Deformity of duodenal bulb, gastric metaplasia of duodenal regenerating mucosa and recurrence of duodenal ulcer: a correlated study.

AIM: To investigate the correlation among the presence and degree of gastric metaplasia of duodenal regenerating mucosa, the deformity of bulb and the recurrence of duodenal ulcer. METHODS: A total of 99 patients with duodenal ulcer were treated with H(2)-antagonist with or without antimicrobial therapy. All patients received follow-up endoscopic examinations 6 wk after treatment. When the ulcer(s) were noted to be healed, two biopsies were taken from the ulcer scar for histological study of gastric metaplasia, and 4 biopsies were taken from antrum for Helicobacter pylori (H pylori) study. Out of these cases, 44 received further follow-up endoscopic examinations after 3, 6 and 12 mo respectively for studying the recurrence rate of duodenal ulcers. The correlation among ulcer recurrence, degree of gastric metaplasia of regenerating mucosa, bulbar deformity, and colonization of H pylori in the stomach was then studied. RESULTS: The results showed that there was a strong correlation between the deformity of duodenal bulb and the degree of gastric metaplasia of regenerating duodenal mucosa. The recurrence rate of duodenal ulcer had a significant difference between patients with and without H pylori colonization in the stomach (P<0.001). The greater the degree of gastric metaplasia of duodenal regenerating mucosa, the higher the recurrence rate of duodenal ulcer (P = 0.021). The more deformed the duodenal bulb, the higher the incidence of recurrence of duodenal ulcer (P = 0.03). CONCLUSION: There is a correlation among deformity of duodenal bulb, gastric metaplasia of duodenal regenerating mucosa and recurrence of duodenal ulcer. A more severely deformed duodenal bulb is closely related to a greater extent of gastric metaplasia. Both factors contribute to the recurrence of duodenal ulcer.

Development of multifocal duodenal erosions after anti-Helicobacter pylori triple therapy.

BACKGROUND AND PURPOSE: Anti-Helicobacter pylori triple therapy is effective for healing duodenal ulcer (DU) diseases and reducing disease recurrence. However, multifocal duodenal erosions or shallow ulcers may develop after triple therapy. The purpose of this study was to investigate the incidence and outcome of duodenal erosions that developed after triple therapy. METHODS: A total of 106 Taiwanese with active DU and with H. pylori infection were enrolled in this study. All patients received anti-H. pylori triple therapy (i.e., 2 weeks of antimicrobial agents combined with treatment for 4 to 6 weeks with acid suppression agents). Follow-up endoscopy was performed immediately after stopping treatment. The incidence of multifocal erosions or shallow ulcers over the bulb and/or second portion of the duodenum was studied. Additional acid suppression agent was given for 4 weeks whenever duodenal erosions or shallow ulcers were found. RESULTS: Out of 106 patients, 11 (10.4%) were found to have multifocal duodenal erosions and/or shallow ulcers on the duodenal bulb and/or second portion of the duodenum at the end of treatment. Ten of the 11 patients with newly developed erosions had healed DU in the S1 or S2 stage, and all 11 had successful H. pylori eradication. The duodenal erosions and/or shallow ulcers of these 11 patients were healed after an additional 4 weeks of histamine-2-receptor antagonist therapy. CONCLUSIONS: Multifocal duodenal erosions and/or shallow ulcers were noted in around 10% of Taiwanese DU patients who received anti-H. pylori triple therapy. An additional 4 weeks therapy with acid suppression agents healed these lesions.

It is difficult to eradicate Helicobacter pylori from dental plaque by triple therapy.

BACKGROUND: Dental plaque has been suggested as a permanent reservoir of Helicobacter pylori (H. pylori) and a potential source of reinfection. The aims of this study were to investigate the presence of H. pylori in both dental plaque and the stomach and to evaluate the therapeutic effect of triple therapy on H. pylori in dental plaque. METHODS: Dental plaque and gastric biopsy samples were obtained from 65 patients with dyspeptic symptoms for endoscopic examination. The prevalence of H. pylori in dental plaque and stomach was determined with rapid urease test, histologic examinations and polymerase chain reaction assay based on the primer pair derived from the cagA gene of H. pylori. Triple therapy was administered to patients infected with H. pylori. H. pylori status was re-evaluated after eradication therapy. RESULTS: Prior to treatment, H. pylori was found in the stomach in 38 of 65 (58%) patients and in dental plaque in 28 of 65 (43%) patients. The coexisting infection rate of H. pylori in both stomach and dental plaque was 74%. After triple therapy, H. pylori was eradicated from the stomach in 32 of 38 (84%) patients, but only 2 of 28 (7%) patients with coexisting H. pylori infections of stomach and dental plaque showed the elimination of H. pylori from dental plaque. CONCLUSIONS: The high coexisting infection rate of H. pylori in both stomach and dental plaque implies that dental plaque can serve as another reservoir of H. pylori. H. pylori in dental plaque was hardly eradicated by triple therapy. Dental plaque may be a potential source for recrudescence of gastric infection after successful systemic therapy.