",
    " </em>",
    " infections. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?29/21/30042?
    source=see_link&amp;anchor=H14#H14\">",
    " \"Epidemiology and clinical spectrum of methicillin-resistant Staphylococcus
    aureus infections in children\", section on 'CA-MRSA infection'",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H9\">",
    " <span class=\"h2\">",
    " Herd effects",
    " </span>",
    " &nbsp;&mdash;&nbsp;Immunization of children with PCV7 has been effective in
    reducing IPD in vaccinated children and, indirectly, in unvaccinated adults (",
    " <a class=\"graphic graphic_figure graphicRef64834 \" href=\"UTD.htm?
    10/26/10658\">",
    " figure 1",
    " </a>",
    " ). Similarly, immunization of children with PCV7 appears to have indirect
    effects on the nasopharyngeal colonization of unvaccinated household contacts and
    community members [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/47,53,54\">",
    " 47,53,54",
    " </a>",
    " ]. Evaluation of household members of children who participated in a trial of
    PCV7 found that adults and unvaccinated children (&lt;5 years) who were contacts of
    vaccinees were less likely to be colonized with vaccine serotypes than contacts of
    controls. However, they had an increase in colonization with nonvaccine serotypes
    (similar to the effects seen in vaccinated children, as described above).",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H10\">",
    " <span class=\"h1\">",
    " ANTIBIOTIC RESISTANCE",
    " </span>",
    " &nbsp;&mdash;&nbsp;The resistance of pneumococci to a variety of antimicrobial
    agents has become a worldwide health problem. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?0/5/81?source=see_link\">",
    " \"Resistance of Streptococcus pneumoniae to beta-lactam antibiotics\"",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?19/15/19704?
    source=see_link\">",
    " \"Resistance of Streptococcus pneumoniae to the macrolides, azalides,
    lincosamines, and ketolides\"",
    " </a>",
    " .) The effects of routine 7-valent pneumococcal conjugate vaccine (PCV7)
    immunization in the United States on antibiotic susceptibility patterns of invasive
    and NP isolates are discussed in this section.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H11\">",
    " <span class=\"h2\">",
    " Invasive isolates",
    " </span>",
    " &nbsp;&mdash;&nbsp;Data from Active Bacterial Core surveillance areas in the
    US indicate that penicillin-nonsusceptible rates of invasive pneumococcal disease
    (IPD) among children younger than five years declined by 64 percent between 1998-
    1999 and 2007-2008 (ie, before and after the introduction of PCV7, respectively;
    but before replacement of PCV7 with PCV13 in 2010) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/55\">",
    " 55",
    " </a>",
    " ]. Rates of IPD nonsusceptible to multiple antibiotics also declined (",
    " <a class=\"graphic graphic_figure graphicRef54045 \" href=\"UTD.htm?
    33/44/34511\">",
    " figure 2",
    " </a>",
    " ).",
    " </p>",
    " <p>",
    " During 2007-2008, the six serotypes in PCV13, but not in PCV7 (",
    " <a class=\"graphic graphic_table graphicRef77274 \" href=\"UTD.htm?
    14/59/15293\">",
    " table 1",
    " </a>",
    " ) (almost exclusively serotype 19A) accounted for 97 percent of penicillin-
    nonsusceptible IPD among children younger than five years, suggesting potential for
    further decline in rates of penicillin-nonsusceptible IPD with the routine use of
    PCV13. Surveillance from eight children&rsquo;s hospitals in the United States
    found a decline in the proportion of isolates nonsusceptible to penicillin and",
    " <a class=\"drug drug_general\" href=\"UTD.htm?10/17/10521?source=see_link\">",
    " ceftriaxone",
    " </a>",
    " after the introduction of PCV13 [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/23\">",
    " 23",
    " </a>",
    " ]. Susceptibility results for",
    " <a class=\"drug drug_general\" href=\"UTD.htm?35/29/36304?source=see_link\">",
    " erythromycin",
    " </a>",
    " ,",
    " <a class=\"drug drug_general\" href=\"UTD.htm?32/21/33104?source=see_link\">",
    " clindamycin",
    " </a>",
    " , and",
    " <a class=\"drug drug_general\" href=\"UTD.htm?4/58/5034?source=see_link\">",
    " trimethoprim-sulfamethoxazole",
    " </a>",
    " were unchanged.",
    " </p>",
    " <p>",
    " Two factors are thought to be responsible for the reduction in antibiotic-
    resistant strains in the pneumococcal conjugate vaccine era [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/41,56\">",
    " 41,56",
    " </a>",
    " ]:",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " Immunization with PCV decreases acquisition of vaccine serotypes that are
    antibiotic-resistant",
    " </li>",
    " <li>",
    " Recipients of PCV receive less antibiotic therapy than nonvaccinated
    children, further reducing the selective pressure to acquire resistant strains",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " Continued surveillance is necessary. In population-based surveillance during
    2007, serotypes 15A, 23A, 35B, and 6C (which are not included in PCV13) accounted
    for 32 percent of invasive isolates nonsusceptible to penicillin [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/57\">",
    " 57",
    " </a>",
    " ].",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H12\">",
    " <span class=\"h2\">",
    " NP isolates",
    " </span>",
    " &nbsp;&mdash;&nbsp;Universal vaccination of infants appears to have an effect
    on the antibiotic resistance of strains carried in the nasopharynx as well as on
    those causing invasive disease. However, the effects are inconsistent, as
    illustrated by the following observations:",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " A cross-sectional survey in children 3 to 59 months in Anchorage, Alaska,
    noted a decrease in the NP carriage of pneumococcal isolates nonsusceptible to",
    " <a class=\"drug drug_general\" href=\"UTD.htm?4/58/5034?source=see_link\">",
    " trimethoprim-sulfamethoxazole",
    " </a>",
    " from 44 to 16 percent between 2000 and 2004, but no change in the NP
    carriage of strains nonsusceptible to penicillin (approximately 36 percent) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/37\">",
    " 37",
    " </a>",
    " ]. Among strains nonsusceptible to penicillin, there was an increase in the
    proportion of serotype 19A (from 10 to 32 percent).",
    " </li>",
    " <li>",
    " A report from St. Louis, Missouri, noted a decrease in the prevalence of
    pneumococcal isolates nonsusceptible to penicillin in the NP cultures of children
    &lt;7 years with acute respiratory infections (from 25 to 12 percent between 2000
    and 2004) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/58\">",
    " 58",
    " </a>",
    " ].",
    " </li>",
    " <li>",
    " Surveillance of Massachusetts children &lt;7 years found that overall NP
    carriage of penicillin-nonsusceptible pneumococci was similar between 2001 and 2009
    [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/48\">",
    " 48",
    " </a>",
    " ]. However, penicillin nonsusceptibility increased among serotypes contained
    in PCV13 (particularly 19A). Multilocus sequence typing of isolates demonstrated
    expansion of previously recognized clones of nonvaccine serotypes (eg, 19A, 15A,
    and 35B), emergence of new clones, and serotype switching, but no evidence of de
    novo acquisition of resistance. (See",
    " <a class=\"local\" href=\"#H7\">",
    " 'Non-PCV7 serotypes'",
    " </a>",
    " above.)",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " The inconsistency of the above observations suggests that factors other than
    immunization with PCV7 may play a role in the antibiotic susceptibility patterns of
    pneumococcal isolates from the nasopharynx. The increased use of",
    " <a class=\"drug drug_general\" href=\"UTD.htm?32/43/33456?source=see_link\">",
    " azithromycin",
    " </a>",
    " may be one such factor [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/59\">",
    " 59",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " These reports highlight the need to continue to monitor the antibiotic
    resistance patterns of strains of pneumococcus carried in the nasopharynx and the
    use of antibiotics with potential to promote multidrug resistance.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H13\">",
    " <span class=\"h1\">",
    " VACCINE LIMITATIONS",
    " </span>",
    " &nbsp;&mdash;&nbsp;The use of pneumococcal conjugate vaccines in children has
    reduced the incidence of invasive pneumococcal disease. However, the issue of
    eliminating noninvasive disease remains critical. Even if the vaccines as currently
    formulated substantially decrease the incidence of upper respiratory infection, the
    effect is not likely to be permanent.",
    " </p>",
    " <p>",
    " The hallmark of pneumococci is their ease of natural DNA transformation as
    evidenced by the diversity and rapidity of spread of antibiotic resistance. As has
    been demonstrated, a strain can enter a day care center as one serotype and acquire
    another serotype capsule within just a few days [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/60\">",
    " 60",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " The molecular flexibility in the capsular locus is based upon its modular gene
    structure [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/61\">",
    " 61",
    " </a>",
    " ]. There are no known limits to capsular exchangeability. Under antibody
    selective pressure, pneumococci can be expected to quickly evolve to circumvent
    vaccines that contain a limited number of serotypes. As described above, there are
    data to suggest this process may have begun. The only long-term solution to this
    problem is the development of a vaccine containing one or several protective
    protein antigens from pneumococcus, rather than serogroup-specific polysaccharide
    antigens [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/601/abstract/62\">",
    " 62",
    " </a>",
    " ].",
    " </p>",
    " <p class=\"headingAnchor\" id=\"PATIENT_INFORMATION\">",
    " <span class=\"h1\">",
    " INFORMATION FOR PATIENTS",
    " </span>",
    " &nbsp;&mdash;&nbsp;UpToDate offers two types of patient education materials,
    &ldquo;The Basics&rdquo; and &ldquo;Beyond the Basics.&rdquo; The Basics patient
    education pieces are written in plain language, at the 5",
    " <sup>",
    " th",
    " </sup>",
    " to 6",
    " <sup>",
    " th",
    " </sup>",
    " grade reading level, and they answer the four or five key questions a patient
    might have about a given condition. These articles are best for patients who want a
    general overview and who prefer short, easy-to-read materials. Beyond the Basics
    patient education pieces are longer, more sophisticated, and more detailed. These
    articles are written at the 10",
    " <sup>",
    " th",
    " </sup>",
    " to 12",
    " <sup>",
    " th",
    " </sup>",
    " grade reading level and are best for patients who want in-depth information
    and are comfortable with some medical jargon.",
    " </p>",
    " <p>",
    " Here are the patient education articles that are relevant to this topic. We
    encourage you to print or e-mail these topics to your patients. (You can also
    locate patient education articles on a variety of subjects by searching on
    &ldquo;patient info&rdquo; and the keyword(s) of interest.)",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " Beyond the Basics topics (see",
    " <a class=\"medical medical_patient\" href=\"UTD.htm?17/42/18084?
    source=see_link\">",
    " \"Patient information: Why does my child need vaccines? (Beyond the
    Basics)\"",
    " </a>",
    " and",
    " <a class=\"medical medical_patient\" href=\"UTD.htm?41/36/42566?
    source=see_link\">",
    " \"Patient information: Vaccines for infants and children age 0 to 6 years
    (Beyond the Basics)\"",
    " </a>",
    " )",
    " </li>",
    " </ul>",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H15\">",
    " <span class=\"h1\">",
    " SUMMARY",
    " </span>",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " The incidence of invasive pneumococcal disease (IPD) in the United States
    has declined dramatically since the pneumococcal conjugate vaccine was added to the
    routine childhood immunization schedule (",
    " <a class=\"graphic graphic_figure graphicRef64834 \" href=\"UTD.htm?
    10/26/10658\">",
    " figure 1",
    " </a>",
    " ). The greatest decline has been noted in pneumococcal bacteremia without a
    focus. (See",
    " <a class=\"local\" href=\"#H2\">",
    " 'Efficacy'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " The large decline in cases of IPD caused by PCV7 vaccine serotypes (",
    " <a class=\"graphic graphic_table graphicRef77274 \" href=\"UTD.htm?
    14/59/15293\">",
    " table 1",
    " </a>",
    " ) was accompanied by a small increase in the number of cases of IPD caused
    by nonvaccine serotypes (eg, replacement serotypes) (",
    " <a class=\"graphic graphic_figure graphicRef64834 \" href=\"UTD.htm?
    10/26/10658\">",
    " figure 1",
    " </a>",
    " ). Most of the replacement serotypes are included in PCV13, which has
    replaced PCV7 in the United States. (See",
    " <a class=\"local\" href=\"#H9889776\">",
    " 'Invasive disease caused by non-vaccine serotypes'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " Widespread use of PCV7 was associated with an increase in the proportion of
    cases of IPD associated with pneumonia",
    " <span class=\"nowrap\">",
    " and/or",
    " </span>",
    " empyema. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?9/34/9770?
    source=see_link\">",
    " \"Epidemiology; clinical presentation; and evaluation of parapneumonic
    effusion and empyema in children\"",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?34/11/35001?
    source=see_link&amp;anchor=H8#H8\">",
    " \"Pneumococcal pneumonia in children\", section on 'Effusion/empyema'",
    " </a>",
    " .)",
    " </li>",
    " <li>",
    " Among children receiving the 7-valent vaccine, serotype 19A was an important
    cause of IPD by replacement serotypes. Serotype 19A is included in the 13-valent
    pneumococcal conjugate vaccine introduced in 2010. However, it remains an important
    cause of IPD. (See",
    " <a class=\"local\" href=\"#H4\">",
    " 'Serotype 19A'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " Universal infant immunization does not appear to have affected the overall
    rate of carriage of pneumococcus in the nasopharynx. However, universal
    immunization has reduced carriage of vaccine serotypes and increased carriage of
    nonvaccine serotypes and",
    " <em>",
    " Staphylococcus aureus",
    " </em>",
    " . The clinical implications of these changes in nasopharyngeal colonization
    remain to be determined. (See",
    " <a class=\"local\" href=\"#H5\">",
    " 'Nasopharyngeal flora'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " Universal infant immunization has been associated with a decrease in the
    rate of penicillin-nonsusceptible and multiple antibiotic-nonsusceptible IPD (",
    " <a class=\"graphic graphic_figure graphicRef54045 \" href=\"UTD.htm?
    33/44/34511\">",
    " figure 2",
    " </a>",
    " ). (See",
    " <a class=\"local\" href=\"#H11\">",
    " 'Invasive isolates'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " Data regarding the effects of universal infant immunization on the
    antibiotic resistance patterns of isolates from the nasopharynx are inconsistent.
    Resistance may be increased through the expansion of clones of antibiotic-resistant
    nonvaccine serotypes. (See",
    " <a class=\"local\" href=\"#H12\">",
    " 'NP isolates'",
    " </a>",
    " above.)",
    " </li>",
    " </ul>",
    " </p>",
    " </div>",
    " <div id=\"topicAgreement\">",
    " Use of UpToDate is subject to the",
    " <a class=\"licenseLink\" href=\"./license\" id=\"sla_in_page\"
    target=\"_blank\">",
    " Subscription and License Agreement",
    " </a>",
    " .",
    " </div>",
    " <div class=\"headingAnchor\" id=\"references\">",
    " <h1>",
    " REFERENCES",
    " </h1>",
    " <ol id=\"reference\">",
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    " Kaplan SL, Barson WJ, Lin PL, et al. Early Trends for Invasive Pneumococcal
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    " Black S. Changing epidemiology of invasive pneumococcal disease: a
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    " Fenoll A, Aguilar L, Granizo JJ, et al. Has the licensing of respiratory
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    " </a>",
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    " Moore MR. Rethinking replacement and resistance. J Infect Dis 2009;
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/27\">",
    " Pai R, Moore MR, Pilishvili T, et al. Postvaccine genetic structure of
    Streptococcus pneumoniae serotype 19A from children in the United States. J Infect
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/28\">",
    " Centers for Disease Control and Prevention (CDC). Emergence of
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/29\">",
    " Kaplan SL, Barson WJ, Lin PL, et al. Serotype 19A Is the most common
    serotype causing invasive pneumococcal infections in children. Pediatrics 2010;
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/30\">",
    " Pichichero ME, Casey JR. Emergence of a multiresistant serotype 19A
    pneumococcal strain not included in the 7-valent conjugate vaccine as an
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    " </a>",
    " </li>",
    " <li>",
    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/31\">",
    " Ongkasuwan J, Valdez TA, Hulten KG, et al. Pneumococcal mastoiditis in
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/32\">",
    " Xu Q, Pichichero ME, Casey JR, Zeng M. Novel type of Streptococcus
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    " McNeil JC, Hulten KG, Mason EO Jr, Kaplan SL. Serotype 19A is the most
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    " Whitney CG. Impact of conjugate pneumococcal vaccines. Pediatr Infect Dis J
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    " Huang SS, Platt R, Rifas-Shiman SL, et al. Post-PCV7 changes in colonizing
    pneumococcal serotypes in 16 Massachusetts communities, 2001 and 2004. Pediatrics
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    " Millar EV, O'Brien KL, Watt JP, et al. Effect of community-wide conjugate
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    " Park SY, Moore MR, Bruden DL, et al. Impact of conjugate vaccine on
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    " Huang SS, Hinrichsen VL, Stevenson AE, et al. Continued impact of
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/39\">",
    " Dagan R, Melamed R, Muallem M, et al. Reduction of nasopharyngeal carriage
    of pneumococci during the second year of life by a heptavalent conjugate
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/40\">",
    " Mbelle N, Huebner RE, Wasas AD, et al. Immunogenicity and impact on
    nasopharyngeal carriage of a nonavalent pneumococcal conjugate vaccine. J Infect
    Dis 1999; 180:1171.",
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/41\">",
    " Dagan R, Givon-Lavi N, Zamir O, Fraser D. Effect of a nonavalent conjugate
    vaccine on carriage of antibiotic-resistant Streptococcus pneumoniae in day-care
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/42\">",
    " Pelton SI, Loughlin AM, Marchant CD. Seven valent pneumococcal conjugate
    vaccine immunization in two Boston communities: changes in serotypes and
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    " </a>",
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/43\">",
    " Ghaffar F, Barton T, Lozano J, et al. Effect of the 7-valent pneumococcal
    conjugate vaccine on nasopharyngeal colonization by Streptococcus pneumoniae in the
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/44\">",
    " Hanage WP, Huang SS, Lipsitch M, et al. Diversity and antibiotic resistance
    among nonvaccine serotypes of Streptococcus pneumoniae carriage isolates in the
    post-heptavalent conjugate vaccine era. J Infect Dis 2007; 195:347.",
    " </a>",
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/45\">",
    " O'Brien KL, Millar EV, Zell ER, et al. Effect of pneumococcal conjugate
    vaccine on nasopharyngeal colonization among immunized and unimmunized children in
    a community-randomized trial. J Infect Dis 2007; 196:1211.",
    " </a>",
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/46\">",
    " Nahm MH, Lin J, Finkelstein JA, Pelton SI. Increase in the prevalence of the
    newly discovered pneumococcal serotype 6C in the nasopharynx after introduction of
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    " </a>",
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/47\">",
    " van Gils EJ, Veenhoven RH, Hak E, et al. Effect of reduced-dose schedules
    with 7-valent pneumococcal conjugate vaccine on nasopharyngeal pneumococcal
    carriage in children: a randomized controlled trial. JAMA 2009; 302:159.",
    " </a>",
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/48\">",
    " Wroe PC, Lee GM, Finkelstein JA, et al. Pneumococcal carriage and antibiotic
    resistance in young children before 13-valent conjugate vaccine. Pediatr Infect Dis
    J 2012; 31:249.",
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/49\">",
    " van Gils EJ, Veenhoven RH, Hak E, et al. Pneumococcal conjugate vaccination
    and nasopharyngeal acquisition of pneumococcal serotype 19A strains. JAMA 2010;
    304:1099.",
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/50\">",
    " Long SS. Capsules, clones, and curious events: pneumococcus under fire from
    polysaccharide conjugate vaccine. Clin Infect Dis 2005; 41:30.",
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/51\">",
    " Regev-Yochay G, Dagan R, Raz M, et al. Association between carriage of
    Streptococcus pneumoniae and Staphylococcus aureus in Children. JAMA 2004;
    292:716.",
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/52\">",
    " Bogaert D, van Belkum A, Sluijter M, et al. Colonisation by Streptococcus
    pneumoniae and Staphylococcus aureus in healthy children. Lancet 2004; 363:1871.",
    " </a>",
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/53\">",
    " Millar EV, Watt JP, Bronsdon MA, et al. Indirect effect of 7-valent
    pneumococcal conjugate vaccine on pneumococcal colonization among unvaccinated
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/54\">",
    " Hammitt LL, Bruden DL, Butler JC, et al. Indirect effect of conjugate
    vaccine on adult carriage of Streptococcus pneumoniae: an explanation of trends in
    invasive pneumococcal disease. J Infect Dis 2006; 193:1487.",
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/55\">",
    " Hampton LM, Farley MM, Schaffner W, et al. Prevention of antibiotic-
    nonsusceptible Streptococcus pneumoniae with conjugate vaccines. J Infect Dis 2012;
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    " Klugman KP. Vaccination: a novel approach to reduce antibiotic resistance.
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/57\">",
    " Gertz RE Jr, Li Z, Pimenta FC, et al. Increased penicillin nonsusceptibility
    of nonvaccine-serotype invasive pneumococci other than serotypes 19A and 6A in
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/58\">",
    " Garbutt J, Rosenbloom I, Wu J, Storch GA. Empiric first-line antibiotic
    treatment of acute otitis in the era of the heptavalent pneumococcal conjugate
    vaccine. Pediatrics 2006; 117:e1087.",
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/59\">",
    " Greenberg D, Givon-Lavi N, Sharf AZ, et al. The association between
    antibiotic use in the community and nasopharyngeal carriage of antibiotic-resistant
    Streptococcus pneumoniae in Bedouin children. Pediatr Infect Dis J 2008; 27:776.",
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/60\">",
    " Nesin M, Ramirez M, Tomasz A. Capsular transformation of a multidrug-
    resistant Streptococcus pneumoniae in vivo. J Infect Dis 1998; 177:707.",
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/61\">",
    " Caimano MJ, Hardy GG, Yother J. Capsule genetics in Streptococcus pneumoniae
    and a possible role for transposition in the generation of the type 3 locus. Microb
    Drug Resist 1998; 4:11.",
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/601/abstract/62\">",
    " Lee CJ, Banks SD, Li JP. Virulence, immunity, and vaccine related to
    Streptococcus pneumoniae. Crit Rev Microbiol 1991; 18:89.",
    " </a>",
    " </li>",
    " </ol>",
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    " <h1>",
    " TOPIC OUTLINE",
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    " <div id=\"outline\">",
    " <ul>",
    " <li>",
    " <a class=\"sr_button\" href=\"#H15\" id=\"summRecButton\">",
    " <span>",
    " SUMMARY",
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    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H1\">",
    " INTRODUCTION",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H2\">",
    " EFFICACY",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H9889776\">",
    " INVASIVE DISEASE CAUSED BY NON-VACCINE SEROTYPES",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H4\">",
    " Serotype 19A",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H5\">",
    " NASOPHARYNGEAL FLORA",
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    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H6\">",
    " PCV7 serotypes",
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    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H7\">",
    " Non-PCV7 serotypes",
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    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H8\">",
    " Staphylococcus aureus",
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    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H9\">",
    " Herd effects",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H10\">",
    " ANTIBIOTIC RESISTANCE",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H11\">",
    " Invasive isolates",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H12\">",
    " NP isolates",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H13\">",
    " VACCINE LIMITATIONS",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#PATIENT_INFORMATION\">",
    " INFORMATION FOR PATIENTS",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H15\">",
    " SUMMARY",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a href=\"#references\">",
    " REFERENCES",
    " </a>",
    " </li>",
    " </ul>",
    " </div>",
    " <h1>",
    " <div class=\"openRelatedGraphics\" id=\"PEDS/6019\" rel=\"outline_link\">",
    " GRAPHICS",
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    " View All",
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    " </h1>",
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    " <li class=\"plainItem\">",
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    " FIGURES",
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    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"graphic graphic_figure\" href=\"UTD.htm?10/26/10658\"
    title=\"figure 1\">",
    " Rates of IPD after PCV7",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"graphic graphic_figure\" href=\"UTD.htm?33/44/34511\"
    title=\"figure 2\">",
    " Nonsusceptibility invasive pneumococcal isolates children",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <div class=\"openRelatedGraphics\" id=\"PEDS/6019|TAB\">",
    " <a href=\"#\" title=\"TABLES\">",
    " TABLES",
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    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"graphic graphic_table\" href=\"UTD.htm?14/59/15293\" title=\"table
    1\">",
    " Pneumococcal vaccines",
    " </a>",
    " </li>",
    " </ul>",
    " </div>",
    " <h1>",
    " RELATED TOPICS",
    " </h1>",
    " <div id=\"relatedTopics\">",
    " <ul>",
    " <li class=\"plainItem\">",
    " <a class=\"medical medical_review\" href=\"UTD.htm?28/60/29642?
    source=related_link\">",
    " Acute otitis media in children: Epidemiology, microbiology, clinical
    manifestations, and complications",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"medical medical_review\" href=\"UTD.htm?29/21/30042?
    source=related_link\">",
    " Epidemiology and clinical spectrum of methicillin-resistant Staphylococcus
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    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"medical medical_review\" href=\"UTD.htm?9/34/9770?
    source=related_link\">",
    " Epidemiology; clinical presentation; and evaluation of parapneumonic
    effusion and empyema in children",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"medical medical_review\" href=\"UTD.htm?7/29/7642?
    source=related_link\">",
    " Invasive pneumococcal (Streptococcus pneumoniae) infections and bacteremia",
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    " <li class=\"plainItem\">",
    " <a class=\"medical medical_patient\" href=\"UTD.htm?41/36/42566?
    source=related_link\">",
    " Patient information: Vaccines for infants and children age 0 to 6 years
    (Beyond the Basics)",
    " </a>",
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    source=related_link\">",
    " Patient information: Why does my child need vaccines? (Beyond the Basics)",
    " </a>",
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    source=related_link\">",
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    " <a class=\"medical medical_review\" href=\"UTD.htm?21/12/21705?
    source=related_link\">",
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    " <a class=\"medical medical_review\" href=\"UTD.htm?0/5/81?
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    " </div>",
    " </div>"].join("\n");
    var title_f0_37_602="Hereditary neuropathies associated with generalized
    disorders";
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    " Hereditary neuropathies associated with generalized disorders",
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    " </a>",
    " <br/>",
    " <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
    0/37/602/contributors\">",
    " Helen V Firth, DM, FRCP, DCH",
    " </a>",
    " <br/>",
    " </div>",
    " <div>",
    " <a class=\"contributor contributor_credentials contributorType\"
    href=\"UTD.htm?0/37/602/contributors\">",
    " Deputy Editor",
    " </a>",
    " <br/>",
    " <a class=\"contributor contributor_credentials\" href=\"UTD.htm?
    0/37/602/contributors\">",
    " John F Dashe, MD, PhD",
    " </a>",
    " <br/>",
    " </div>",
    " </div>",
    " <div id=\"disclosures\">",
    " <a href=\"UTD.htm?0/37/602/contributor-disclosure\" target=\"_blank\">",
    " Disclosures",
    " </a>",
    " </div>",
    " <div id=\"reviewProcess\">",
    " <span>",
    " All topics are updated as new evidence becomes available and our",
    " </span>",
    " <a href=\"/home/editorial-policy\" target=\"_blank\">",
    " peer review process",
    " </a>",
    " <span>",
    " is complete.",
    " </span>",
    " </div>",
    " <div id=\"literatureReviewDate\">",
    " <span class=\"emphasis\">",
    " Literature review current through:",
    " </span>",
    " Oct 2013.",
    " <span class=\"pipeSpace\">",
    " |",
    " </span>",
    " <span class=\"emphasis\">",
    " This topic last updated:",
    " </span>",
    " Apr 9, 2013.",
    " </div>",
    " <div id=\"topicText\">",
    " <p class=\"headingAnchor\" id=\"H1\">",
    " <span class=\"h1\">",
    " INTRODUCTION",
    " </span>",
    " &nbsp;&mdash;&nbsp;The hereditary peripheral neuropathies have been classified
    based upon clinical characteristics, mode of inheritance, electrophysiologic
    features, metabolic defect, and, more recently, specific genetic markers. The
    primary hereditary neuropathies predominantly affect peripheral nerves and produce
    symptoms of peripheral nerve dysfunction. Other hereditary neuropathies affect both
    the central and peripheral nervous systems and, in some cases, other organs; in
    such patients, symptoms related to the peripheral neuropathy may be overshadowed by
    additional manifestations of the disease (",
    " <a class=\"graphic graphic_table graphicRef74269 graphicRef72307
    graphicRef56567 graphicRef52324 \" href=\"UTD.htm?11/20/11584\">",
    " table 1A-D",
    " </a>",
    " ).",
    " </p>",
    " <p>",
    " The last group of disorders is reviewed here. The primary motor-sensory and
    sensory&ndash;autonomic neuropathies are discussed separately. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?34/59/35770?
    source=see_link\">",
    " \"Hereditary primary motor sensory neuropathies, including Charcot-Marie-
    Tooth disease\"",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?42/16/43272?
    source=see_link\">",
    " \"Hereditary sensory and autonomic neuropathies\"",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H21258726\">",
    " <span class=\"h1\">",
    " SPINOCEREBELLAR ATAXIAS",
    " </span>",
    " &nbsp;&mdash;&nbsp;The spinocerebellar ataxias (SCA) are a heterogeneous group
    of inherited disorders with different neuropathological profiles reflecting the
    degree of cerebellar and brainstem dysfunction or degeneration. A peripheral
    neuropathy is described in some but not all (",
    " <a class=\"graphic graphic_table graphicRef74269 \" href=\"UTD.htm?
    10/59/11198\">",
    " table 1A",
    " </a>",
    " ). Peripheral neuropathy has been best characterized in SCA type 4, in which a
    prominent axonal neuropathy is present [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/1\">",
    " 1",
    " </a>",
    " ]. A mild peripheral neuropathy with decreased deep tendon reflexes and
    reduced vibration sense has been described in type 1 [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/2\">",
    " 2",
    " </a>",
    " ], type 2 [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/3\">",
    " 3",
    " </a>",
    " ], type 3 [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/4\">",
    " 4",
    " </a>",
    " ], and type 6 [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/5\">",
    " 5",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " A detailed review of the spinocerebellar ataxias is found separately. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?28/35/29242?
    source=see_link\">",
    " \"The spinocerebellar ataxias\"",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H2\">",
    " <span class=\"h1\">",
    " INFANTILE NEUROAXONAL DYSTROPHY",
    " </span>",
    " &nbsp;&mdash;&nbsp;Infantile neuroaxonal dystrophy (INAD; MIM 256600), also
    called PLA2G6-associated neurodegeneration or Seitelberger disease, is an autosomal
    recessive disorder. It is considered one of several subtypes of neurodegeneration
    with brain iron accumulation (NBIA). (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?15/36/15943?
    source=see_link&amp;anchor=H10#H10\">",
    " \"Bradykinetic movement disorders in children\", section on
    'Neurodegeneration with brain iron accumulation'",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " The classification of infantile neuroaxonal dystrophy has been evolving since
    the discovery that nearly 80 percent of children with infantile neuroaxonal
    dystrophy have mutations in the PLA2G6 gene with a locus on chromosome 22q13.1 [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/6-8\">",
    " 6-8",
    " </a>",
    " ]. Mutations in the PLA2G6 gene have also been detected in patients previously
    diagnosed with other subtypes of NBIA, and it now appears that the PLA2G6 mutation
    is associated with a characteristic clinical and radiologic phenotype called
    PLA2G6-associated neurodegeneration (PLAN) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/7\">",
    " 7",
    " </a>",
    " ].",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H3\">",
    " <span class=\"h2\">",
    " Clinical features",
    " </span>",
    " &nbsp;&mdash;&nbsp;Children with infantile neuroaxonal dystrophy typically
    present by two to three years of age [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/9\">",
    " 9",
    " </a>",
    " ]. In a series of 14 children with PLAN, the median age of symptom
    presentation was 14 months (range 12 to 22 months) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/7\">",
    " 7",
    " </a>",
    " ]. Of these, five died at median age of nine years (range 6.5 to 14 years).",
    " </p>",
    " <p>",
    " Symptoms related to infantile neuroaxonal dystrophy reflect involvement of the
    peripheral nerves, central nervous system, and autonomic nervous system (",
    " <a class=\"graphic graphic_table graphicRef72307 \" href=\"UTD.htm?
    31/28/32204\">",
    " table 1B",
    " </a>",
    " )&nbsp;[",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/9,10\">",
    " 9,10",
    " </a>",
    " ]. The peripheral neuropathy is characterized by loss of distal sensation,
    which may lead to limb mutilation and muscle atrophy. Hypotonia and loss of motor
    milestones are associated with early onset of the disease. Deep tendon reflexes
    typically are hypoactive.",
    " </p>",
    " <p>",
    " Central nervous system manifestations include cognitive deterioration,
    spasticity, optic atrophy, and hypothalamic dysfunction with diabetes insipidus and
    hypothyroidism [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/11\">",
    " 11",
    " </a>",
    " ]. Autonomic symptoms may include urinary retention, decreased tearing, and
    dysfunction of temperature regulation. Early studies reported rare seizures in
    children with late-onset neuroaxonal dystrophy [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/12\">",
    " 12",
    " </a>",
    " ], but seizures have not been reported in children with PLA2G6 mutations [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/7\">",
    " 7",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " Electromyography shows signs of chronic denervation; fast rhythms may be
    present on electroencephalography, and visual evoked potentials are usually
    abnormal [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/7,10\">",
    " 7,10",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " Magnetic resonance imaging (MRI) may be suggestive of the diagnosis.
    Cerebellar atrophy and gliosis is universally present, with increased signal on
    fluid-attenuated inversion recovery (FLAIR) and T2-weighted MRI sequences [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/7,10,13\">",
    " 7,10,13",
    " </a>",
    " ]. Other common MRI findings include hypointensity of the globus pallidus,
    dentate nuclei, and substantia nigra on high susceptibility gradient echo (T2*)
    sequences, and hypointensity of the globus pallidus on fast spin echo sequences [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/7,14\">",
    " 7,14",
    " </a>",
    " ].",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H4\">",
    " <span class=\"h2\">",
    " Pathology",
    " </span>",
    " &nbsp;&mdash;&nbsp;The pathologic findings, which are seen best by electron
    microscopy, are similar in the peripheral, central, and autonomic nervous systems.
    Spheroids containing mitochondria, glycogen-like granules, and dense bodies occur
    in both central and peripheral nerve fibers [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/15,16\">",
    " 15,16",
    " </a>",
    " ]. Spheroid formation leads to axonal swelling.",
    " </p>",
    " <p>",
    " Other abnormalities in the central nervous system include cerebellar atrophy
    with neuronal atrophy and astrogliosis and involvement of the corticospinal tracts.
    Immunohistochemistry reveals the presence of ubiquitin but not beta-tuberculin or
    beta-amyloid [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/17\">",
    " 17",
    " </a>",
    " ]. These findings suggest that loss of microtubule function is part of the
    mechanism of spheroid formation.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H5\">",
    " <span class=\"h2\">",
    " Diagnosis",
    " </span>",
    " &nbsp;&mdash;&nbsp;The presence of infantile neuroaxonal dystrophy is
    suggested by the progressive neurologic symptoms beginning in infancy, but further
    testing is required to establish the diagnosis.",
    " </p>",
    " <p>",
    " The diagnosis of infantile neuroaxonal dystrophy generally is confirmed by the
    demonstration of spheroids on peripheral nerve or conjunctival biopsy [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/9,15,18\">",
    " 9,15,18",
    " </a>",
    " ]. An abnormal conjunctival biopsy is not dependent upon the presence of optic
    atrophy. Where available, PLA2G6 mutation analysis may confirm the diagnosis in
    patients with PLA2G6-associated neurodegeneration [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/7\">",
    " 7",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " The differential diagnosis of infantile neuroaxonal dystrophy includes other
    subtypes of NBIA, as these exhibit broad phenotypic overlap. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?15/36/15943?
    source=see_link&amp;anchor=H10#H10\">",
    " \"Bradykinetic movement disorders in children\", section on
    'Neurodegeneration with brain iron accumulation'",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H6\">",
    " <span class=\"h1\">",
    " TANGIER DISEASE",
    " </span>",
    " &nbsp;&mdash;&nbsp;Tangier disease is an autosomal codominant condition in
    which homozygotes have no serum high density lipoprotein (HDL) and heterozygotes
    have serum HDL concentrations of approximately one-half of those in normal
    individuals [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/19\">",
    " 19",
    " </a>",
    " ]. HDL-mediated cholesterol efflux from macrophages and intracellular lipid
    trafficking are impaired in this disorder, leading to the presence of foam cells in
    macrophages and other cells of the reticuloendothelial system throughout the body
    (",
    " <a class=\"graphic graphic_table graphicRef72307 \" href=\"UTD.htm?
    31/28/32204\">",
    " table 1B",
    " </a>",
    " )&nbsp;[",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/20\">",
    " 20",
    " </a>",
    " ].",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H7\">",
    " <span class=\"h2\">",
    " Genetics",
    " </span>",
    " &nbsp;&mdash;&nbsp;The defect in Tangier disease appears to involve mutations
    in the ATP-binding cassette transporter A1 (ABCA1) gene on chromosome 9q31, which
    encodes for the cholesterol efflux regulatory protein [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/19,21-24\">",
    " 19,21-24",
    " </a>",
    " ]. ABCA1 appears to play a central role in intracellular cholesterol transport
    and is associated with increased HDL catabolism [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/24,25\">",
    " 24,25",
    " </a>",
    " ]. One suggestion is that reduced cholesterol efflux onto nascent HDL
    particles leads to lipid depleted particles that are then rapidly catabolized [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/26\">",
    " 26",
    " </a>",
    " ]. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?39/2/39978?
    source=see_link&amp;anchor=H4#H4\">",
    " \"HDL metabolism and approach to the patient with abnormal HDL-cholesterol
    levels\", section on 'HDL metabolism'",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H8\">",
    " <span class=\"h2\">",
    " Clinical manifestations",
    " </span>",
    " &nbsp;&mdash;&nbsp;Homozygotes develop cholesterol ester deposition in tonsils
    (orange tonsils), liver, spleen, gastrointestinal tract, lymph nodes, bone marrow,
    and Schwann cells. The main clinical manifestations are hepatosplenomegaly and
    premature coronary disease; a neuropathy occurs in at least 50 percent of patients
    and is the most debilitating feature of the disease [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/20\">",
    " 20",
    " </a>",
    " ]. In a review in which the findings in 51 patients with homozygous Tangier
    disease were compared to over 3,000 controls, the patients were more likely to have
    both peripheral neuropathy (54 versus &lt;1 percent) and cardiovascular disease,
    defined as angina, myocardial infarction, or stroke (20 versus 5 percent overall
    and 44 versus 7 percent in those between the ages of 35 and 65) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/20\">",
    " 20",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " Two major types of neurologic syndromes are seen [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/27\">",
    " 27",
    " </a>",
    " ]:",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " A peripheral neuropathy occurs in childhood with fluctuating numbness,
    tingling, distal sensory loss, and distal weakness with muscle atrophy [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/28\">",
    " 28",
    " </a>",
    " ].",
    " </li>",
    " <li>",
    " Progressive loss of sensory and motor function in the upper body in a
    pattern similar to that which occurs in syringomyelia (a cystic degeneration of the
    spinal cord) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/29\">",
    " 29",
    " </a>",
    " ].",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " The major pathologic findings on nerve biopsy are loss of smaller myelinated
    and unmyelinated nerve fibers and lipid vacuole accumulation in Schwann cells. The
    cause of nerve death is unknown, but nerve loss appears to precede the development
    of the lipid-laden Schwann cells [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/30\">",
    " 30",
    " </a>",
    " ].",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H9\">",
    " <span class=\"h2\">",
    " Treatment",
    " </span>",
    " &nbsp;&mdash;&nbsp;Initiation of a low-fat diet may reduce the number of
    abnormal particles and can be associated with symptomatic improvement in the
    peripheral neuropathy. The administration of drugs that can increase serum HDL in
    other patients (",
    " <a class=\"drug drug_general\" href=\"UTD.htm?42/42/43686?source=see_link\">",
    " gemfibrozil",
    " </a>",
    " , niacin, or a statin) has little effect in those with Tangier disease [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/20\">",
    " 20",
    " </a>",
    " ]. Possible future therapies involve pharmacologic manipulation of the reverse
    cholesterol transport pathway such as increasing cellular ABC1 expression to
    augment cellular efflux of cholesterol to HDL; preventing the catabolism of HDL
    without interfering with its cholesterol transport function; or increasing the rate
    of hepatic HDL cholesterol uptake [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/31\">",
    " 31",
    " </a>",
    " ].",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H10\">",
    " <span class=\"h1\">",
    " ABETALIPOPROTEINEMIA",
    " </span>",
    " &nbsp;&mdash;&nbsp;Abetalipoproteinemia (Bassen-Kornzweig syndrome) is
    reviewed here briefly and discussed in detail separately (see",
    " <a class=\"medical medical_review\" href=\"UTD.htm?33/2/33833?
    source=see_link&amp;anchor=H1983214#H1983214\">",
    " \"Neuroacanthocytosis\", section on 'Abetalipoproteinemia'",
    " </a>",
    " ). It is a rare autosomal recessive disorder caused by mutations in the
    microsomal triglyceride transfer protein. The neurologic manifestations result from
    the inability to absorb and transport vitamin E and include progressive ataxia,
    sensory-motor neuropathy, and vision impairment with retinitis pigmentosa. Other
    clinical manifestations include acanthocytosis along with fat malabsorption and
    steatorrhea.",
    " </p>",
    " <p>",
    " The diagnosis is made in the setting of the typical clinical findings
    accompanied by laboratory findings of acanthocytosis, very low triglyceride and
    total cholesterol levels, and absent beta-lipoproteins. Neurologic manifestations
    can be prevented and partially reversed with the administration of vitamin E (150",
    " <span class=\"nowrap\">",
    " mg/kg",
    " </span>",
    " per day) along with other fat soluble vitamins. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?33/2/33833?
    source=see_link&amp;anchor=H1983214#H1983214\">",
    " \"Neuroacanthocytosis\", section on 'Abetalipoproteinemia'",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H13\">",
    " <span class=\"h1\">",
    " REFSUM DISEASE",
    " </span>",
    " &nbsp;&mdash;&nbsp;Refsum disease (MIM #266500), previously known as
    hereditary motor and sensory neuropathy IV, is a disorder of peroxisomal function.
    Peroxisomes are subcellular organelles that catalyze numerous functions in cellular
    metabolism. A group of genetic diseases in which impairment in one or more
    peroxisomal functions exists is expanding. The peroxisomal disorders usually are
    classified into three groups according to the presence or absence of intact
    peroxisomes and whether one or more than one peroxisomal enzyme or function is
    affected. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?8/23/8570?
    source=see_link\">",
    " \"Peroxisomal disorders\"",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " Refsum disease has been classified into classic and infantile forms; both are
    associated with abnormal phytanic acid accumulation. Classic Refsum disease
    (heredopathia atactica polyneuritiformis) is an autosomal recessive disorder
    associated with the accumulation of phytanic acid in plasma and tissues. Phytanic
    acid is a branched-chain fatty acid present in the typical human diet. Normally it
    is metabolized by activation to its CoA ester, phytanoyl-CoA and then alpha-
    oxidation to pristanic acid (",
    " <a class=\"graphic graphic_table graphicRef72307 \" href=\"UTD.htm?
    31/28/32204\">",
    " table 1B",
    " </a>",
    " ). (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?8/23/8570?
    source=see_link&amp;anchor=H40#H40\">",
    " \"Peroxisomal disorders\", section on 'Refsum disease'",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " Patients with Refsum disease are unable to degrade phytanic acid because of
    deficient activity of phytanoyl-CoA hydroxylase (PhyH), a peroxisomal enzyme that
    catalyzes the first step of phytanic acid alpha-oxidation; this abnormality is
    caused by mutations in the PHYH gene that lead to an enzymatically inactive PhyH
    protein.",
    " </p>",
    " <p>",
    " A small number of patients with classic adult Refsum disease have defects
    involving the PEX7 gene rather than the PhyH gene. The PEX7 gene encodes the
    peroxin 7 receptor protein, which is required for peroxisomal import of proteins,
    and which plays a role in the incorporation of PhyH into peroxisomes. Defects in
    the PEX7 gene are also found in another hereditary disorder, rhizomelic
    chondrodysplasia punctata type 1. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?8/23/8570?
    source=see_link&amp;anchor=H34#H34\">",
    " \"Peroxisomal disorders\", section on 'Rhizomelic chondrodysplasia punctata
    type 1'",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " A different defect is present in infantile Refsum disease, which is one of a
    group of lethal peroxisome biogenesis disorders (the others being Zellweger
    syndrome and neonatal adrenoleukodystrophy). This disorder is characterized by
    mutations in PEX1 or PEX6, which encode for members of the AAA protein family
    (ATPases associated with multiple cellular activities). (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?8/23/8570?
    source=see_link&amp;anchor=H29#H29\">",
    " \"Peroxisomal disorders\", section on 'Infantile Refsum disease'",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H14\">",
    " <span class=\"h2\">",
    " Clinical features",
    " </span>",
    " &nbsp;&mdash;&nbsp;The age of onset varies, but most patients are symptomatic
    by 20 years of age. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?8/23/8570?
    source=see_link&amp;anchor=H40#H40\">",
    " \"Peroxisomal disorders\", section on 'Refsum disease'",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " Classic Refsum disease is characterized by the presence of four clinical
    abnormalities:",
    " </p>",
    " <p>",
    " <ul class=\"bulletCompact-block\">",
    " <li>",
    " Retinitis pigmentosa",
    " </li>",
    " <li>",
    " Peripheral polyneuropathy",
    " </li>",
    " <li>",
    " Cerebellar ataxia",
    " </li>",
    " <li>",
    " Elevated cerebrospinal fluid protein concentration (100 to 600",
    " <span class=\"nowrap\">",
    " mg/dL)",
    " </span>",
    " without an increase in cells",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " Affected patients also may have sensorineural deafness, ichthyosis, anosmia,
    and cardiac conduction defects. Nerve conduction studies typically show a slowed
    conduction velocity. Peripheral nerve biopsy reveals hypertrophic changes with
    onion bulb formation and paracrystalline inclusions on electron microscopy.",
    " </p>",
    " <p>",
    " The diagnosis usually is made clinically and can be confirmed by measurement
    of serum phytanic acid concentrations. Strict reduction in dietary phytanic acid
    intake may be associated with a significant improvement in the clinical
    manifestations in patients with classic Refsum disease. Another method to reduce
    serum phytanic acid in these patients is plasmapheresis, which can be performed
    serially if necessary.",
    " </p>",
    " <p>",
    " Refsum disease is discussed in greater detail elsewhere. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?8/23/8570?
    source=see_link&amp;anchor=H40#H40\">",
    " \"Peroxisomal disorders\", section on 'Refsum disease'",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H21258209\">",
    " <span class=\"h1\">",
    " CHEDIAK-HIGASHI SYNDROME",
    " </span>",
    " &nbsp;&mdash;&nbsp;Chediak-Higashi syndrome (CHS) is an autosomal recessive
    disorder characterized by recurrent infections, partial albinism,
    hepatosplenomegaly, an increased risk of lymphoreticular malignancy, and multiple
    neurologic abnormalities. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?41/18/42278?
    source=see_link\">",
    " \"Chediak-Higashi syndrome\"",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " Patients who survive early childhood despite serious infections develop severe
    neurologic manifestations in adolescence and early adulthood. Both the peripheral
    and central nervous systems are involved [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/32-34\">",
    " 32-34",
    " </a>",
    " ]. Neurologic features may include nystagmus, photosensitivity, seizures,
    mental retardation, generalized weakness, spinocerebellar degeneration, and
    parkinsonism. Biopsy of peripheral nerves reveals perivascular intracytoplasmic
    inclusions, loss of myelinated sensory fibers, and the presence of peroxidase
    positive granules in Schwann cells, similar to those seen in leukocytes, which are
    thought to be giant lysosomes [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/32,35,36\">",
    " 32,35,36",
    " </a>",
    " ]. Muscle biopsy reveals neurogenic atrophy with peroxidase positive granules
    similar to those seen in leukocytes.",
    " </p>",
    " <p>",
    " Patients who do not die from infection eventually enter the accelerated phase
    of the disease characterized by massive lymphohistiocytic infiltration of virtually
    all organ systems. Treatment with hematopoietic cell transplantation prevents
    infections and the accelerated phase, but patients still develop neurologic
    deficits. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?41/18/42278?
    source=see_link&amp;anchor=H9#H9\">",
    " \"Chediak-Higashi syndrome\", section on 'Treatment'",
    " </a>",
    " and",
    " <a class=\"medical medical_review\" href=\"UTD.htm?41/18/42278?
    source=see_link&amp;anchor=H10#H10\">",
    " \"Chediak-Higashi syndrome\", section on 'Prognosis'",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H15\">",
    " <span class=\"h1\">",
    " LYSOSOMAL STORAGE DISEASES",
    " </span>",
    " &nbsp;&mdash;&nbsp;Lysosomes are acidic cellular organelles that function as
    terminal degradative compartments. Lysosomal storage diseases are a group of
    approximately 36 heterogeneous disorders characterized by the accumulation of
    undigested macromolecules within the lysosomes. They result from a deficiency of a
    specific lysosomal enzyme or protein, although how the accumulated substrates
    relate to the observed pathology is not known. Many are associated with a
    neurodegenerative phenotype, and a peripheral neuropathy occurs in Fabry disease,
    Krabbe disease, metachromatic leukodystrophy, and Niemann-Pick disease (",
    " <a class=\"graphic graphic_table graphicRef56567 \" href=\"UTD.htm?
    36/27/37308\">",
    " table 1C",
    " </a>",
    " ).",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H16\">",
    " <span class=\"h2\">",
    " Fabry disease",
    " </span>",
    " &nbsp;&mdash;&nbsp;Fabry disease (also called angiokeratoma corporis diffusum,
    ceramide trihexosidosis, and Anderson-Fabry disease) is an X-linked recessive
    glycolipid storage disease. The clinical manifestations, diagnosis and treatment of
    Fabry disease are discussed separately. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?26/49/27414?
    source=see_link\">",
    " \"Neurologic manifestations of Fabry disease\"",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H17\">",
    " <span class=\"h2\">",
    " Krabbe disease",
    " </span>",
    " &nbsp;&mdash;&nbsp;Krabbe disease (globoid cell leukodystrophy) is an
    autosomal recessive disorder caused by the deficiency of galactocerebrosidase
    (GALC). The genetics, clinical manifestations, diagnosis and treatment of Krabbe
    disease are discussed separately. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?3/60/4038?
    source=see_link\">",
    " \"Krabbe disease\"",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H18\">",
    " <span class=\"h2\">",
    " Metachromatic leukodystrophy",
    " </span>",
    " &nbsp;&mdash;&nbsp;Metachromatic leukodystrophy (MLD, sulfatide lipidosis) is
    an autosomal recessive lysosomal storage disease that occurs in 1 of 40,000 births.
    The genetics, clinical manifestations, diagnosis and treatment of Metachromatic
    leukodystrophy are discussed separately. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?41/27/42421?
    source=see_link\">",
    " \"Metachromatic leukodystrophy\"",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H19\">",
    " <span class=\"h2\">",
    " Niemann-Pick disease",
    " </span>",
    " &nbsp;&mdash;&nbsp;Niemann-Pick disease (NPD, sphingomyelin-cholesterol
    lipidosis) is a group of autosomal recessive disorders associated with
    splenomegaly, variable neurologic deficits, and the storage of sphingomyelin. The
    different types of Niemann-Pick disease are discussed separately. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?20/0/20489?
    source=see_link\">",
    " \"Overview of Niemann-Pick disease\"",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H20\">",
    " <span class=\"h1\">",
    " MITOCHONDRIAL DISORDERS",
    " </span>",
    " &nbsp;&mdash;&nbsp;Defects in structure or function of mitochondria, mainly
    involving the oxidative phosphorylation, mitochondrial biogenesis and other
    metabolic pathways, are associated with a wide spectrum of clinical phenotypes.
    Peripheral neuropathy is a prominent feature in several (",
    " <a class=\"graphic graphic_table graphicRef52324 \" href=\"UTD.htm?
    39/16/40204\">",
    " table 1D",
    " </a>",
    " ).",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H21\">",
    " <span class=\"h2\">",
    " Leigh syndrome",
    " </span>",
    " &nbsp;&mdash;&nbsp;Leigh syndrome (subacute necrotizing encephalomyelopathy)
    is an inherited neurodegenerative disorder of infancy or childhood. It is
    characterized by developmental delay or psychomotor regression, signs of brainstem
    dysfunction, ataxia, dystonia, external ophthalmoplegia, seizures, lactic acidosis,
    vomiting, and weakness [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/37-39\">",
    " 37-39",
    " </a>",
    " ]. Peripheral neuropathy with reduced nerve conduction velocity and
    demyelination also are frequent findings [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/40,41\">",
    " 40,41",
    " </a>",
    " ]. The prognosis is poor, with survival typically being a matter of months
    after disease onset.",
    " </p>",
    " <p>",
    " The pathologic hallmarks are bilateral, symmetric necrotizing lesions with
    spongy changes and microcysts in the basal ganglia, thalamus, brainstem, and spinal
    cord [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/38\">",
    " 38",
    " </a>",
    " ]. The mammary bodies are spared. Magnetic resonance imaging shows abnormal
    white matter signal in the putamen, basal ganglia, and brainstem with T2 images.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H22\">",
    " <span class=\"h3\">",
    " Pathogenesis",
    " </span>",
    " &nbsp;&mdash;&nbsp;The phenotype of Leigh syndrome appears to be related to
    altered mitochondrial metabolism. Alterations in the mitochondrial respiratory
    chain complex I [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/42-44\">",
    " 42-44",
    " </a>",
    " ], pyruvate dehydrogenase complex (PDHC) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/45-47\">",
    " 45-47",
    " </a>",
    " ] or in mitochondrial DNA (mtDNA) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/45,47,48\">",
    " 45,47,48",
    " </a>",
    " ] have been associated with autosomal, X-linked, or mtDNA mutations
    (maternally-inherited Leigh syndrome). A deficiency in cytochrome c oxidase (COX),
    the fourth multisubunit complex of the respiratory chain, is a common finding that
    is inherited as an autosomal recessive trait [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/47,49\">",
    " 47,49",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " The relative frequency of these abnormalities was assessed in a study of 100
    Japanese patients with a clinical diagnosis of Leigh syndrome [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/47\">",
    " 47",
    " </a>",
    " ]. Enzymatic defects were found in 21 patients: 15 involved COX and four
    involved PDH. In addition, mtDNA mutations in the ATPase 6 coding region occurred
    in 18 patients; different point mutations were associated with different clinical
    courses.",
    " </p>",
    " <p>",
    " Despite the frequency of COX deficiency, no mutations of the nuclear encoded
    COX subunit genes have been found [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/50\">",
    " 50",
    " </a>",
    " ]. However, mutations of SURF1, a gene located on chromosome 9q34, have been
    identified in many COX-deficient patients with Leigh syndrome [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/51-53\">",
    " 51-53",
    " </a>",
    " ]. In one series, loss of function SURF-1 mutations were found in 18 of 24 (75
    percent) patients with COX deficiency [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/52\">",
    " 52",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " Another nuclear gene that causes COX deficiency was identified through genetic
    linkage analysis of a consanguineous African family with an isolated COX defect [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/54\">",
    " 54",
    " </a>",
    " ]. The gene is located on chromosome 17p13.1-q11.1, a region that encompasses
    two genes that encode proteins involved in COX assembly: SCO1 and COX10. The COX10
    gene encodes heme A:farnesyltransferase, which catalyzes the first step in the
    conversion of protoheme to the heme A prosthetic groups. SCO1 is thought to be
    involved in mitochondrial copper transport to COX [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/55\">",
    " 55",
    " </a>",
    " ].",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H23\">",
    " <span class=\"h2\">",
    " Leber hereditary optic neuropathy",
    " </span>",
    " &nbsp;&mdash;&nbsp;Leber hereditary optic neuropathy (LHON) is a maternally
    inherited bilateral subacute optic neuropathy caused by mutations in the
    mitochondrial genome. It is the first human disease to be associated with a
    mitochondrial DNA point mutation [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/56\">",
    " 56",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " Three LHON mtDNA mutations at nucleotide positions 3460, 11778, and 14484 are
    specific for LHON. These mutations account for more than 90 percent of worldwide
    cases and are designated as primary [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/57\">",
    " 57",
    " </a>",
    " ]. They are missense mutations in the subunit genes for the subunits of the
    electron transport chain complexes I, III, and IV. The three primary LHON mutations
    appear to cause profound impairment of complex I-dependent ATP synthesis,
    suggesting that they result in a common disease-causing mechanism [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/58\">",
    " 58",
    " </a>",
    " ]. However, the pathogenesis remains uncertain [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/56\">",
    " 56",
    " </a>",
    " ]. At least 15 other secondary mutations have been identified, but their
    pathogenicity is unclear; they may serve as exacerbating genetic factors.",
    " </p>",
    " <p>",
    " LHON typically produces severe and permanent visual loss in men [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/59,60\">",
    " 59,60",
    " </a>",
    " ]. The initial symptoms include visual dysfunction with blurring of vision and
    loss of central vision, most often beginning in the late teens. However,
    variability in the age of onset, spectrum of clinical expression, and outcome
    exists.",
    " </p>",
    " <p>",
    " In one series of 72 patients with the 11778 mutation, 82 percent were males
    [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/60\">",
    " 60",
    " </a>",
    " ]. The age at onset of visual loss ranged from 8 to 60 years, the time
    interval between affected eyes averaged 1.8 months, and progression to visual
    acuity of",
    " <span class=\"nowrap\">",
    " 20/200",
    " </span>",
    " or worse occurred in 98 percent of eyes over an average time of 3.7 months.
    Telangiectatic microangiopathy, disk pseudoedema, and vascular tortuosity, which
    are classic features of LHON, were seen in 58 percent of patients.",
    " </p>",
    " <p>",
    " However, not all patients have such rapid progression, as illustrated in a
    report of 53 patients, 15 of whom had favorable outcomes [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/61\">",
    " 61",
    " </a>",
    " ]. In the latter group, seven had subclinical disease; two had slowly
    progressive LHON with a favorable visual outcome; and six had classic acute onset
    followed by spontaneous visual recovery. The visual outcome was better in families
    with the 3460 mutation than in those with the 11778 mutation.",
    " </p>",
    " <p>",
    " Numerous factors have been considered as potential explanations for the male
    predominance, variable penetrance, and variable phenotype [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/62\">",
    " 62",
    " </a>",
    " ]. These factors include an additional X locus, impaired mitochondrial
    respiratory chain activity, mtDNA heteroplasmy, environmental factors and
    autoimmunity.",
    " </p>",
    " <p>",
    " Among environmental factors, smoking and alcohol intake may influence the
    expression of disease. Support for this hypothesis comes from an epidemiologic
    study of 125 LHON pedigrees with 196 affected and 206 unaffected carriers [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/63\">",
    " 63",
    " </a>",
    " ]. Both light and heavy cumulative smoking were independent risk factors for
    visual loss. In men who smoked, the lifetime clinical penetrance of visual loss was
    93 percent. In addition, there was a trend towards increased visual failure with
    heavy alcohol intake.",
    " </p>",
    " <p>",
    " Features other than visual loss, including tremor and a multiple sclerosis-
    like illness, occasionally are present [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/64\">",
    " 64",
    " </a>",
    " ]. Additional findings that can occur in children include an extrapyramidal
    syndrome, seizures, ataxia, spasticity, mental retardation, and peripheral
    neuropathy.",
    " </p>",
    " <p>",
    " Muscle biopsy shows abnormal mitochondria in the subsarcolemmal region by
    electron microscopy [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/59,65\">",
    " 59,65",
    " </a>",
    " ]. In the CNS, demyelination of the optic tracts and cell loss and gliosis of
    the geniculate bodies occur, but the visual cortex is normal. Axonal depletion
    centrally in the optic nerve is present, as is loss of ganglion cells in the
    retina.",
    " </p>",
    " <p>",
    " The diagnosis typically is made by demonstration of the DNA point mutations.
    They can be detected using whole white blood cells. In addition, the defects in
    respiratory enzymes in the abnormal mitochondria can be demonstrated on muscle
    biopsy.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H24\">",
    " <span class=\"h1\">",
    " DNA REPAIR DISORDERS",
    " </span>",
    " &nbsp;&mdash;&nbsp;The DNA repair disorders are characterized by
    susceptibility to chromosomal breakages, increased frequency of breaks, and
    interchanges occurring either spontaneously or following exposure to various DNA
    damaging agents. The underlying defect in these syndromes is the inability to
    repair a particular type of DNA damage [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/66\">",
    " 66",
    " </a>",
    " ]. The inheritance of these disorders is autosomal recessive and they show an
    increased tendency to develop malignancies. Two of these disorders, xeroderma
    pigmentosum and the Cockayne syndrome, manifest a peripheral neuropathy (",
    " <a class=\"graphic graphic_table graphicRef52324 \" href=\"UTD.htm?
    39/16/40204\">",
    " table 1D",
    " </a>",
    " ).",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H25\">",
    " <span class=\"h2\">",
    " Xeroderma pigmentosum",
    " </span>",
    " &nbsp;&mdash;&nbsp;Xeroderma pigmentosum (XP) is a multigenic, multiallelic
    autosomal recessive disease that occurs in the United States at a frequency of
    approximately 1:250,000. Homozygotes have severe sun sensitivity that leads to
    degeneration of regions of the skin and eyes, leading to various forms of cutaneous
    malignancy. Mutations in eight genes have been identified. Seven of these genes
    (ie, XPA to XPG) are involved in nucleotide excision repair of carcinogen adducts
    after UV irradiation, while the other (ie, XPV) is involved in error-free
    replication of DNA damaged by UV irradiation. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?6/26/6569?
    source=see_link&amp;anchor=H12#H12\">",
    " \"Inherited susceptibility to melanoma\", section on 'Xeroderma pigmentosum
    genes'",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " Approximately 25 percent of patients with XP have neurologic abnormalities of
    varying severity caused by primary neuronal degeneration [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/67\">",
    " 67",
    " </a>",
    " ]. Neurologic features may be mild or severe and can include progressive
    cognitive impairment, ataxia, choreoathetosis, sensorineural hearing loss,
    spasticity, seizures, and peripheral neuropathy with diminished or absent deep
    tendon reflexes [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/67-69\">",
    " 67-69",
    " </a>",
    " ]. Acquired microcephaly also may be seen.",
    " </p>",
    " <p>",
    " The dermatologic manifestations of XP are discussed elsewhere. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?24/56/25482?
    source=see_link&amp;anchor=H16#H16\">",
    " \"Epidemiology and risk factors for cutaneous squamous cell carcinoma\",
    section on 'Xeroderma pigmentosum'",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H26\">",
    " <span class=\"h2\">",
    " Cockayne syndrome",
    " </span>",
    " &nbsp;&mdash;&nbsp;Cockayne syndrome is a rare multisystem disorder with
    characteristic physical features and progressive dementia. The child typically is
    considered normal until two years of age. An unusual facies with large ears and
    sunken eyes occurs. The syndrome is characterized by severe physical and mental
    retardation, short stature, microcephaly, progressive neurologic dysfunction caused
    by demyelination, retinal degeneration with a pigmented retinopathy and optic
    atrophy, kyphoscoliosis, gait defects, and sun sensitivity but no increased
    frequency of cancer [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/70\">",
    " 70",
    " </a>",
    " ]. In 13 cases confirmed with biochemical assays (unscheduled DNA synthesis
    and recovery of RNA synthesis in skin fibroblasts after exposure to UV
    irradiation), there was wide variation in the clinical manifestations ranging from
    prenatal features to normal psychomotor development [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/71\">",
    " 71",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " These observations suggest that Cockayne syndrome should be considered in
    children with growth retardation, microcephaly and one of the characteristic
    features (eg, sunken eyes, limb ataxia, abnormal auditory evoked responses, or
    increased ventricular size and white matter changes on neuroimaging).",
    " </p>",
    " <p>",
    " Affected patients have white matter demyelination in the CNS, with atrophy of
    the cerebrum and cerebellum. Perivascular calcifications are seen in the basal
    ganglia and cerebellum. MRI scans show increased signal in the white matter with T2
    images.",
    " </p>",
    " <p>",
    " Two complementation groups (CS-A and CS-B) have been identified, and 80
    percent of patients have been assigned to the CS-B complementation group [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/72,73\">",
    " 72,73",
    " </a>",
    " ]. The CS-A gene encodes a WD repeat protein, which interacts with the CS-B
    protein to enhance the transcription factor II subunit of RNA polymerase II [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/74,75\">",
    " 74,75",
    " </a>",
    " ]. The CS-B protein is a helicase involved in the preferential repair of
    active genes [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/76\">",
    " 76",
    " </a>",
    " ].",
    " </p>",
    " <p>",
    " Like XP, CS cells are hypersensitive to the lethal effects of UV light, but
    nucleotide excision repair of the bulk of genomic DNA is unaffected. CS cells are
    defective in a subpathway of nucleotide excision repair, known as transcription-
    coupled repair, whereby damage in the transcribed strand of active genes is rapidly
    and preferentially repaired [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/77,78\">",
    " 77,78",
    " </a>",
    " ]. Thus, in CS cells, damage in active genes is repaired at the same
    relatively slow rate as in the bulk DNA. It appears to be sufficient to prevent a
    predisposition to cancer.",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H27\">",
    " <span class=\"h1\">",
    " HEREDITARY TYROSINEMIA",
    " </span>",
    " &nbsp;&mdash;&nbsp;Four autosomal recessive disorders result from deficiencies
    in specific enzymes in the tyrosine catabolic pathway: hereditary tyrosinemia (HT)
    types 1, 2, and 3, and alkaptonuria. These disorders summarized briefly below and
    discussed in detail separately. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?23/4/23624?
    source=see_link\">",
    " \"Disorders of tyrosine metabolism\"",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " Tyrosinemia type 1 (HT1) is the most severe disorder of tyrosine metabolism.
    It is characterized by severe progressive liver disease and renal tubular
    dysfunction. HT1 is caused by mutations in the fumarylacetoacetate hydrolase gene
    (FAH), which encodes the last enzyme in the tyrosine catabolic pathway.",
    " </li>",
    " <li>",
    " Tyrosinemia type 2 (Richner-Hanhart syndrome) is characterized by keratitis,
    palmoplantar hyperkeratosis, mental retardation, and elevated blood tyrosine levels
    [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/79\">",
    " 79",
    " </a>",
    " ]. The disease is caused by deficiency in hepatic tyrosine aminotransferase
    (TAT).",
    " </li>",
    " <li>",
    " Tyrosinemia type 3 is caused by deficiency of 4-hydroxyphenylpyruvate
    dioxygenase. It is an extremely rare disorder associated with hypertyrosinemia and
    elevated urinary excretion of 4-hydroxyphenyl derivatives. Affected patients have
    neurologic dysfunction, including ataxia, seizures, and mild psychomotor
    retardation, but no other systemic involvement.",
    " </li>",
    " </ul>",
    " </p>",
    " <p>",
    " Severe neurologic manifestations can occur in children with HT1. These are due
    to the accumulation of succinylacetone, which is a potent inhibitor of ALA
    dehydratase (porphobilinogen synthase) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/80,81\">",
    " 80,81",
    " </a>",
    " ]. Thus, patients may have symptoms of ALA dehydratase porphyria. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?5/33/5656?
    source=see_link\">",
    " \"ALA dehydratase porphyria\"",
    " </a>",
    " .)",
    " </p>",
    " <p>",
    " In one study of 48 children with tyrosinemia identified with neonatal
    screening, neurologic crises resembling the crises of the neuropathic porphyrias
    occurred in 20 (42 percent) [",
    " <a class=\"abstract\" href=\"UTD.htm?0/37/602/abstract/82\">",
    " 82",
    " </a>",
    " ]. These acute episodes of peripheral neuropathy were characterized by severe
    pain with extensor hypertonia (in 75 percent), vomiting or paralytic ileus (69
    percent), muscle weakness (29 percent), and self-mutilation (8 percent). Eight
    children required mechanical ventilation because of paralysis. Between crises, most
    survivors regained normal function. Electrophysiologic studies in seven patients
    and neuromuscular biopsies in three patients showed axonal degeneration and
    secondary demyelination. (See",
    " <a class=\"medical medical_review\" href=\"UTD.htm?23/4/23624?
    source=see_link\">",
    " \"Disorders of tyrosine metabolism\"",
    " </a>",
    " .)",
    " </p>",
    " <p class=\"headingAnchor\" id=\"H21258289\">",
    " <span class=\"h1\">",
    " SUMMARY",
    " </span>",
    " </p>",
    " <p>",
    " <ul class=\"bullet-block\">",
    " <li>",
    " The spinocerebellar ataxias are a heterogeneous group of inherited disorders
    with different neuropathological profiles reflecting the degree of cerebellar and
    brainstem dysfunction or degeneration. A peripheral neuropathy is described in some
    but not all. (",
    " <a class=\"graphic graphic_table graphicRef74269 \" href=\"UTD.htm?
    10/59/11198\">",
    " table 1A",
    " </a>",
    " ). (See",
    " <a class=\"local\" href=\"#H21258726\">",
    " 'Spinocerebellar ataxias'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " Infantile neuroaxonal dystrophy is an autosomal recessive disorder. It is
    considered one of several subtypes of neurodegeneration with brain iron
    accumulation (NBIA). Symptoms reflect involvement of the peripheral nerves, central
    nervous system, and autonomic nervous system (",
    " <a class=\"graphic graphic_table graphicRef72307 \" href=\"UTD.htm?
    31/28/32204\">",
    " table 1B",
    " </a>",
    " ). The usual onset ranges from ages 1 to 3 years. Manifestations include
    motor and cognitive regression, spasticity, muscle atrophy, hypotonia, cerebellar
    ataxia, dystonia, optic atrophy, and distal sensory loss. (See",
    " <a class=\"local\" href=\"#H2\">",
    " 'Infantile neuroaxonal dystrophy'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " Tangier disease is an autosomal codominant condition in which homozygotes
    have no serum high density lipoprotein (HDL) and heterozygotes have serum HDL
    concentrations of approximately one-half of those in normal individuals.
    Homozygotes develop cholesterol ester deposition in tonsils (orange tonsils),
    liver, spleen, gastrointestinal tract, lymph nodes, bone marrow, and Schwann cells.
    The main clinical manifestations are hepatosplenomegaly and premature coronary
    disease; a neuropathy occurs in at least 50 percent of patients and is the most
    debilitating feature of the disease. (See",
    " <a class=\"local\" href=\"#H6\">",
    " 'Tangier disease'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " Abetalipoproteinemia (Bassen-Kornzweig syndrome) is a rare autosomal
    recessive disorder that is characterized by defective assembly and secretion of
    apolipoprotein B (apo B) and apo B containing lipoproteins. A spectrum of clinical
    manifestations can be seen (",
    " <a class=\"graphic graphic_table graphicRef72307 \" href=\"UTD.htm?
    31/28/32204\">",
    " table 1B",
    " </a>",
    " ). All patients have neurologic manifestations such as retinitis pigmentosa,
    peripheral neuropathy, and ataxia. (See",
    " <a class=\"local\" href=\"#H10\">",
    " 'Abetalipoproteinemia'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " Refsum disease is a disorder of peroxisomal function. Classic Refsum disease
    is characterized by retinitis pigmentosa, peripheral polyneuropathy, cerebellar
    ataxia, and elevated cerebrospinal fluid protein concentration (",
    " <a class=\"graphic graphic_table graphicRef72307 \" href=\"UTD.htm?
    31/28/32204\">",
    " table 1B",
    " </a>",
    " ). Additional features may include sensorineural deafness, ichthyosis,
    anosmia, and cardiac conduction defects. (See",
    " <a class=\"local\" href=\"#H13\">",
    " 'Refsum disease'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " Chediak-Higashi syndrome is an autosomal recessive disorder characterized by
    recurrent infections, partial albinism, hepatosplenomegaly, an increased risk of
    lymphoreticular malignancy, and multiple neurologic abnormalities (",
    " <a class=\"graphic graphic_table graphicRef72307 \" href=\"UTD.htm?
    31/28/32204\">",
    " table 1B",
    " </a>",
    " ). (See",
    " <a class=\"local\" href=\"#H21258209\">",
    " 'Chediak-Higashi syndrome'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " Lysosomal storage diseases are a group of approximately 36 heterogeneous
    disorders characterized by the accumulation of undigested macromolecules within the
    lysosomes. They result from a deficiency of a specific lysosomal enzyme or protein.
    Many are associated with a neurodegenerative phenotype, and a peripheral neuropathy
    occurs in Fabry disease, Krabbe disease, metachromatic leukodystrophy, and Niemann-
    Pick disease (",
    " <a class=\"graphic graphic_table graphicRef56567 \" href=\"UTD.htm?
    36/27/37308\">",
    " table 1C",
    " </a>",
    " ). (See",
    " <a class=\"local\" href=\"#H15\">",
    " 'Lysosomal storage diseases'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " Defects in structure or function of mitochondria, mainly involving the
    oxidative phosphorylation, mitochondrial biogenesis and other metabolic pathways,
    are associated with a wide spectrum of clinical phenotypes. Peripheral neuropathy
    is a prominent feature in several (",
    " <a class=\"graphic graphic_table graphicRef52324 \" href=\"UTD.htm?
    39/16/40204\">",
    " table 1D",
    " </a>",
    " ). (See",
    " <a class=\"local\" href=\"#H20\">",
    " 'Mitochondrial disorders'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " The DNA repair disorders are characterized by susceptibility to chromosomal
    breakages, increased frequency of breaks, and interchanges occurring either
    spontaneously or following exposure to various DNA damaging agents. The underlying
    defect in these syndromes is the inability to repair a particular type of DNA
    damage. The inheritance of these disorders is autosomal recessive and they show an
    increased tendency to develop malignancies. Two of these disorders, xeroderma
    pigmentosum and the Cockayne syndrome, manifest a peripheral neuropathy (",
    " <a class=\"graphic graphic_table graphicRef52324 \" href=\"UTD.htm?
    39/16/40204\">",
    " table 1D",
    " </a>",
    " ). (See",
    " <a class=\"local\" href=\"#H24\">",
    " 'DNA repair disorders'",
    " </a>",
    " above.)",
    " </li>",
    " <li>",
    " Four autosomal recessive disorders result from deficiencies in specific
    enzymes in the tyrosine catabolic pathway; these are hereditary tyrosinemia (HT)
    types 1, 2, and 3, and alkaptonuria. Severe neurologic manifestations can occur in
    children with HT1, including acute episodes of peripheral neuropathy characterized
    by severe pain. (See",
    " <a class=\"local\" href=\"#H27\">",
    " 'Hereditary tyrosinemia'",
    " </a>",
    " above.)",
    " </li>",
    " </ul>",
    " </p>",
    " </div>",
    " <div id=\"topicAgreement\">",
    " Use of UpToDate is subject to the",
    " <a class=\"licenseLink\" href=\"./license\" id=\"sla_in_page\"
    target=\"_blank\">",
    " Subscription and License Agreement",
    " </a>",
    " .",
    " </div>",
    " <div class=\"headingAnchor\" id=\"references\">",
    " <h1>",
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    " Uemura A, Osame M, Nakagawa M, et al. Leber's hereditary optic neuropathy:
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    " Newman NJ, Lott MT, Wallace DC. The clinical characteristics of pedigrees of
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    " Nikoskelainen EK, Huoponen K, Juvonen V, et al. Ophthalmologic findings in
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    " Chalmers RM, Schapira AH. Clinical, biochemical and molecular genetic
    features of Leber's hereditary optic neuropathy. Biochim Biophys Acta 1999;
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    " Kirkman MA, Yu-Wai-Man P, Korsten A, et al. Gene-environment interactions in
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    " Charlmers RM, Harding AE. A case-control study of Leber's hereditary optic
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    " Wallace DC, Singh G, Lott MT, et al. Mitochondrial DNA mutation associated
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    " Kraemer KH, Patronas NJ, Schiffmann R, et al. Xeroderma pigmentosum,
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    " Kanda T, Oda M, Yonezawa M, et al. Peripheral neuropathy in xeroderma
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    " Anttinen A, Koulu L, Nikoskelainen E, et al. Neurological symptoms and
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    " Nance MA, Berry SA. Cockayne syndrome: review of 140 cases. Am J Med Genet
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    " Pasquier L, Laugel V, Lazaro L, et al. Wide clinical variability among 13
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    " Cleaver JE, Thompson LH, Richardson AS, States JC. A summary of mutations in
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    " <a class=\"nounderline abstract\" href=\"UTD.htm?0/37/602/abstract/73\">",
    " Mallery DL, Tanganelli B, Colella S, et al. Molecular analysis of mutations
    in the CSB (ERCC6) gene in patients with Cockayne syndrome. Am J Hum Genet 1998;
    62:77.",
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    " Henning KA, Li L, Iyer N, et al. The Cockayne syndrome group A gene encodes
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    " Selby CP, Sancar A. Cockayne syndrome group B protein enhances elongation by
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    " Troelstra C, van Gool A, de Wit J, et al. ERCC6, a member of a subfamily of
    putative helicases, is involved in Cockayne's syndrome and preferential repair of
    active genes. Cell 1992; 71:939.",
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    " van der Horst GT, van Steeg H, Berg RJ, et al. Defective transcription-
    coupled repair in Cockayne syndrome B mice is associated with skin cancer
    predisposition. Cell 1997; 89:425.",
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    " van Hoffen A, Natarajan AT, Mayne LV, et al. Deficient repair of the
    transcribed strand of active genes in Cockayne's syndrome cells. Nucleic Acids Res
    1993; 21:5890.",
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    " Goldsmith LA, Kang E, Bienfang DC, et al. Tyrosinemia with plantar and
    palmar keratosis and keratitis. J Pediatr 1973; 83:798.",
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    " Sassa S, Kappas A. Hereditary tyrosinemia and the heme biosynthetic pathway.
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    " Lindblad B, Lindstedt S, Steen G. On the enzymic defects in hereditary
    tyrosinemia. Proc Natl Acad Sci U S A 1977; 74:4641.",
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    " Mitchell G, Larochelle J, Lambert M, et al. Neurologic crises in hereditary
    tyrosinemia. N Engl J Med 1990; 322:432.",
    " </a>",
    " </li>",
    " </ol>",
    " </div>",
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    " <a href=\"#\" title=\"Collapse Topic Outline\">",
    " <img alt=\"\" src=\"./../images/orange_arrow_left.myextg\"/>",
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    " <h1>",
    " TOPIC OUTLINE",
    " </h1>",
    " <div id=\"outline\">",
    " <ul>",
    " <li>",
    " <a class=\"sr_button\" href=\"#H21258289\" id=\"summRecButton\">",
    " <span>",
    " SUMMARY",
    " </span>",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H1\">",
    " INTRODUCTION",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H21258726\">",
    " SPINOCEREBELLAR ATAXIAS",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H2\">",
    " INFANTILE NEUROAXONAL DYSTROPHY",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H3\">",
    " Clinical features",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H4\">",
    " Pathology",
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    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H5\">",
    " Diagnosis",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H6\">",
    " TANGIER DISEASE",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H7\">",
    " Genetics",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H8\">",
    " Clinical manifestations",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H9\">",
    " Treatment",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H10\">",
    " ABETALIPOPROTEINEMIA",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H13\">",
    " REFSUM DISEASE",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H14\">",
    " Clinical features",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H21258209\">",
    " CHEDIAK-HIGASHI SYNDROME",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H15\">",
    " LYSOSOMAL STORAGE DISEASES",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H16\">",
    " Fabry disease",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H17\">",
    " Krabbe disease",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H18\">",
    " Metachromatic leukodystrophy",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H19\">",
    " Niemann-Pick disease",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H20\">",
    " MITOCHONDRIAL DISORDERS",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H21\">",
    " Leigh syndrome",
    " </a>",
    " </li>",
    " <li class=\"dashItem\">",
    " <a class=\"outlineLink\" href=\"#H22\">",
    " - Pathogenesis",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H23\">",
    " Leber hereditary optic neuropathy",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H24\">",
    " DNA REPAIR DISORDERS",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H25\">",
    " Xeroderma pigmentosum",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"outlineLink\" href=\"#H26\">",
    " Cockayne syndrome",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H27\">",
    " HEREDITARY TYROSINEMIA",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a class=\"outlineLink\" href=\"#H21258289\">",
    " SUMMARY",
    " </a>",
    " </li>",
    " <li class=\"plainItem\">",
    " <a href=\"#references\">",
    " REFERENCES",
    " </a>",
    " </li>",
    " </ul>",
    " </div>",
    " <h1>",
    " <div class=\"openRelatedGraphics\" id=\"PEDS/6226\" rel=\"outline_link\">",
    " GRAPHICS",
    " <a class=\"graphics_icon\" href=\"#\" title=\"View All Related Graphics\">",
    " View All",
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    " <a href=\"#\" title=\"TABLES\">",
    " TABLES",
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    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"graphic graphic_table\" href=\"UTD.htm?10/59/11198\" title=\"table
    1A\">",
    " Characteristics of SCA types",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"graphic graphic_table\" href=\"UTD.htm?31/28/32204\" title=\"table
    1B\">",
    " Syndromic hereditary neurop I",
    " </a>",
    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"graphic graphic_table\" href=\"UTD.htm?36/27/37308\" title=\"table
    1C\">",
    " Lysosomal storage disorders",
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    " </li>",
    " <li class=\"bulletItem\">",
    " <a class=\"graphic graphic_table\" href=\"UTD.htm?39/16/40204\" title=\"table
    1D\">",
    " Syndromic hereditary neurop II",
    " </a>",
    " </li>",
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    " </div>",
    " <h1>",
    " RELATED TOPICS",
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    var title_f0_37_603="Criteria for gestational HTN";
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    " &copy;2013 UpToDate",
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    " Criteria for gestational hypertension",
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    " Systolic blood pressure &ge;140 mmHg",
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    " <td>",
    " <strong>",
    " OR",
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    " </td>",
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    " Developing",
    " <strong>",
    " AFTER",
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    " the 20th week of gestation in women known to be normotensive before
    pregnancy. Blood pressure should be elevated on at least two occasions at least six
    hours apart.",
    " </td>",
    " </tr>",
    " </tbody>",
    " </table>",
    " </div>",
    " <div class=\"lgnd\">",
    " <div class=\"footnotes\">",
    " </div>",
    " <div class=\"reference\">",
    " </div>",
    " </div>",
    " </div>",
    " </div>",
    "</div>"].join("\n");
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    var title_f0_37_604="Natural history of chronic AR";
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    title=\"Email graphic(s)\"/>",
    " </a>",
    " <a class=\"icontxt textLink etacLink\" href=\"#\" title=\"Email graphic(s)\">",
    " Email",
    " </a>",
    " </div>",
    " </div>",
    " <div class=\"graphic\">",
    " <div class=\"figure\">",
    " <div class=\"ttl\">",
    " Natural history of chronic aortic regurgitation mostly based upon data from
    nine series with a total of 593 patients followed for a mean of 6.6 years",
    " </div>",
    " <div class=\"cntnt\">",
    " <table cellspacing=\"0\">",
    " <tbody>",
    " <tr>",
    " <td class=\"subtitle1_left\" colspan=\"2\" rowspan=\"1\">",
    " Asymptomatic patients with normal left ventricular (LV) systolic
    function",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " Progression to symptoms and/or LV dysfunction",
    " </td>",
    " <td>",
    " Less than 6 percent/year",
    " </td>",
    " </tr>",
    " <tr>",
    " <td class=\"sublist1_start\" colspan=\"2\" rowspan=\"1\">",
    " Progression to symptoms, LV dysfunction, or death",
    " </td>",
    " </tr>",
    " <tr>",
    " <td class=\"sublist1\" colspan=\"2\" rowspan=\"1\">",
    " According to LV end-systolic dimension*",
    " </td>",
    " </tr>",
    " <tr>",
    " <td class=\"sublist2\">",
    " &gt;50 mm",
    " </td>",
    " <td class=\"sublist_other\">",
    " 19 percent/year",
    " </td>",
    " </tr>",
    " <tr>",
    " <td class=\"sublist2\">",
    " 40 to 50 mm",
    " </td>",
    " <td class=\"sublist_other\">",
    " 6 percent/year",
    " </td>",
    " </tr>",
    " <tr>",
    " <td class=\"sublist2\">",
    " &lt;40 mm",
    " </td>",
    " <td class=\"sublist_other\">",
    " 0 percent/year",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " Progression to asymptomatic LV dysfunction",
    " </td>",
    " <td colspan=\"1\">",
    " Less than 3.5 percent/year",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " Sudden death",
    " </td>",
    " <td colspan=\"1\">",
    " Less than 0.2 percent/year",
    " </td>",
    " </tr>",
    " <tr>",
    " <td class=\"subtitle1_left\" colspan=\"2\" rowspan=\"1\">",
    " Asymptomatic patients with LV systolic dysfunction",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " Progression to cardiac symptoms",
    " </td>",
    " <td colspan=\"1\">",
    " More than 25 percent/year",
    " </td>",
    " </tr>",
    " <tr>",
    " <td class=\"subtitle1_left\" colspan=\"2\" rowspan=\"1\">",
    " Symptomatic patients",
    " </td>",
    " </tr>",
    " <tr>",
    " <td>",
    " Mortality rate",
    " </td>",
    " <td colspan=\"1\">",
    " More than 10 percent/year",
    " </td>",
    " </tr>",
    " </tbody>",
    " </table>",
    " </div>",
    " <div class=\"lgnd\">",
    " <div class=\"footnotes\">",
    " </div>",
    " <div class=\"reference\">",
    " Data from Bonow, RO, Lakatos, E, Maron, BJ, et al. Serial long-term
    assessment of the natural history of asymptomatic patients with chronic aortic
    regurgitation and normal left ventricular systolic function. Circulation 1991;
    84:1625.",
    " </div>",
    " </div>",
    " </div>",
    " </div>",
    "</div>"].join("\n");
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    var outline_f0_37_604=null;
    var title_f0_37_605="Heart rate and VO2";
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    " <div class=\"graphic\">",
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    " <div class=\"ttl\">",
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    " </div>",
    " <div class=\"lgnd\">",
    " Relation between attained heart rate and oxygen uptake during exercise. One
    metabolic equivalent (MET) is defined as 3.5 mL O2 uptake/kg per min. Mean values
    of approximately 10 METs (VO2 35 mL/kg per min) can be achieved by nonathletic,
    healthy, middle-aged men; this should occur at a heart rate of approximately 175
    beats/min.",
    " <div class=\"footnotes\">",
    " </div>",
    " <div class=\"reference\">",
    " </div>",
    " </div>",
    " </div>",
    " </div>",
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    s=);\">",
    " </div>",
    " <div class=\"lgnd\">",
    " Data from the EPISTENT trial of 2399 patients undergoing emergent or elective
    angioplasty. Top panel: The 30-day incidence of the primary endpoint (death, MI, or
    need for urgent revascularization) was significantly lower among patients receiving
    a stent with abciximab compared to those undergoing angioplasty with abciximab
    therapy or stenting alone (5.3, 6.9, and 10.8 percent, respectively). Bottom panel:
    The benefit from abciximab primarily reflected a reduced incidence of death and of
    large non-Q wave MI (shown in blue).",
    " <div class=\"footnotes\">",
    " </div>",
    " <div class=\"reference\">",
    " Data from The EPISTENT Investigators. Lancet 1998; 352:87.",
    " </div>",
    " </div>",
    " </div>",
    " </div>",
    "</div>"].join("\n");
    var script_f0_37_607=[""].join("\n");
    var outline_f0_37_607=null;

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