Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We defined optimal Helicobacter pylori (Hp) treatment as Hp eradication rate about 90%, well-tolerated with few side-effects. Two centers carried out randomized trials including 90 patients (74% men, 26% women, ages ranging from 18 to 65, mean age 42 +/- 8) with active duodenal ulcers (DU). Patients were treated with the combination of Omeprazole (O) 20 mg bd + Clarithromycin (C) 250 mg bd + Tinidazole (T) (500 mg bd) or with Lansoprazole (L) 15 mg bd + Amoxicillin (A) 750 mg bd + Metronidazole (M) 500 mg bd administered for one week. The DU healing rate was evaluated by endoscopy and the Hp status by rapid urease CLO-test and 14C-urea breath test (UBT). The healing rate of the DU in a group treated with the combination of O + C + T was 91% and in group treated with L + A + M was 93%. The eradication of Hp in group O + C + T and L + A + M averaged 91% and 87%, respectively. There was no statistically significant difference in the DU healing rate and the Hp eradication rate between these two groups. Both treatments were accompanied by a marked rise in the basal and postprandial plasma gastrin levels and the rise in the intragastric pH but these alterations returned to the pre-treatment values 4 weeks after the termination of the therapy. Both treatments were well tolerated and the only side effect was the taste disturbance observed in few patents treated with O + C + T. None of patients discontinued the treatment because of the adverse events. We conclude that one week treatment using O + C + T or L + A + M are highly and equally effective in the healing of DU and in the eradication of Hp.
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PMID:One week treatment with omeprazole, clarithromycin and tinidazole or lansoprazole, amoxicillin and metronidazole for cure of Helicobacter pylori infection in duodenal ulcer patients. 877 3

The discovery of Helicobacter pylori has changed our understanding of the pathophysiology of peptic ulcer disease. An estimated one billion people harbour the organism worldwide but the highest prevalence is found in developing countries with up to 80% of people infected. The most favoured modes of transmission are faeco-oral and oral-oral. The mechanisms of H pylori-induced gastroduodenal disease include the provocation of local inflammatory reaction with the release of toxic cytokines, elevation of gastrin concentration and cytotoxic epithelial injury from the activity of urease and other enzymes produced by the bacterium. However, a large proportion of infected persons have no disease or are asymptomatic thereby suggesting that there may be other factors apart from H pylori infection necessary for ulcer formation. The simple finger prick test, a variant of serology and the newly developed ELISA-based Faecal Antigen Test hold the ace for large-scale epidemiological studies. The eradication of H pylori is now a very important goal of treatment of gastric and duodenal ulcers. Most H pylori eradication regimens combine anti-secretory agent, usually a proton pump inhibitor or H2-receptor antagonist and two antibiotics (usually, Clarithromycin and Amoxycillin or Metronidazole). Emergence of antibiotic resistance is worrisome but a quadruple therapy that incorporates bismuth may be used if the triple therapy fails.
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PMID:Helicobacter pylori and the pathogenesis of gastroduodenal disease: Implications for the management of peptic ulcer disease. 1638 Jul 42