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.

BackgroundGrowth factor, cytokine and chemokine-induced activation of PI3K enzymes constitutes the start of a complex signalling cascade, which ultimately mediates cellular activities such as proliferation, differentiation, chemotaxis, survival, trafficking, and glucose homeostasis. The PI3K enzyme family is divided into 3 classes; class I (subdivided into IA and IB), class II (PI3K-C2α, PI3K-C2β and PI3K-C2γ) and class III PI3K. Expression of these enzymes in human tissue has not been clearly defined.MethodsIn this study, we analysed the immunohistochemical topographical expression profile of class IA (anti-p85 adaptor) and class II PI3K (PI3K-C2α and PI3K-C2β) enzymes in 104 formalin-fixed, paraffin embedded normal adult human (age 33–71 years, median 44 years) tissue specimens including those from the gastrointestinal, genitourinary, hepatobiliary, endocrine, integument and lymphoid systems. Antibody specificity was verified by Western blotting of cell lysates and peptide blocking studies. Immunohistochemistry intensity was scored from undetectable to strong.ResultsPI3K enzymes were expressed in selected cell populations of epithelial or mesenchymal origin. Columnar epithelium and transitional epithelia were reactive but mucous secreting and stratified squamous epithelia were not. Mesenchymal elements (smooth muscle and endothelial cells) and glomerular epithelium were only expressed PI3K-C2α while ganglion cells expressed p85 and PI3K-C2β. All three enzymes were detected in macrophages, which served as an internal positive control. None of the three PI3K isozymes was detected in the stem cell/progenitor compartments or in B lymphocyte aggregates.ConclusionsTaken together, these data suggest that PI3K enzyme distribution is not ubiquitous but expressed selectively in fully differentiated, non-proliferating cells. Identification of the normal in vivo expression pattern of class IA and class II PI3K paves the way for further analyses which will clarify the role played by these enzymes in inflammatory, neoplastic and other human disease conditions.

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.

Helicobacter pylori eradication after simple closure of duodenal ulcer perforation gives better result than the operation plus antisecretory non-eradication therapy for prevention of ulcer recurrence. All duodenal ulcer perforation patients should be tested for H. pylori infection, and eradication therapy is required in all infected patients.