Ranitidine bismuth citrate-based triple therapies as a second-line therapy for Helicobacter pylori in Turkish patients.

BACKGROUND: Quadruple therapy with a proton pump inhibitor, bismuth, metronidazole and tetracycline is recommended as the optimal second-line therapy of Helicobacter pylori infection in the Maastricht Consensus Report. The aim of the present paper was to evaluate the efficacy of ranitidine bismuth citrate (RBC)-based regimens as second-line therapies after failure of the standard Maastricht triple therapy. MATERIALS AND METHODS: One hundred and sixteen H. pylori-positive patients were given omeprazole 20 mg b.d., clarithromycin 500 mg b.d., and amoxicillin 1 g b.d for 10 days. Patients remaining H. pylori-positive (n = 29) were combined with 27 patients enrolled after an initial eradication failure from proton-pump inhibitor (PPI), amoxicillin and clarithromycin therapy for at least 7 days and were randomly given one of the following second-line 10-day treatments: RBC 400 mg b.d., amoxicillin 1 g b.d and clarithromycin 500 mg b.d. (RAC group, n = 28) and RBC 400 mg b.d., metronidazole 500 mg b.d and tetracycline 500 mg b.d. (RMT group, n = 28). Eradication was assessed by either histology and rapid urease test or (13)C urea breath test 8 weeks after therapy. RESULTS: The eradication rate of first-line Maastricht therapy was 67% for intention-to-treat analysis (95% confidence interval [CI]: 58-75). Per-protocol and intention-to-treat eradication was achieved in 60.7% of patients (95%CI: 42-79) in the RAC group and in 85.7% of patients (95%CI: 73-98) in the RMT group (P = 0.03). Fifty-three percent of patients in the RAC and 50% of patients in the RMT group experienced at least one slight side-effect (P = 0.6). CONCLUSIONS: RMT is an effective and well-tolerated second-line therapy after H. pylori eradication failure from PPI, amoxicillin, and clarithromycin.

Alverine citrate induced acute hepatitis.

Alverine citrate is a commonly used smooth muscle relaxant agent. A MEDLINE search on January 2004 revealed only 1 report implicating the hepatotoxicity of this agent. A 34-year-old woman was investigated because of the finding of elevated liver function tests on biochemical screening. Other etiologies of hepatitis were appropriately ruled out and elevated enzymes were ascribed to alverine citrate treatment. Although alverine citrate hepatotoxicity was related to an immune mechanism in the first case, several features such as absence of predictable dose-dependent toxicity of alverine citrate in a previous study and absence of hypersensitivity manifestations in our patient are suggestive of a metabolic type of idiosyncratic toxicity.