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hypersensitivity

pneumonitis (extrinsic
allergic alveolitis)
INTRODUCTION
an immunologic reaction to an
inhaled agent, particularly an organic
antigen, occurring within the
pulmonary parenchyma
Farmer's lung is one of the most
common forms of HP, affecting 0.4 to
7 percent of the farming population
ETIOLOGIC AGENTS:
Farming, vegetable, or dairy cattle workers
Bagassosis
Sugar cane inhalation of dust from
bagasse (the residue of cane after
extraction of sugar).
thermoactinomycetes sacchari
Byssinosis
also called "brown lung disease" or
"Monday fever",
caused by exposure to cotton dust
Pathogenesis

Most patients have circulating


immunoglobulin G antibodies that are
specific for the offending antigen.
The antibody (called precipitating
antibody) reacts with a specific antigen to
form a precipitation.
initially thought to be an immunocomplex-
mediated process, subsequent studies
showed that cell-mediated immunity is
more important
Early response to the antigen is characterized
by an increase in neutrophils in the alveoli and
small airways followed by an influx of
mononuclear cells.
release proteolytic enzymes, prostaglandins,
and leukotrienes.
Alveolar macrophages are activated and an
array of proinflammatory cytokines, such as
TNF-a, IL-1 and IL-8, are produced.
lead to progressive inflammation and the
formation of granulomas,
clinical presentations of HP

ACUTE HP
SUBACUTE OR INTERMITTENT HP
CHRONIC PROGRESSIVE HP
ACUTE HP
abrupt onset (four to six hours following exposure)
fever, chills, malaise, nausea, cough, chest
tightness, and dyspnea without wheezing.
Physical examination is notable for tachypnea and
diffuse fine crackles. Wheezing is rarely present.
Removal from exposure to the inciting antigen in
acute HP results in subsiding of symptoms within
12 hours to several days and complete resolution
of clinical and radiographic findings within several
weeks.
The disease may recur with reexposure.
Laboratory tests are of limited utility.
The erythrocyte sedimentation rate and quantitative
immunoglobulins are elevated in many patients.
elevated C-reactive protein, and circulating immune
complexes also may be found.
The serum LDH may be high in acute phases of the
disease and may decline as clinical indices improve.
Positive precipitating IgG serum antibodies to common
antigens may be demonstrated
bronchoalveolar lavage (BAL) lymphocytosis is usually
present
chest film is frequently normal
Pathologically, acute HP is
characterized by poorly formed,
noncaseating interstitial granulomas
or mononuclear cell infiltration in a
peribronchial distribution, often with
prominent giant cells
SUBACUTE OR
INTERMITTENT HP
gradual development of productive
cough, dyspnea, fatigue, anorexia,
and weight loss.
tachypnea and diffuse crackles. T
The major laboratory abnormalities
are bronchoalveolar lavage (BAL)
lymphocytosis
chest radiograph may be normal or
show micronodular or reticular
opacities
CHRONIC PROGRESSIVE HP
may lack a history of acute episodes
usually reports the insidious onset of
cough, dyspnea, fatigue, and weight
loss.
Digital clubbing may be seen in
advanced disease
removal from exposure usually
results in only partial improvement,
DIAGNOSTIC CRITERIA
1. Known exposure to offending antigen(s)
identified by:
A. History of appropriate exposure.
B. Aerobiologic or microbiologic
investigations of the environment that
confirm the presence of an inciting
antigen .
C. The presence of specific IgG
antibodies in serum against the identified
antigen (serum precipitins
2. Compatible clinical, radiographic, or physiologic
findings:
A. Respiratory ( constitutional) symptoms
and signs, such as crackles on chest exam,
weight loss, cough, breathlessness, febrile
episodes, wheezing, and fatigue. These findings
are especially suggestive if present, appearing,
or worsening several hours after antigen
exposure .

B. Reticular, nodular, or ground glass opacity


on chest radiograph or HRCT.

C. Altered spirometry and/or lung volumes


(may be restrictive, obstructive, or mixed
3. BAL with lymphocytosis:
A. Usually with low CD4 to CD8 ratio
B. Positive specific immune response to the
antigen by lymphocyte transformation testing
(currently not available in most centers)

4. Positive inhalation challenge testing by:


A. Reexposure to the environment
B. Inhalation challenge to the suspected antigen in a
hospital setting

5. Histopathology showing compatible changes:


A. Poorly formed, noncaseating granulomas OR B.
Mononuclear cell infiltrate
Prevention
diminishing exposure to provocative
antigens.
minimizing contact with potential
inciting agents, reducing microbial
contamination of the work or home
environment, or using protective
equipment.
Treatment
Glucocorticoids

Patients with persistent symptoms (eg, dyspnea,


cough, fatigue, weight loss),
abnormal lung function tests (eg, lung
restriction and reduced diffusing capacity)
hypoxemia
radiographic evidence of extensive lung
involvement
initiated with prednisone 0.5 to 1 mg per
kilogram of ideal body weight per day (up to a
maximum daily dose of 60 mg per day)
tappering