Genetic differences in interleukin-1 betapolymorphisms among four Asian populations: an analysis of the Asian paradox between H. pylori infection and gastric cancer incidence.

The prevalence of Helicobacter pylori infection is high among Asian populations, but the incidences of gastric cancer differ greatly among northern and southern Asian populations. Here, we studied histopathological findings in stomach tissue using an updated Sydney System and the frequencies of interleukin (IL)-1betapolymorphisms, thought to be associated with an increased risk of gastric cancer, in four Asian populations. Endoscopic-guided biopsies from three regions of the stomach and the -511 T-to-C polymorphism in the IL-1betagene were examined in 228 Japanese, 116 Chinese, 159 Thai and 83 Vietnamese patients with gastric diseases. H. pylori colonization, inflammation and activity were more severe in the Japanese and Thai populations than in the Chinese and Vietnamese populations and these scores were more antrum-predominant in the Thai and Vietnamese populations than in the Japanese and Chinese populations, with the most severe degree of atrophy and intestinal metaplasia occurring in the angulus region of the Japanese population. The IL-1betapolymorphisms did not differ among the four populations overall, but in cases with severe mucosal atrophy (pepsinogen I/II ratio <3.0), the CC polymorphism was dominant in the Japanese population and the TT+TC polymorphism was dominant in the Chinese population; no difference in C and T allele frequencies was found in the Thai and Vietnamese populations. In conclusion, the incidence of gastric cancer is extremely low, but the prevalence of H. pylori infection is high in the Thai population (Asian paradox). In the Thai population, the scores for corpus gastritis and intestinal metaplasia, which are associated with a high risk of gastric cancer, were low in comparison with the Japanese population. IL-1betapolymorphisms were correlated with mucosal atrophy in the Japanese and Chinese populations, but not in the Thai and Vietnamese populations.

Helicobacter pylori infection in the remnant stomach after gastrectomy: with special reference to the difference between Billroth I and II anastomoses.

Helicobacter pylori infection is associated with many gastric diseases, such as peptic ulcer and gastric cancer. We examined the remnant stomach for H. pylori infection after gastrectomy for gastric cancer or peptic ulcer between October 1992 and July 1997. H. pylori DNA in the gastric juice of 109 patients [mean age 62.4 years, male/female 78/31, gastrectomy for gastric cancer 83/peptic ulcer 26, Billroth I (BI) anastomosis 72/Billroth II (BII) 37, mean postoperative interval 6.0 years] was amplified by PCR and detected by Southern blot hybridization. The serum of 135 patients was assayed by ELISA for IgG antibody against H. pylori (mean age 61.8 years, male/female 99/36, gastrectomy for gastric cancer 111/peptic ulcer 24, BI anastomosis 93/BII 42, mean postoperative interval 5.4 years). H. pylori was positive in 68/109 (62.4%) by PCR and 113/ 135 (83.7%) by ELISA. H. pylori cytotoxin gene cagA, a H. pylori virulence factor gene, was found in 15/16 (93.8%) cases by PCR. A significant difference in H. pylori positivity by PCR was found according to the type of anastomosis (BI vs. BII) but not according to age group, sex, disease (cancer or ulcer), or postoperative interval by PCR and ELISA. BII anastomosis was followed by a significantly lower rate of H. pylori infection (17/37; 45.9%) than BI anastomosis (51/72; 70.8%; p=0.01) according to the results of PCR. Moreover, some patients with BII anastomosis (3/8; 37.5%) showed positive to negative seroconversion for H. pylori infection after the operation (mean 2.47 years) according to the results of ELISA, but this phenomenon was not observed in patients with BI (0/12) anastomosis. This may reflect the role of bile reflux, which is more common in BII than BI, because bile reflux interferes with colonization by H. pylori.

Role of Helicobacter pylori infection in perforation of peptic ulcer: an age- and gender-matched case-control study.

Evidence showed a marked decrease in recurrence rate of peptic ulcer after eradication of Helicobacter pylori infection. However, whether H. pylori infection is etiologically related to perforation of peptic ulcer remains to be clarified. We therefore conducted an age- and gender-matched case-control study between perforated and nonsurgical peptic ulcers in H. pylori infection and examined differences in the cytotoxin genes cagA and vacA. Serum H. pylori IgG antibody (ELISA) was positive in 20/21 (95%) of perforated vs. 37/40 (93%) of nonsurgical duodenal ulcers and in 5/5 (100%) of perforated vs. 24/28 (86%) of nonsurgical gastric ulcer patients. Positivity of H. pylori DNA in gastric juice, which was amplified by PCR and identified by Southern blot hybridization, was 17/23 (74%) of perforated vs. 32/45 (71%) in the nonsurgical duodenal ulcer group. Positivity of the cytotoxin genes cagA and vacA in H. pylori DNA-positive gastric juice was as follows: perforated vs. nonsurgical duodenal ulcer, cagA 11/ 13 (85%) vs. 24/27 (89%); vacA1: 9/13 (69%) vs. 22/27 (82%); vacA2 8/13 (62%) vs. 21/27 (78%). There were no significant differences between the perforated and nonsurgical peptic ulcer groups for these H. pylori serum and gene markers. It is assumed that H. pylori infection is not etiologically related to perforation of peptic ulcer.