Impact of drug combination of clopidogrel and pantoprazole In the prognosis of patients with transient ischemic attack

The study aimed to investigate the impact of clopidogrel combined with proton pump inhibitors [PPI] pantoprazole treatment on the prognosis of patients with transient ischemic attack [TIA]. A total of 478 cases of TIA patients treated with clopidogrel were randomly assigned half to clopidogrel combined with pantoprazole treatment and the control groups [clopidogrel treatment alone] from January 2012 to January 2014. The platelet aggregation before and after treatment and cerebrovascular events incidence within 90 days were compared and analyzed. Multivariate analysis was used to estimate the incidence of cerebrovascular events within 90 days. The platelet aggregation rate before treatment was 73.2 +/- 6.1% in the treatment group, 74.1 +/- 8.8% in the control group. The platelet aggregation rate after treatment was 38.1 +/- 10.7% in the treatment group, 36.8 +/- 9.7% in the control group. The platelet aggregation before and after treatments between the two groups had not significant difference [P>0.05]. The incidence of cerebrovascular events within 90 days [11.7% in the treatment group, 9.6% in the control group] between the two groups had not significant difference [P>0.05]. Multivariate analysis showed that the incidence of cerebrovascular events within 90 day was associated with hypertension [P=0.008], diabetes [P=0.000], hyperlipidemia [P=0.002] and ABCD2 score >3 points [P=0.000]. Clopidogrel combined with pantoprazole treatment had no significant effect on the prognosis of TIA patients

Role of oxidative stress in lansoprazole-mediated gastric and hepatic protection in Wistar rats.

BACKGROUND AND AIM: Lansoprazole, a benzimidazole derivative, is a widely-used proton-pump inhibitor. In addition, it has been reported to have an independent gastroprotective action. Since free radicals and antioxidant mechanisms appear to counter-act tissue-related injury, we studied the effect of lansoprazole on oxidative stress in acid-ethanol gastric injury. As this drug is metabolized in the liver, we also studied its effect on the liver. METHODS: Wistar rats were divided into three groups: control group, group I (vehicle treatment) and group II (lansoprazole treatment for eight days). In all the groups, injury was induced by ethanol-HCl administration. The effect of lansoprazole on free-radical generation and various antioxidants, e.g. superoxide dismutase (SOD), catalase, reduced glutathione (GSH), glutathione-s-transferase (GST) and glutathione reductase was evaluated in the gastric mucosal and liver homogenates. RESULTS: Ethanol-HCl administration initiated injury as shown by increase in malondialdehyde (MDA) levels in both gastric mucosa and liver. There was an increase in SOD and GST activity and a decrease in catalase, glutathione reductase and GSH in the gastric mucosa. In liver, ethanol-HCl administration decreased the activity of SOD, catalase and GSH and increased GST activity. Lansoprazole pretreatment led to decrease in the levels of MDA and increase in SOD, catalase, GSH, glutathione reductase and GST in both the gastric mucosa and liver. CONCLUSIONS: Lansoprazole has a protective action on gastric mucosa and the liver. This protection is mediated by a decrease in oxidative stress and a concomitant in-crease in antioxidants.