R E V I E W A R T I C L E
Helicobacter Pylori Infection : Current Status
YK Joshi*
Peptic ulcer disease (PUD) is a common problem
encountered by physicians in day-to-day practice.
Its prevalence varies from country to country and
from place to place within the country. Till recently
a number of factors were incriminated as the cause
of the disease. These included food habits,
smoking, heredity, physical stress, psychological
stress, alcohol, coffee, drugs, infectious agents like
virus, etc. All these factors were thought to be
responsible for increased acid output, which is the
requirement for the occurrence of the ulcer. It was
believed that “no acid, no ulcer”. During the last
two decades there has been a tremendous
progress in understanding the aetiology,
pathogenesis and management of the disease.
Now, it is certain that the bacterial infection by H.
pylori is the main aetiological agent of peptic ulcer.
Of course, acid remains in the limelight and it
does play an important role. This review deals with
the role of H.pylori in peptic ulcer and its
management.
Epidemiology and Prevalence 1-3
Humans are the only host for H.pylori, which is
found in stomach, and in duodenum, oesophagus
and rectum on areas of metaplastic gastric
epithelium. Other helicobacter species have been
isolated from the animals. Animal models of
Helicobacter infection have been developed due
to shared characteristics of other Helicobacters like
H.mustelae and H. felis with H.pylori.
H.pylori exists the world over and its prevalence
in the population increases with age. In developed
countries, prevalence increases about 1% per year
of age where it is rare in children, and reaches
70% in the seventh decade. In developing
* Additional Professor,
Deptt. of Gastroenterology & HNU,
All India Institute of Medical Sciences,
Ansari Nagar, New Delhi 110 029
countries, more than 50% children acquire the
infection by the age of 10 years, and more than
80% of the population gets infected by the age of
20 years. In asymptomatic individuals prevalence
of H.pylori infection varies from 31%-84%.
H.pylori infection is chronic and once acquired
remains life long, unless eradicated by antibiotics
given for some other conditions. Humoral and
tissue immune response by the host is usually not
sufficient to clear the infection. Though the mode
of transmission is not yet well established, most
probably it takes place by oral-oral or faeco-oral
route and important risk factors are socio-
economic status and age. Overcrowding, poor
socio-economic status and poor hygiene are
associated with high infection rate. Re-infection
rate after eradication is quite high in developing
countries due to the above mentioned risk factors.
Colonisation of H.Pylori occurs by producing
urease and gastric acid inhibitory protein. It can
colonise only in gastric type epithelium and can-
not stay anywhere else in the GI tract in absence
of gastric mucosa. Metaplasia, which is present
in more than 90% of patients of duodenal ulcer,
occurs by replacing the columnar cells, normally
covering the duodenal villi, by gastric type
epithelium. Adhesion of H.pylori to the gastric
epithelium occurs by tissue specific proteins.
Colonisation of the duodenal bulb by H.pylori
leads to mucosal inflammation which makes it
vulnerable to attack by acid or pepsin or bile
resulting into ulceration, however, factors leading
to gastric metaplasia in the duodenal bulb are
not known. Stimulation of the immune system of
H.pylori contributes to host damage and it evades
the immunological clearance.
Bacterial Factors4-7
Direct damage to the host occurs by urease and
other enzymes and toxins produced by the
bacteria. Depending on the enzymes and toxins
production, H.pylori strains phenotypically can be
divided into two groups, i.e., type 1 and type 2.
Type 1 contains vacuolating toxin, encoded by the
gene vacA(94-kda vacA) and cytotoxin associated
protein encoded by the gene cagA(120-128-
kcagA). The second group, i.e., type 2 contains
non-cytotoxic vacA and cagA negative strains. It
has been observed that type 1 strains cause more
intensive inflammation than type 2. Such strain
diversity may explain why some infected individuals
do not develop diseases while some may develop
peptic ulcer and gastric cancer which may be due
to different type of strains. The studies from other
countries have reported that about 70% of strains
isolated from patients with DU produce this toxin
compared to about 30% isolated from non-ulcer
dyspepsia. There is also some evidence to suggest
that the degree of inflammation and subsequently
clinical consequences of H.pylori infection are
related to density of bacterial colonisation. The
enzyme produced by both types of strains plays
an important role in the pathogenesis. Urease
hydrolyses urea into ammonia and creates alkaline
surroundings, thus creating a neutral
microenvironment for the bacteria. It may also
have a role in H.pylori metabolism as a part of
nitrogen cycle. It has been presumed that the
ammonia produced by the urease activity works
with cytotoxin inducing vacuoles.
Though H.pylori is strongly antigenic and leads to
humoral and cellular immune response, the
human host is unable to clear the infection which
may persist life long. The local inflammatory
response leads to accumulation of a number of
different cytokines which includes IL-8 and tumour
necrosis factor alpha. These two cytokines play
an important role in the formation of inflammatory
infiltrate. Type 1 H.pylori strains have been shown
to induce significantly higher IL-8 than type 2
strains.
Effects on Gastric Secretions8-11
Gastrin produced by the G cells stimulates the acid
secretion and has a trophic action on mucosal
Journal of Indian Academy of Clinical Medicine
Vol. 5
cells in the stomach. It has been found that H.pylori
increases the fasting serum gastrin levels in healthy
subjects and also in patients with duodenal ulcer.
The main inhibitor of gastrin secretion and
excretion somatostatin is produced by the D cells.
Somatostatin levels are decreased in H.pylori
positive individuals. H.pylori also decreases the
gastric body mucosal histamine. There are two
main opposite effects of H.pylori on acid secretion
function of the stomach, viz., its effect on fundal
histamine decreases acid output while the effect
on somatostatin leading to hypergastrinaemia
increases the gastric acid output. The basal and
peak acid output changes after eradication of
H.pylori supports the hypothesis that H.pylori
causes impairment in the inhibitory control of
gastric acid. In the early stage of infection acid
output increases, leading to gastric metaplasia in
duodenum, which in turn gets infected with
H.pylori and development of duodenal ulcer. With
diffuse disease the acid output falls.
Diseases associated with H.Pylori12-14
H.pylori infection is found to be associated with
gastritis, non-ulcer dyspepsia (NUD), duodenal
ulcer, gastric ulcer, gastric cancer, gastric
lymphoma of mucosa associated lymphoid tissue
(MALT), non-Hodgkin’s lymphoma and even
coronary heart disease.
It has now been well established that H.pylori is
the cause of almost all duodenal ulcers (DU) and
chronic benign gastric ulcers (GU) which are not
associated with NSAIDs. More than 95% of DU
and 90% of GU are associated with H.pylori
infection and there is a dramatic decrease in their
relapse rate after the H.pylori eradication. Right
now there is no convincing evidence that NUD
symptoms are due to H.pylori infection. Prevalence
of H.pylori infection is comparable between
healthy individuals and patients with the symptoms
of NUD. Recurrent abdominal pain in children
suggestive of NUD subsides after the eradication
of H.pylori which indirectly associates H.pylori
infection with NUD. However, further studies are
necessary in this regard and at present there is no

No. 2 149
indication to eradicate H.pylori in NUD. there if the number of bacteria in the specimen is
less or if the antral biopsy is taken after one week
Association between H.pylori and gastric cancer
of proton pump inhibitors, antibiotics or bismuth
has been reported in several retrospective
treatment, when H.pylori colonize in body or
epidemiological studies. It is postulated that
fundus.
starting with acute gastritis, H.pylori infection leads
to chronic atrophic gastritis, intestinal metaplasia, PCR is highly sensitive and specific but it may detect
dysplasia and ultimately progression to gastric DNA of non-viable bacteria also giving false
adenocarcinoma. High H.pylori infection rate has positive results and also has a limited role in
been reported in patients with gastric cancers confirming eradication of H.pylori after treatment.
compared to healthy subjects. The WHO has put It is usually used for molecular typing of H.pylori
H.pylori in group I, a definite carcinogen. H.pylori and for research.
has also been found to be associated with
Non-invasive tests include serology and urea
development of MALT and subsequent
breath test (UBT). Commercially available ELISA
transformation to malignant lymphoma.
kits detect IgG antibodies in sera. This test is useful
Eradication of H.pylori has shown regression of
to screen the patients for H.pylori infection, usually
low-grade b cell gastric lymphoma of MALT type.
to find out prevalence of H.pylori infection in the
There is some epidemiological evidence that
community. It is a relatively sensitive and specific
H.pylori infection is associated with non-Hodgkin’s
test and also inexpensive. But it has a limited role
lymphoma which is comparatively rare in stomach.
in diagnosing acute infection and in confirming
eradication.
Diagnosis 15-17
UBT is a good non-invasive test. Although it is
A number of invasive and non-invasive tests with
expensive, it is highly sensitive (95%) and specific
almost comparable sensitivity and specificity are
(100%) and also ideal to check the post-treatment
available. Invasive tests require upper GI
eradication. Detection of labelled CO2 (13C or 14C)
endoscopy and biopsy from stomach for histology,
in expired air indicates hydrolysis of urea and
bacterial culture, rapid urease test (RUT) and PCR.
presence of urease producing organism in
Biopsy is fixed in 10% formalin and stained with stomach. Difference between 13C UBT and 14C UBT
haematoxylin and eosin or by modified Giemsa are shown in Table I.
stain. Biopsy can also provide additional
Table I: 13
C- and 14
C-UBT
information on gastritis, metaplasia and dysplasia.
In experienced hands histology has >90% 13
C-UBT 14
C-UBT
sensitivity and >95% specificity. Biopsy specimen Sensitivity 90-100% 90-100%
can also be used for bacterial culture in selective Specificity 90-100% 90-100%
or non-selective media. Though the sensitivity and Radioactive No Yes
specificity of this test is >95% and >80% Analysis Isotope ratio mass Liquid scintillation
Spectrometry counter
respectively, it is time consuming and expensive
Advantages Simple to do Cheap
and also it is not easy to culture this bacteria.
Commercially Immediate results
RUT is 90% sensitive and 100% specific, available
inexpensive and provides results within 20 minutes. Disadvantages High Cost Nuclear Medicine
Department regulations
Urease produced by the bacteria hydrolyses urea
into ammonia. A change in pH changes colour of Follow-up tests to check the eradication should
the indicator from yellow to pink. In case of low be done atleast four weeks after the completion
urease activity it may take as long as 24 hours to of treatment to minimize the likelihood of false
change the colour. False negative result may be negative results. At present, no single test is the

150 Journal of Indian Academy of Clinical Medicine
Vol. 5
No. 2

gold standard for diagnosis of H.pylori. The
combination of two or more of above mentioned
tests are used for this purpose.
Treatment 18-23
The main aim of treating H.pylori is to eradicate
the organism from the foregut. Eradication is
defined as negative test results for H.pylori four
weeks or longer after the antibacterial therapy.
The National Institute of Health of USA
recommends eradication of all H.pylori in all
patients with active peptic ulcer disease or a history
of it and proved infection.
Antimicrobial treatment of H.pylori is difficult, as
the bacteria are located below the mucus layer,
adherent to gastric mucosa where the access of
antimicrobial drugs, given either by enteral or
parenteral route is limited and H.pylori may
acquire resistance to commonly or frequently used
antibacterial drugs. These vary from country to
country depending on the use of different
antibacterial drugs. For example, resistance of
H.pylori to clarithromycin in UK is less than 5%
while in Spain and France it is as high as 15-
17%. It is because of this problem, the treatment
regimens using two or three antimicrobial agents
have been developed.
The ideal therapy for any infection should be
simple, safe, free from side effects, with 100%
efficiency and low cost and same applies to
H.pylori infection also. The ideal treatment
regimen has not yet been established, so there is
no definite recommendation for the optimal
treatment schedule. The treatment for H.pylori
should be given only after the clinical diagnosis
and proper indication for eradication. Eradication
therapy should not be taken lightly. All the
treatment schedules have side effects but they are
mild and usually do not interfere with patient’s
compliance if given with proper instructions.
Effect of the antimicrobial agent depends on the
acid environment of stomach which may decrease
the effectiveness of some antibiotics. Usually the
concentration of antibiotics is low in stomach.
Journal of Indian Academy of Clinical Medicine
Vol. 5
Colloidal bismuth subcitrate (CBS) penetrates
transmucosally, and has been shown to block
adhesion of H.pylori to epithelial cells and to form
protective complexes with glycoproteins and to
stimulate mucosal bicarbonate secretion. In vitro
studies have shown bacteriostatic effect of proton
pump inhibitors (PPI) on H.pylori. PPI also may
interfere with energy production of bacteria. All
the PPI have also been found to cause decrease
in antral H.pylori density during the therapy,
although the fundal count may increase leading
to fundal gastritis. This is an important effect one
has to keep in mind while keeping the patient on
maintenance therapy for gastroesophageal reflux
disease. Clarithromycin is one of the most effective
antimicrobial agent against H.pylori in vitro. It is
quickly absorbed and at pH 5.5, obtained with
the help PPIs, it is the most effective antimicrobial
agent.
Indication for H.pylori Eradication
Treatment for H.pylori in asymptomatic carrier, in
order to decrease reservoir of infection in
community and to prevent the development of
various conditions caused by H.pylori, is
controversial and supported by only a few studies.
It is advised that it should be treated only if chronic
carrier status is proved to initiate the disease
process.
Non-ulcer Dyspepsia
Treatment for H.pylori associated with symptoms
of non-ulcer dyspepsia is also controversial and
at present there is no convincing evidence that
H.pylori is responsible for these symptoms.
Moreover, prevalence of H.pylori in this group
of patients is not higher than the general
population without symptoms. Although a
subset of patients may have their symptoms due
to presence of H.pylori, there is no clear
evidence that they benefit after H.pylori
eradication. At present there is no indication
that patients with non-ulcer or functional
dyspepsia should be treated for H.pylori, till the
results from large trials are available.

No. 2 151
Duodenal and Gastric Ulcer
It has now been well established that H.pylori is
the main cause of most of the duodenal ulcers
and chronic benign gastric ulcers that are not
associated with NSAIDs. More than 95% of
patients with duodenal ulcer are positive for
H.pylori and eradication of infection results in rapid
healing and a dramatic decrease in relapse rate
to less than 5% each year. Duodenal ulcer heals
completely after the eradication therapy and a
course of antisecretory drugs after healing is not
required, unless it is associated with complications
like recent haemorrhage, perforation, etc. There
is some data suggesting prevention of recurrence
of bleeding from ulcer after eradication of H.pylori.
Those who have recurrence of symptoms after
successful eradication, without recurrence of
duodenal ulcer, other causes for such symptoms,
like gastroesophageal reflux disease, gallstones
should be investigated. The clinical benefit of
H.pylori eradication in NSAIDs induced duodenal
or gastric ulcer is not well established. However,
there is some evidence that NSAIDs induced
mucosal damage may be less in the absence of
H.pylori and thus there is some justification to
eradicate H.pylori in NSAIDs induced gastric or
duodenal ulcer.
Though there is a strong circumstantial evidence
to link the H.pylori infection with the development
of gastric adenocarcinoma and WHO has
classified H.pylori as a group I definite carcinogen,
less than 1% of H.pylori infected individuals will
ever develop gastric cancer and so far there is no
evidence that, eradication of H.pylori will decrease
the risk of gastric cancer. It is also not known where
exactly the point of no return is in the gastritis-
atrophy-metaplasia-dysplasia-cancer sequence of
events. With a family history of gastric cancer, if
an individual has an evidence of atrophy,
metaplasia or dysplasia in early life, he may be
offered H.pylori eradication treatment. H.pylori
infection has been associated with MALT
lymphoma, which subsequently develops into
malignant lymphoma. It has been found that
H.pylori specific T-lymphocytes act as a growth
152 Journal of Indian Academy of Clinical Medicine
stimulant for MALT, which suggests that early
tumour may respond if this stimulus is withdrawn.
H.pylori eradication therapy results in regression
of low-grade b-cell gastric lymphoma of MALT
type.
Epidemiological evidence has suggested that
H.pylori infection is also associated with non-
Hodgkin’s lymphoma but there is no data on effect
of H.pylori eradication in this condition.
H.pylori infection has been found in more than
90% patients with hypertrophic gastropathy
(Menetrier’s disease). Eradication of H.pylori has
been reported to return the stomach and protein
concentration to normal in this condition.
Eradication Regimens24-34
H.pylori infection can be cured with antibacterial
therapy and with presently available combination
more than 90% eradication can be achieved. The
present therapeutic standards are clear,
eradication in atleast 90% after one week of
treatment and less than 5% of the patients dropout
from the treatment because of side effects. It
should be remembered that all currently available
treatments are associated with side effects. Various
therapeutic regimens that have been tried are as
follows :
Monotherapy : Single drug therapy is not effective
in eradication of H.pylori. With a single antibiotic,
eradication rate has been reported from 0-54%.
Clarithromycin has been found as the most
effective single drug. However a single antibiotic
should not be prescribed as it is not only ineffective
but also it may produce a resistant strain. H2
receptor antagonists have no effect on H.pylori
and despite in vitro effect of PPI on H.pylori, they
are not effective in eradicating the bacteria.
Bismuth compounds do suppress the H.pylori, but
as monotherapy, bismuth does not eradicate this
bacteria. Due to the ineffectiveness and possibility
of development of resistant strain, monotherapy
is not recommended.
Dual therapy: Combinations that have been tried
for eradication of H.pylori include two antibiotics;

Vol. 5
No. 2
H2 receptor antagonists with antibiotics; bismuth rate was 96%.
with antibiotics; omeprazole (PPI) with amoxycillin;
and omeprazole (PPI) with clarithromycin. Table II : Dual therapy with amoxycillin35
Combination of any two antibiotics is not effective Omeprazole Ranitidine Bismuth
in H.pylori eradication. High dose H2RAs given Amoxycillin Citrate, Amoxycillin
along with antibiotic (amoxycillin or clarithromycin) Dosing 20-40 mg b.i.d. 400-800 mg b.i.d.
500 mg q.i.d. or 1g b.i.d 500 mg q.i.d.
for two weeks may eradicate H.pylori in upto 60%
Duration 2 weeks 2 weeks
of patients. Colloidal bismuth subcitrate (CBS) with
Hp Eradication 50-85% 65%
metronidazole have been found effective in almost
Side effects common:diarrhoea common:diarrhoea
85% in small studies. Ranitidine bismuth citrate
(RBC) in combination with either amoxycillin or
Table III: Dual therapy with clarithromycin 35
clarithromycin given for two weeks has shown
eradication rate from 65% to 80% depending upon Omeprazole Ranitidine Bismuth
Clarithromycin Citrate, Clarithromycin
the dosage.
Dosing 40 mg b.i.d. 400 mg b.i.d.
Triple Therapy: Various combinations of three 500 mg t.i.d. 500 mg b.i.d.
drugs have been tried. Drugs that have been used Duration 2 weeks 2 weeks
in triple therapy are CBS, RBC, H2RA, PPI, Hp Eradication 60-80% 80%
amoxycillin, tetracycline, clarithromycin, Side effects common: taste common:taste
metronidazole and tinidazole. There are wide disturbances, diarrhaea disturbances, diarrhoea
dosage variation and different treatment schedules
with eradication rate varying from 35 to 95% have Table IV: Low-dose, 1 week triple therapies35
been reported in the literature. Such different PPI PPI PPI
findings are because of dissimilarities in patient Clarithromycin Amoxycillin Amoxycillin
Metronidazole Clarithromycin Metronidazole
populations, resistance to metronidazole and other
Dosing o.d. or b.i.d. b.i.d. o.d.
antibiotics and variation in compliance by the
250 mg b.i.d. 1g b.i.d 500 mg t.i.d
patients. Classical triple therapy given for seven 400mg b.i.d. 250-500 mg b.i.d. 400 mg t.i.d
days has not been always successful. On the Duration 7 days 7 days 7 days
contrary, there is no further benefit if the treatment Hp eradication 85-95% 85-95% 75-90%
is given for 14 days or more. Tetracycline or Side effects Minimal:nausea common:diarrhoea, common:diarrhoea,
amoxycillin based therapy has no significant nausea nausea
difference in eradication. The combinations used
for triple therapy are; bismuth+antibiotics+PPI, Table V: Triple therapy combinations with
H 2 RA+metronidazole+amoxycillin, PPI+ amoxycillin and metronidazole 35
Metronidazole/tinidazole+amoxycillin/clarithro-
CBS PPI Ranitidine
mycin. Newer PPIs like lansoprazole and Amoxycillin Amoxycillin Amoxycillin
pantoprazole also have been used in these Metronidazole Metronidazole Metronidazole
combinations. Various combinations with their Dosing 120 mg q.i.d. o.d. 300 mg o.d.
efficacies are shown in Tables II-IV. 500 mg q.i.d. 500mg t.i.d 750 mg t.i.d.
200-400mg q.i.d. 400mg t.i.d. 500 mg t.i.d.
Quadruple Therapy: Combination of four Duration 2 weeks 1 week 12 days
drugs also have been tried, though these have Hp eradication 60-90% 75-90% 68-90%
more side effects and compliance problems. Side effects common:diarrhoea, common:diarrhoea, common:diarrhoea,
Drugs that have been given for one week in nausea nausea nausea
this combination were omeprazole (20mg bid),
CBS(120mg bid), tetracycline (500mg bid) and It is very difficult to eradicate metronidazole
metronidazole (500 mg bid). The eradication resistant H.pylori. Combination therapy consisting

Journal of Indian Academy of Clinical Medicine
Vol. 5
No. 2 153

metronidazole may not be very effective against
metronidazole resistant strains (eradication rate
may be less than 50%). Primary or acquired
metronidazole resistance of H.pylori is 20-30% in
western countries and as high as 66% in India.
Metronidazole or tinidazole resistance may be
reduced by combining with bismuth or by giving
quadruple therapy for 10 days.
Inspite of large available data, it is yet not possible
to give final recommendation as to the best
regimen to eradicate H.pylori as there are very
few large trials. It is quite likely that there is no
significant difference between triple and quadruple
regimens. The effective eradication also depends
upon other factors like compliance, metronidazole
resistant status and side effects of the drugs. Cost
is also an important consideration and also the
relapse rate. However, for all practical purposes
the triple drug regimen in a suitable combination
is preferable for the treatment of H.pylori infection.
In high metronidazole resistant areas preference
should be given to a combination without
metronidazole.
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