الفهرس 
StomachOnly 14 pages are availabe for public view
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Abstract
in developing world, where infection may appear early in life in
childhood, and may arise to an incidence of 80% among young adults. In
developed countries, childhood infection is uncommon, but prevalence
arise after the age of 40.
It was suggested that the eradication of H.pylori does play an
important role in the reduction of non ulcer dyspepsia symptoms in the
long term, and that the persistence of infection with H.pylori results in
more dyspeptic symptoms.
It was now recognized that H.pylori infection can cause acute
gastritis.
Studies from many regions of the world have confirmed the
association of H.pylori infection with chronic antral gastritis; H.pylori
infection specifically associated with type B gastritis.
H.pylori cause chronic inflammation, gastritis which does not
generally resolve until the bacterium is eradicated by antimicrobial
treatment.
It is now well established that H.pylori is associated with more
than 90% of duodenal ulcers and 70-80% of gastric ulcers and the cure of
this infection results in long term remission.
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It has been shown that eradiation of H.pylori speeds up gastric
ulcer healing with a 6 weeks healing rate of 85%.
Recently H.pylori has been designated a class I carcinogen by the
world health organization. H.pylori is present up to 92% of patients of
gastric MALT lymphoma compared with 50% of control. H.pylori is the
major cause of chronic atrophic gastritis and is likely to be an important
etiological factor in the development of gastric cancer.
The role of H.pylori in the pathogenesis of esophageal reflux has
not been elucidated; gastric acid hypersecretion may be implicated and
isolation of the organism in patients with reflux- induced gastric
metaplasia of the esophagus has been reported in 0-25%of patients.
Also GERD may develop de novo or it may be unmasked after
successful eradication of H.pylori; on the other hand another study had
shown that H.pylori may play a protecting role against GERD.So the role
of H.pylori in GERD is still under study to show whether it is positive or
negative role.
We can say that colorectal carcinoma over express gastrin; and
receptors for gastrin (CCKB-R) and (Cox-2), increased plasma level of
gastrin should be considered as suitable biomarker of CRC; H.pylori
infection may contribute to colonic carcinogenesis by enhancing
expression of gastrin and Cox-2, they may account for stimulation of the
tumour growth, angiogenesis, and reduction in a apoptosis as evidenced
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by an increased ratio of mRNA expression for anti-apoptotic Bcl2 over
proapoptotic Bax proteins.
H.Pylori positive patients who developed CRC should be subjected
to H.Pylori eradication; this is expected to reduce hypergastrinemia and
to attenuate Cox-2 expression. so treatment of patient with CRC with
Cox-2 selective inhibitors now gained a strong support as a preventive
measure.
However, recent reports have shown that Crohn’s disease patients
have lower prevalence of H.pylori infection it was also observed that
previous use of sulphasalazine is associated with reduced risk of
Helicobacter pylori infection in IBD patients. We can say that the
clinical course of Crohn’s disease may be ”sui genesis” connected with
H.pylori infection but the exact mechanisms remain to be discovered.
H.pylori DNA has been found within the livers of patients with
HCC;however culture results have been negative, and a causative
association remains unproven. Helicobacter genus bacterium may take
part in the pathogenesis of primary biliary cirrhosis and primary
sclerosing cholangitis, but its role in the pathogenesis of gallstones is still
unknown and needs more clinical trials. Further studies are warranted to
illustrate this possibility and whether Helicobacter pylori is involved in
the development of malignant liver and biliary tract diseases or not.
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Among the various tests described for diagnosis of H.pylori,
histological examination seems to be the best. It could detect not only the
causative agent (H.pylori), but also the disease without significant false
positive results. Biopsy is 99% sensitive-99% specific, serology is 95%
sensitive-90% specific and ureabreath test is98% sensitive-100% specific.
Patient noncompliance and antibiotic resistance are two of the most
important reasons for failure of H.pylori therapy. Patient compliance is
influenced by a variety of factors including the duration of therapy and
severity of treatment associated side effects. There is emerging evidence
that sequential therapy may be superior to clarithromycin triple therapy in
the eradication of clarithromycin – resistant H.pylori, studies also
confirms superiority of 10 days of levofloxacin triple therapy to 7 days of
bismuth quadruple therapy.
Finally, an effective, safe vaccine that prevents infection with
H.pylori would clearly be the optimal intervention strategy in those
countries where gastric cancer remains a major problem. Within the next
five years, a few vaccines will most likely to be tested in humans.