Background-Development of gastric mucosa associated lymphoid tissue (MALT) lymphoma is thought to be closely associated with host immune reactions to Helicobacter pylori. Aim-To investigate humoral immune responses in patients with MALT lymphoma to antigens shared by H pylori and human gastric epithelial cells. Methods-Sera were obtained from H pylori positive patients with MALT lymphoma (n = 11) or other gastroduodenal diseases (peptic ulcer, n = 40; nonulcer dyspepsia, n = 20) and from H pylori negative healthy control subjects (n = 10). Antibodies to HGC-27 human gastric epithelial cells and human recombinant heat shock protein (Hsp) 60 were examined using an enzyme linked immunosorbent assay (ELISA) and immunoblotting. Results-Antibody titres to HGC-27 cells were significantly elevated in H pylori positive patients with MALT lymphoma when compared with titres in patients with other gastroduodenal diseases and in healthy subjects. Immunoblotting of sera from patients with MALT lymphoma often detected a band with a molecular mass corresponding to Hsp60, and both ELISA and immunoblotting showed elevated antibody titres to the recombinant human Hsp60. Antigenic similarity between Hsp60 and H pylori HspB was documented by immunoblotting experiments. Conclusions-Autoantibodies reactive with host gastric epithelial cells are often increased in MALT lymphoma, and Hsp60 is a major target antigen. Immune responses induced by immunological cross reactivity between H pylori HspB and human Hsp60 in gastric epithelium may be involved in the development of MALT lymphoma. (Gut 1999;45:20-23)

Infection with Helicobacter pylori induces humoral immune responses against various antigens of the bacterium. Heat shock proteins (hsps) are immunodominant antigens in various diseases including H. pylori infection. In the present study, we measured the anti-hsp antibody titers in 42 patients with H. pylori-infected peptic ulcers during a bacterial eradication study. The patients were treated with a proton pump inhibitor and antimicrobial agents to eradicate the organism. Their sera were obtained at pretreatment and at 1 month and 6 months after the eradication therapy. The titers of immunoglobulin G antibodies to the H. pylori hsp, wholecell lysate, and urease (30-kDa subunit) antigens in serum were measured by a capture enzyme-linked immunosorbent assay. The levels of H. pylori hsp60 antibodies in sera collected 1 month after treatment had declined significantly, even when changes in the titers of antibodies to whole-cell and urease antigens were not apparent. These results suggest that measurement of antibodies to H. pylori hsp60 in serum is useful for the early monitoring of the effectiveness of eradication therapy.Helicobacter pylori is associated with gastritis and peptic ulcer disease in humans. H. pylori infection induces the host's constitutional immune response against various antigens of this bacterium. The detection of immunoglobulin G (IgG) antibodies to H. pylori is useful for the diagnosis of infection. Some investigators reported that the titers of these antibodies declined during therapy for H. pylori eradication (1,12,14,15,17,18). Kosunen (13) reported that a consistent decrease in the IgG antibody titer within 6 months of antimicrobial therapy reliably indicated the eradication of H. pylori (13). However, a serological test that can be used to judge the success of treatment earlier in the follow-up period has not yet been established. In this study we measured the titers of IgG antibodies to the heat shock protein (hsp) hsp60, urease, and whole-cell lysates of H. pylori in sera from patients with peptic ulcer during antimicrobial treatment of H. pylori and then assessed its usefulness for the monitoring of eradication therapy. MATERIALS AND METHODSPatients studied. We investigated 20 subjects with gastric ulcer (GU) (17 men and 3 women; age range, 35 to 74 years; mean age, 52 years) and 17 subjects with duodenal ulcer (DU) (13 men and 4 women; age range, 22 to 51 years; mean age, 36.6 years). All patients underwent gastroduodenoscopy because of gastrointestinal symptoms. Examinations were performed in the First Department of Internal Medicine, Okayama University School of Medicine, and its affiliated hospitals. At the initial diagnostic endoscopy, all patients were diagnosed as having a peptic ulcer.Status of H. pylori infection. H. pylori infection status was evaluated by bacterial culture, measurement of urease activity, and histologic analysis. A patient was judged to be H. pylori positive if culture and/or histologic analysis of specimens retrieved endoscopically was positive for the org...

Background and AimBleeding is an inevitable and often severe complication after endoscopic sphincterotomy (EST). We aimed to investigate the factors associated with post‐EST bleeding in patients treated with anticoagulants.MethodsThe data of patients who underwent EST at 15 hospitals between July 2015 and June 2017 were extracted. We investigated the incidence of post‐EST bleeding and risk factors for bleeding in patients treated with anticoagulants.ResultsOne hundred forty‐nine patients undergoing EST who met the inclusion criteria were included in this study. The total‐EST bleeding (bleeding occurring during or after EST) rate did not differ between the heparin replacement (8.0%, 6/75) and continuation (16.6%, 2/12; P = 0.37) groups of warfarin users. The total‐EST‐bleeding rate in the heparin replacement group (12.9%, 4/31) was significantly higher than that in the continuation group (0%, 0/31; P = 0.016) in direct oral anticoagulant (DOAC) users. The rate of total‐EST bleeding with continuation of DOAC (0%, 0/31) was significantly lower with continuation of warfarin (16.6%, 2/12; P = 0.021). During‐EST bleeding (bleeding occurring during EST) (P = 0.0083) and precut (P = 0.033) were significant risk factors for post‐EST bleeding in all 149 patients. Heparin replacement was only a significant risk factor for total‐EST bleeding (P = 0.033) in DOAC users.ConclusionHeparin replacement was a significant risk factor for post‐EST bleeding in DOAC users; however, there was no significant difference between the bleeding rate of heparin replacement and that of continuation groups in patients taking warfarin. During EST and precut were significant risk factors for post‐EST bleeding in all patients treated with anticoagulants.

Objective Gastric endoscopic submucosal dissection (ESD) under heparin replacement (HR) of warfarin reportedly has a high risk of delayed bleeding (24-57%). It is possible that the delayed bleeding risk may have changed over the years. We evaluated the current risk of delayed bleeding after gastric ESD under HR of anticoagulant agents. Methods We retrospectively reviewed the delayed bleeding rate and analyzed the risk factors for delayed bleeding. Patients Consecutive patients who underwent gastric ESD under HR of anticoagulant agents from July 2015 to June 2017. Results A total of 32 patients with a solitary early gastric cancer and taking anticoagulant agents were analyzed, including 24 patients on warfarin (the warfarin group) and 8 patients on direct oral anticoagulants (the DOAC group). Three (9.4%) patients experienced delayed bleeding: three (12.5%) patients in the warfarin group and no patients in the DOAC group. Continued aspirin treatment was identified to be a risk factor of delayed bleeding (p=0.01). Conclusion Careful management may be required for patients undergoing gastric ESD under continued aspirin treatment in addition to HR of anticoagulant agents; although the delayed bleeding risk after gastric ESD under HR of anticoagulant agents might have decreased over the years.