ABSTRACT
BACKGROUND The aim of the study is to detect and define the role of H. pylori virulence factors and host IL-1 polymorphisms to prevent from further gastric cancer. mwom 5ml of blood samples were collected from each of 42 patients who had abdominal complaint, after informed consent was obtained. All patients were Mongolian nationality. The biopsy specimens were stored in liquid nitrogen and homogenized before DNA isolation. After tissue lysation with proteinase K. DNA isolation was performed with "Promege" tissue kit. according to the manufacturer's instructions. PCR amplification of H. pylori gene loci was performed for the cagA gene and the vacAs mosaics vac As 1 and vacAs2. RESULTS Result of histological findings shows 84.7% from all patients were diagnosed with II. pylori infection 83% (35/42). Histologically LI'G 50% (42/21). Gastric atrophy 30% (42/13). Intestinal metaplasia 9% (42/4). Gastroduodcnal ulcer 4% (42/2), Dys¬plasia 11% (42/5), Adinocarcinoma 2% (42/1), 3 patients (42/3, 7%) were none patho¬logic change. 62% (26/42) patients infected with H. pylori, as determined by Urease test. H. pylori were investigated in all 42 patients and 83% (35/42) were infected with II. pylori, as determined by histology (haematoxylin- eosin and (iiemsa-stained). Strain characteristics of H. pylori were investigated in all 42 patients and 83% (35/42) were infected with //. pylori, as determined by UreC PCR. Result of histological findings revealed Bacilla form 48,5% (17/35), Coccoid form 28,5% (12/35), mixed form 14% (5/35) from all patients were found //. pylori. 76% (13/17) of all patients were revealed coccoid form of H. pylori were taken anti-//. pylori treatment. The vacAs 1 genotype was found in 38% (16/42) of all UreC+ patients, and cagA was found in 23% (10/42) of UreC+ patients. 16.9% of all patients were IL-RN*2 positive (7/42), (IL-1B 31C/51 IT).