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Title: Unhealed duodenal ulcers despite Helicobacter pylori eradication.
Author: Gisbert JP, Boixeda D, Martín De Argila C, Alvarez Baleriola I, Abraira V, García Plaza A.
Journal: Scand J Gastroenterol; 1997 Jul; 32(7):643-50. PubMed ID: 9246702.
Abstract:
BACKGROUND: Our aims were 1) to study the influence of several factors (age, sex, smoking, previous ulcer disease, ulcer size, chronic gastritis, serum gastrin and pepsinogen I levels, therapy regimen and, especially, eradication of Helicobacter pylori) on duodenal ulcer healing; 2) to evaluate the frequency of duodenal ulcer healing failure despite eradication of H. pylori, to study why this failure occurs, and to verify its evolution without antisecretory therapy; and 3) to confirm whether a week's prescription of omeprazole is sufficient to obtain ulcer healing. METHODS: Three-hundred and eight patients (mean age, 45 +/- 13 years; 71% males) with duodenal ulcer and H. pylori infection were studied prospectively. Biopsy specimens were obtained at initial endoscopy, and serum gastrin and pepsinogen I levels were measured. A repeat endoscopy (with biopsies) was performed 1 month after eradication therapy had been completed, and a 13C-urea breath test was also carried out. Three eradication therapies were used: omeprazole plus amoxycillin for 2 weeks (OA group, n = 61); 'classic' triple therapy (with bismuth; CTT group, n = 65); and 'new' triple therapies for 1 week (NTT group, n = 182): omeprazole plus two of the following antibiotics: clarithromycin, metronidazole, and amoxycillin. When the ulcer did not heal despite successful H. pylori eradication, antacids were prescribed on an as-needed basis, and endoscopy was repeated 1 month later (2nd control endoscopy). If the ulcer was still present, the acid output (basal and pentagastrin-stimulated) was measured, a secretin test was performed, and a final endoscopy (3rd control endoscopy) was carried out after an additional month. The statistical method used was multiple logistic regression. RESULTS: Overall eradication was achieved in 69% (n = 212) of the patients, and ulcer healing in 76% (n = 233): 57% in the OA group, 80% in the CTT group, and 81% in the NTT group (P < 0.01 when comparing the OA group with the others). Ulcer healing was achieved in 90% of H. pylori-eradicated patients and in only 45% of patients with eradication therapy failure (P < 0.001). Similar results were obtained when only patients treated with NTT were considered: ulcer healing in 90% of patients with the organisms eradicated. Eradication of H. pylori (odds ratio (OR), 11.8; 95% confidence interval (CI), 6.3-22) and sex (OR, 2.5; 95% CI, 1.2-5.1) were the only variables that correlated with ulcer healing in the multivariate analysis. The ulcer persisted despite successful eradication of H. pylori in 22 patients. The duodenal ulcer had healed spontaneously in 73% of these patients at the 2nd control endoscopy. Finally, by the 3rd control endoscopy, only three patients still had duodenal ulcer. Therefore, ulcer healing was finally achieved in 98.1% (95-99%) of patients in whom H. pylori was eradicated. Gastrin, pepsinogen I, acid output, and the secretin test had normal values in all patients. CONCLUSIONS: Eradication of H. pylori favours ulcer healing, which is achieved in most patients in whom the organism is eradicated. Just 1 week of omeprazole therapy (that is, the antibiotic administration period in the new triple therapies) is enough to obtain a high ulcer healing rate. Most duodenal ulcers that do not heal initially despite H. pylori eradication will ultimately do so after several weeks without additional therapy.

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