Comparison of PPIs and H2-receptor antagonists plus prokinetics for dysmotility-like dyspepsia.

AIM: To compare efficacy of proton pump inhibitors (PPIs) with H(2)-receptor antagonists (H(2)RAs) plus prokinetics (Proks) for dysmotility-like symptoms in functional dyspepsia (FD). METHODS: Subjects were randomized to receive open-label treatment with either rabeprazole 10 mg od (n = 57) or famotidine 10 mg bid plus mosapride 5 mg tid (n = 57) for 4 wk. The primary efficacy endpoint was change (%) from baseline in total dysmotility-like dyspepsia symptom score. The secondary efficacy endpoint was patient satisfaction with treatment. RESULTS: The improvement in dysmotility-like dyspepsia symptom score on day 28 was significantly greater in the rabeprazole group (22.5% ± 29.2% of baseline) than the famotidine + mosapride group (53.2% ± 58.6% of baseline, P < 0.0001). The superior benefit of rabeprazole treatment after 28 d was consistent regardless of Helicobacter pylori status. Significantly more subjects in the rabeprazole group were satisfied or very satisfied with treatment on day 28 than in the famotidine + mosapride group (87.7% vs 59.6%, P = 0.0012). Rabeprazole therapy was the only significant predictor of treatment response (P < 0.0001), defined as a total symptom score improvement ≥ 50%. CONCLUSION: PPI monotherapy improves dysmotility-like symptoms significantly better than H(2)RAs plus Proks, and should be the treatment of first choice for Japanese FD.

[Clinical investigation of perforated duodenal ulcer--with special reference to the presence of Helicobacter pylori infection and rate of recurrence].

Perforated duodenal ulcer was clinically evaluated with respect to Helicobacter pylori infection and rate of recurrence in 38 ulcer patients perforated and 154 patients with non-perforated duodenal ulcer who visited our hospital in past 5 years and 6 months. The frequency of occurrence of H. pylori-positivity was 42.1% in patients with perforated duodenal ulcer, significantly lower than that of 92.9% in patients with non-perforated lesions. This result suggests that H. pylori is hardly involved in the development of perforated duodenal ulcer. The rate of recurrence was significantly lower for perforated duodenal ulcer than for non-perforated ulcer. In particular, perforated duodenal ulcer did not recur in the group on maintenance therapy with H2-recepter antagonists. Maintenance therapy using inhibitors of gastric acid secretion seems effective for the prevention of recurrence of perforated duodenal ulcer.

Helicobacter pylori in patients receiving long-term dialysis.

BACKGROUND: Helicobacter pylori (H. pylori) is considered to cause gastritis and gastric ulcer. In dialysis patients, digestive tract hemorrhage is sometimes fatal. However, in regard to H. pylori infection in patients with end-stage renal disease (ESRD), many issues remain to be clarified. METHODS: This study included 76 symptom-free patients with ESRD. The subjects consisted of 25 patients with chronic renal failure who had not received dialysis and 51 patients receiving dialysis. On upper digestive tract endoscopy, specimens were taken for analysis of H. pylori. Urease test, culture, and microscopy were performed. RESULTS: In non-dialysed patients, the prevalence of H. pylori-positive patients was 56.0%. In dialysed patients, the percentage was significantly lower (27.5%). In dialysed patients, the mean duration of dialysis was 8.1 +/- 7.5 months (mean +/- SD) in H. pylori-positive patients and 56.2 +/- 60.9 months (mean +/- SD) in H. pylori-negative patients (p < 0.001). 11 of 13 non-dialysed patients with chronic gastritis were positive for H. pylori. However, only 5 of 24 dialysed patients were positive for H. pylori infection. CONCLUSIONS: Long-term dialysis decreased the prevalence of H. pylori. The reduction of gastric acid secretion related to chronic gastritis may be involved.