Helicobacter pylori reinfection rate, in patients with cured duodenal ulcer.

OBJECTIVE: To determine the reinfection rate of the gastric mucosa in patients previously cured of duodenal ulcers, following the eradication of Helicobacter pylori. Only those remaining H. pylori-negative beyond 12 months of follow-up were studied, to minimize the potential inclusion of patients with H. pylori recrudescence. METHODS: Patients with endoscopically proven duodenal ulcers who had been treated with triple therapy, resulting in documented eradication of H. pylori and cure of the ulcer for at least 4 years, were recalled and had their H. pylori status determined by the 14C-urea breath test. Those found positive for H. pylori underwent endoscopic confirmation of the infection. RESULTS: Of the 94 patients restudied, with a follow-up period range of 48-96 months or a total of 549.8 yr, only two (2.2%) were again H. pylori positive. This gives an effective reinfection rate of 0.36% per patient year. In the two H. pylori-positive patients, one had normal mucosa endoscopically, whereas duodenitis without active ulceration was present in the other. The former was asymptomatic, whereas the latter patient was using ranitidine daily for symptom control. CONCLUSION: In the Australian setting, following cure of duodenal ulcer disease by eradication of H. pylori, subsequent reinfection is an unusual phenomenon. We conclude that efforts aimed at eradication of H. pylori in duodenal ulcer are justified and are worthwhile.

Use of high efficacy, lower dose triple therapy to reduce side effects of eradicating Helicobacter pylori.

OBJECTIVES: To evaluate two triple-therapy (TT) regimens of colloidal bismuth subcitrate (CBS), metronidazole, and tetracycline HCl in eradicating Helicobacter pylori, with particular attention to the frequency of resulting adverse effects of the two therapies. METHODS: A prospective, randomized controlled trial was conducted in patients with symptoms of dyspepsia who were positive for H. pylori. Subjects received a 14-day course of either 4 x/day therapy of CBS (108 mg), tetracycline HCl (500 mg), and metronidazole (250 mg), or 5 x/day therapy of CBS (108 mg), tetracycline HCl (250 mg), and metronidazole (200 mg). H. pylori status was determined endoscopically by urease test, histology, and culture. Standard questionnaires were administered to determine compliance to treatment and side effects of therapy. RESULTS: H. pylori was eradicated in 196/213 (92%) patients in the 4 x/day group and 202/210 (96%) in the 5 x/day group (p = 0.07). Side effects were significantly less frequent and less severe in the 5 x/day group (p < 0.01). CONCLUSIONS: We conclude that a lower dose, 5 x/day triple therapy treatment of H. pylori is equally efficacious to the standard 4 x/day therapy, but is accompanied by fewer and milder adverse effects.

Apparent reversal of early gastric mucosal atrophy after triple therapy for Helicobacter pylori.

Helicobacter pylori may be difficult to detect in individuals with intestinal metaplasia or atrophic gastritis, even though bacteria may persist in the mucosa in low numbers, maintaining elevated serum H. pylori antibody levels. We report a patient with marked, endoscopically visible gastric mucosal changes and focal changes of histological atrophic gastritis, who was negative for H. pylori on urease test, culture, and histology, but had positive H. pylori serology. When treated with triple therapy and reassessed at 6 months, his H. pylori antibody titer fell to low/negative levels, abnormal mucosa was replaced by a velvety, normal lining, and the previous evidence of histological atrophic gastritis was no longer detectable.

Smoking does not contribute to duodenal ulcer relapse after Helicobacter pylori eradication.

Cigarette smoking is believed to be one of the major factors influencing duodenal ulcer (DU) recurrence. However, the influence of cigarette smoking on DU recurrence after the eradication of Helicobacter pylori has not been separately addressed. The aim of this study was to investigate DU relapse rate in smokers and nonsmokers, both with confirmed eradication of H. pylori. Patients with H. pylori eradication, demonstrated at endoscopy 4 wk post-treatment, were included in the study. Smoking history was obtained with a standard questionnaire, and patients were followed endoscopically, both yearly and at symptomatic recurrence, to detect anatomical DU recurrence. Of the 197 (121M:76F) patients enrolled in the study and followed for 1-6 yr, 80 (41%) were smokers, smoking 5-40 cigarettes/day. The 117 (59%) nonsmokers included 31 (26%) patients who had ceased smoking 4-20 yr ago. Another seven (9%) smokers ceased smoking during the follow-up period. In the 197 patients with eradicated H. pylori and cured DU, there has been no recurrence of ulcer, regardless of smoking status. We conclude that in patients with DU in whom H. pylori infection is eradicated, ulcer disease does not recur, as observed for up to 6 yr. Furthermore, cigarette smoking is not a risk factor for DU recurrence, provided H. pylori is eradicated.

Helicobacter pylori-negative gastric ulcer.

Causes of Helicobacter pylori (HP)-negative gastric ulcers (GUs) have not previously been systematically studied. In this study we examined possible causes of HP-negative GUs. Among 115 consecutive patients with endoscopic diagnoses of GU, 71 (62%) had HP infection, and 44 (38%) were found to be HP-negative. Of the 71 HP-positive patients, 47 (66%) had no other detectable causal factors, 21 (30%) were regularly taking nonsteroidal antiinflammatory drugs (NSAIDs), and three (4%) had malignant GU. Of the 44 HP-negative patients, 29 (66%) were taking NSAIDs, two (5%) had a malignant GU, whereas 13/44 (30%) (11% of total 115) patients had no identifiable cause. These patients were classified as having "idiopathic GU." Some 38/115 (33%) GUs occurred on the lesser curve, and these were more often (p = 0.012) HP-positive (76%) than prepyloric GUs (60/115 (52%)). We conclude that although most patients have an identifiable cause of GU, around 11% will have no apparent contributing factor. HP-positive GUs are more frequently located on the lesser curve. It is now important to identify the cause of GU, because this may dictate choice of management.