PubMed · 12082341
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C A Desai, B D Samant. Rabeprazole.. https://pubmed.ncbi.nlm.nih.gov/12082341/
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AIM: To establish a triple therapy regimen for Helicobacter pylori eradication in patients with chronic renal insufficiency. METHODS: Eighty-eight patients with chronic renal insufficiency and H. pylori infection were evenly randomized into two groups receiving 1-week lansoprazole, 30 mg, clarithromycin, 500 mg, and either amoxicillin, 750 mg, or metronidazole, 500 mg, twice daily. The adverse events and compliance with triple therapy were reviewed at the week 1 visit. Patients provided stool samples at week 6 to assess the success of H. pylori eradication by H. pylori-specific stool antigen. The serum creatinine levels were monitored at enrollment, at weeks 1, 2 and 6 and on any unscheduled visit after triple therapy. RESULTS: The success of H. pylori eradication was higher in the lansoprazole-clarithromycin-metronidazole group than in the lansoprazole-clarithromycin-amoxicillin group (intention-to-treat analysis: 84% vs. 66%, P < 0.05: per protocol analysis: 93% vs. 76%, P < 0.05). Complete drug compliance was also better in the lansoprazole-clarithromycin-metronidazole group than in the lansoprazole-clarithromycin-amoxicillin group (77% vs. 52%, P < 0.05). Patients in the lansoprazole-clarithromycin-metronidazole group had a lower risk of acute renal failure than those in the lansoprazole-clarithromycin-amoxicillin group (2% vs. 18%, P < 0.05; relative risk, 0.128, 95% confidence interval, 0.016-0.979). CONCLUSIONS: Triple therapy with metronidazole and clarithromycin, but not amoxicillin, can be used for H. pylori eradication in patients with chronic renal insufficiency, because it is more effective, well tolerated and less likely to cause deterioration of renal function.
AIM: To compare H2-receptor antagonists and proton pump inhibitors as adjuvants to triple therapy for Helicobacter pylori eradication. METHODS: H. pylori-infected patients with peptic ulcer were randomized to receive either 300 mg nizatidine or 30 mg lansoprazole plus 1 g amoxicillin and 500 mg clarithromycin taken b.d. for 7 days. H. pylori eradication was assessed 4 weeks after therapy. Using meta-analytical techniques, we combined the results of this study with other randomized controlled comparisons of H2-receptor antagonists and proton pump inhibitors as adjuvants to triple therapy. RESULTS: One hundred and one patients were randomized. H. pylori eradication was 94% (47/50) [95% confidence interval (CI), 83-99%] (intention-to-treat) in the H2-receptor antagonist group vs. 86% (44/51) (95% CI, 74-94%) in the proton pump inhibitor group (P = 0.3). There has been a total of 12 similar studies (1415 patients). The overall efficacy was similar in intention-to-treat analysis: 78% (549/701) with H2-receptor antagonists vs. 81% (575/714) with proton pump inhibitors (odds ratio, 0.86; 95% CI, 0.66-1.12). A non-significant trend favouring H2-receptor antagonist (79% vs. 69%; odds ratio, 1.14; 95% CI, 0.76-1.71; P = 0.5) was seen in the comparison of clarithromycin-containing regimens. In contrast, in non-clarithromycin-containing trials, there was a slight, but significant, advantage with proton pump inhibitors (85% vs. 78%; odds ratio, 0.64; 95% CI, 0.45-0.92; P = 0.02). CONCLUSION: Overall, proton pump inhibitor and H2-receptor antagonist antisecretory agents appear to be similarly effective as adjuvants for H. pylori triple therapy. It is unlikely that the direct anti-H. pylori effect of proton pump inhibitors is responsible for their ability to enhance anti-H. pylori therapy.
To examine the physiological role of the histamine H(2) receptor, histamine H(2) receptor-null mice were generated by homologous recombination. Histamine H(2) receptor-null mice, which developed normally and were fertile and healthy into adulthood, exhibited markedly enlarged stomachs and marked hypergastrinemia. The former was due to hyperplasia of gastric gland cells (small-sized parietal cells, enterochromaffin-like cells and mucous neck cells which were rich in mucin), but not of gastric surface mucous cells, which were not increased in number as compared with those in wild-type mice despite the marked hypergastrinemia. Basal gastric pH was slightly but significantly higher in histamine H(2) receptor-null mice. Although carbachol but not gastrin induced in vivo gastric acid production in histamine H(2) receptor-null mice, gastric pH was elevated by both muscarinic M(3) and gastrin antagonists. Thus, both gastrin and muscarinic receptors appear to be directly involved in maintaining gastric pH in histamine H(2) receptor-null mice. Interestingly, gastric glands from wild-type mice treated with an extremely high dose of subcutaneous lansoprazole (10 mg/kg body weight) for 3 months were very similar to those from histamine H(2) receptor-null mice. Except for hyperplasia of gastric surface mucous cells, the findings for gastric glands from lansoprazole-treated wild-type mice were almost identical to those from gastric glands from histamine H(2) receptor-null mice. Therefore, it is possible that the abnormal gastric glands in histamine H(2) receptor-null mice are secondary to the severe impairment of gastric acid production, induced by the histamine H(2) receptor disruption causing marked hypergastrinemia. Analyses of the central nervous system (CNS) of histamine H(2) receptor-null mice revealed these mice to be different from wild-type mice in terms of spontaneous locomotor activity and higher thresholds for electrically induced convulsions. Taken together, these results suggest that (1) gastrin receptors are functional in parietal cells in histamine H(2) receptor-null mice, (2) abnormal gastric glands in histamine H(2) receptor-null mice may be secondary to severe impairment of gastric acid production and secretion and (3) histamine H(2) receptors are functional in the central nervous system.