Helicobacter pylori, efficacy of the new triple therapy in six and twelve-day schedules.

OBJECTIVE: Assessment of four eradicating patterns of 6 and 12 days duration with new triple therapies adapted to our environment. PATIENTS: After an endoscopic diagnosis of Duodenal or Gastric Ulcer, and the confirmation of the presence of Helicobacter pylori using a rapid urease test in antral biopsies, 274 patients were treated with one of four eradicating therapies, verifying its efficacy with the C-13 urea breath test, at least one month after the end of the treatment and 10 days after withdrawal of proton pump inhibitors. RESULTS: Maximum eradicating efficacy was achieved with Omeprazole (20 mg/12 hours), Clarithromycin (500 mg/12 hours) and Amoxycillin (1 g/12 hours), given for 12 days (96.6%), and Omeprazole (20 mg/12 hours), Tinidazole (500 mg/12 hours) and Clarithromycin (500 mg/12 hours), also given for 12 days (95.2%). The same drugs and doses, when given during six days, achieved percentages of 78.3% and 82.2% respectively. Results with Tinidazole suggest lack of resistance to this drug in the Community of Madrid.

Nitric oxide stimulates tyrosine phosphorylation of p125(FAK) and paxillin in rat pancreatic acini.

Some of the effects of several oncogenes, integrins, growth factors, and neuropeptides are mediated by tyrosine phosphorylation of the non-receptor tyrosine kinase p125(FAK) and the cytoskeletal protein paxillin. We have demonstrated that different stimuli cause tyrosine phosphorylation of p125(FAK) and paxillin in rat pancreatic acini. The aim of the present study was to determine whether exogenous NO activates this pathway. We demonstrate that in isolated rat pancreatic acini, a NO donor, sodium nitroprusside (SNP) stimulates, in a dose- and time-dependent way, tyrosine phosphorylation of p125(FAK) and paxillin. The same effects could be observed after incubating acini with 8-Br-cGMP. Moreover, the stimulation caused by SNP was completely abolished by two different guanylyl cyclase inhibitors, methylene blue, and LY-83583. These inhibitors also diminished unstimulated phosphorylation of p125(FAK) and paxillin. We conclude that in rat pancreatic acini exogenous NO causes p125(FAK) and paxillin tyrosine phosphorylation that is mediated by a guanylyl cyclase-dependent pathway.