The IL-1beta-511/-31 and TNF-alpha-308/-857/-863/-1031 genotypes were determined in Helicobacter pylori-positive patients with gastritis only (n = 164), gastric ulcers (n = 110), duodenal ulcers (n = 94), or gastric cancers (n = 105), and in H. pylori-negative controls (n = 172).
To investigate this inconsistency, we performed a meta-analysis of 36 studies for TNFA -308G>A polymorphism to evaluate the effect of TNFA on genetic susceptibility for gastritis and GC.
A total of 31% of children with duodenal disease were infected with iceA1 positive strains and had the -238 G to A polymorphism in the TNF-alpha gene vs only 1.6% of children with gastritis alone (P < 0.0005).
Since allelic variation in cagA exists and distinct H. pylori subgenotypes may circulate in different regions, PCR using primers for a variable 3' region of the cagA gene according to a Japanese methodology and for a consensus cagA 3' region used in Western methods was used for cagA detection. cagA was present in 53 (71%) of 75 H. pylori-positive cases when analyzed by the consensus region method and was associated with duodenal ulcer disease (P = 0.02), but not with gastric ulcer (P = 0.26), when compared to patients with duodenitis or gastritis.
Summarized odds ratios and corresponding 95% confidence intervals (CIs) for IL-1β-511 and IL-1β-31 polymorphisms and gastritis risk were estimated using fixed- or random-effects models when appropriate.
Functional oipA genes were correlated with cagA gene; both genes were significantly associated with gastritis activity, peptic ulcer and gastric adenocarcinoma.
The IL-8-251 A/T polymorphism and the polymorphisms in H pylori vacA gene are involved in limiting the infection outcome to gastritis and peptic ulcer or in favoring cancer onset in Iranian patients.
Studies from the West have indicated that the cagA gene and the associated EPIYA genotype of H. pylori is closely linked to the development of severe gastritis and gastric carcinoma; however, as yet no consistent correlation has been found among the bacteria from East Asia.
In the case of T-251A of IL-8, the frequency of the A/A genotype was significantly increased in gastritis (P=0.049) and IM (P=0.038) groups as compared with the histologically negative ones.
We investigated the effects of an interleukin 8 (IL-8) gene polymorphism on the risk of gastroduodenal diseases, the degree of H pylori induced gastritis, and IL-8 gene transcription.
We evaluated the presence of the homA, homB, and cagA genes in 286 strains isolated from patients in the U.S. and Colombian populations (126 with gastritis, 96 with duodenal ulcer, and 64 with gastric cancer) by PCR.
Although the cagA gene sequence was completely identical between the gastric corpus and the antrum in all patients, the corpus gastritis was more prominent in patients with gastric cancer than those with duodenal ulcer.
The IL-8 -251 A/T polymorphism and the polymorphisms in H pylori vacA gene are involved in limiting the infection outcome to gastritis and peptic ulcer or in favoring cancer onset in Iranian patients.
Electron spin resonance spectroscopy analysis showed a significant increase in free radical levels in gastritis samples compared with normal, intestinal metaplasia and cancer samples, suggesting that free radicals present in gastritis may contribute to p53 mutations.
The IL-8 heterozygote mutant variant was detected with a significantly higher frequency among the DU patients and those with gastritis than among the H. pylori-positive controls.
When the patients with different clinical manifestations were compared according to the presence of cagA gene or various vacA genotypes, only the vacA genotypes were significantly different among gastritis, peptic ulcer and gastric cancer patients (chi 2 = 17.8; P = 0.001).