INTRODUCTION: Helicobacter Pylori was brought to the worlds attention 1983by Warren and Morshall, it is now acknowledged that H.Pylori gastritis is the one of the most common human bacterial infectious disease and is causally linked with gastritis , peptic ulcer disease, gastric adeno- carcinoma ,and gastric B.cell lymphoma.(1)
H.Pylori is a slow growing , microaerophilic, highly motile, Gram negative spiral organism whose most striking biochemical characteristic is the abundant production of urease enzyme which is an important indirect marker of the organisms presence because it is the bases of biopsy rapid unease test, the urea broth test and as an antigen for serologic detection . The prevalence of H.Pylori among healthy individuals varies depending on age , socioeconomic class, country of origin. In developing countries children are typically infected by age 10 years, whereas in developed countries there is an age related increase in prevalence (1,2 ).The major risk factor for infection is the socioeconomic status of the family during childhood as reflected by number of persons in a house hold, sharing a bed ,and absence of a fixed hot water supply all of which probably are markers for the level of sanitation and house hold hygiene(3,4,5 ).
* Immunology Unit, Teaching Laboratories-
It is not known how often an acute infection with H.Pylori sponteneously clears , studies in children suggest that sponteneous loss of infection may be common (6 ).Infection in adults appears to be typically long lived and is probably life long.(7 ) . Most infected individuals have chronic active, non atrophic superficial gastritis .This histological form is usually asymptomatic but may be associated with duodenal ulcer; chronic atrophic gastritis , gastric adeno carcinoma or gastric lymphoma. (6,7 ) Diagnostic tests for H.Pylori can be divided into those that do and do not require samples of gastric mucosa, mucosal biopsy of histological examination of the specimen for the presence of H.Pylori and or gastritis has been the diagnostic method of choice until recently :to increase diagnostic yield ,use of large cup biopsy and 3 samples biopsy (lesser curve Angularis ,greater curve pre pyloric and greater curve body ) examined by both Giemsa stain as a standard stain and hematoxylin & eosin stain which is excellent to determine histologic chronic or chronic active gastritis and demonstrates H.Pylori if large number of organisms are present ( 1,6) . Biopsies may also be tested for the presence of unrease enzyme production by agar gel slide test such as rapid urease test which is excellent for screening for the presence of H.Pylori in patients with peptic ulcer.
Tests that do not require a mucosal biopsy include serologic tests as urea broth test, detection of
infection in adults To determine the prevalence of H.Pylori undergoing oesphagogastrodudenoscopy by two methods serology (ELISA technique) comparing it with histopathology.
Forty patients referred to the GIT clinic of AL-Yarmok teaching hospital for GI endoscopy were involved in this study; their biopsies and sera send to histopathology and immunology department respectively for detection of H.Pylori. RESULTS:
H.Pylori Abs(IgG) were detected in the sera of 25(63%) patients by ELISA,15 (37.50%) of them H.Pylori was also seen in their biopsies by Giemsa s stain. Most patients with detectable antibodies are those with chronic gastritis ;however patients complaining from reflux oesophagitis showed a significant absentees of these Abs.
Most patients with gastritis had detectable H,Pylori Abs in their sera; However the study reveled a significant decrease in H.Pylori Ab detection in patients sera with reflex esophagitis (R.O).