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.

Helicobacter pylori-negative duodenal ulcer.

Most patients with chronic duodenal ulcer (DU) craters have gastritis associated with Helicobacter pylori (HP), now thought to be the major cause of DU. A smaller proportion of DU patients have no detectable HP. In this study, we examined the frequency and causes of HP-negative duodenal ulcers. In 302 consecutive patients with endoscopic diagnosis of duodenal ulcer, 284 (94%) were found to have associated HP gastritis, whereas 18 (6%) were HP-negative on histology, culture, and urease test. The largest subgroup of HP-negative patients (8/18) was made up of those who had been taking nonsteroidal antiinflammatory drugs (NSAIDs), followed closely (4/18) by patients with recent intake of antibiotics. Causes of DU in the remaining subgroups included two patients with duodenal Crohn's disease, two with Gastrospirillum hominis infection, one with penetrating carcinoma of the pancreas and one with no detectable cause. We conclude that, although the most common causal factor of duodenal ulcer is HP, some 6% of DU's will be HP-negative, signaling unusual etiology. It is now important to identify the cause of duodenal ulcer so as to initiate appropriate therapy.