Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Omeprazole (CAS 73590-58-6), an H+, K+ ATPase inhibitor, is a potent suppressor of gastric acid secretion and a very active substance in the treatment of duodenal and gastric ulcers. The kinetic profile of omeprazole is well defined for healthy volunteers and for some high-risk population, but not so far for patients with liver disease. As the substance is mainly metabolized in the liver, changes in liver circulation and/or function might lead to changes in the pharmacokinetics of omeprazole. Aim of the study was to evaluate the kinetic profile in patients with liver disease and compare the results obtained in healthy volunteers, 16 subjects were included in the study: 8 patients with liver cirrhosis and 8 healthy volunteers. A single oral dose of omeprazole 20 mg was administered: plasma samples were collected for 24 h since omeprazole administration. The principal pharmacokinetic parameters were estimated for the two studied populations.
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PMID:Pharmacokinetics of omeprazole in cirrhotic patients. 185 16

Omeprazole is frequently used in patients with cirrhosis of the liver to treat peptic ulcer disease. It is also used for the healing of mucosal lesions after endoscopic sclerotherapy of esophageal varices in cirrhosis and extraheptic portal vein obstruction (EHPVO). This study was carried out with the aim of determining the pharmacokinetics of omeprazole in different degrees of liver cirrhosis and in patients with EHPVO, compared with healthy volunteers. Ten healthy volunteers, 30 patients with cirrhosis of the liver, divided into 3 groups of 10 depending on severity (according to Child-Pugh classification A, B and C) and ten patients with EHPVO participated in the study. The subjects received an omeprazole 20 mg capsule after an overnight fast. Blood samples were collected at 0, 0.5, 1, 1.5, 2, 2.5, 3, 6, 9 and 24 h after drug administration. Omeprazole level in plasma was estimated by reverse-phase high performance liquid chromatography (HPLC). The elimination half-life was significantly (p < 0.05) increased to 2.38 +/- 0.16, 3.26 +/- 0,12, 3.58 +/- 0.31 and 2.59 +/- 0.22 h in patients with different grades of cirrhosis (A, B and C) and also in patients with EHPVO, respectively, compared with 1.054 + 0.10 h in healthy volunteers. A similar significant increase (p < 0.05) was observed in the AUC(0alpha), while C(max) was significantly increased to 400.40 +/- 27.89 and 602 +/- 55.13 ng/ml in only grade C cirrhosis patients and EHPVO patients, compared with 303.5 +/- 36.42 ng/ml in healthy volunteers. No significant difference was observed in T(max). It was concluded that the metabolism of omeprazole was significantly impaired in both liver cirrhosis and EHPVO in comparison with healthy volunteers.
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PMID:Pharmacokinetics of omeprazole in patients with liver cirrhosis and extrahepatic portal venous obstruction. 1467 80

Esomeprazole is efficient for acid-dependent diseases of the gastrointestinal tract in patients with chronic hepatitis and hepatic cirrhosis as it can reduce the disease symptoms and cause the epithelization of erosive and ulcerative defects of the mucous coat. The terms of the cicatrisation of erosive and ulcerative defects of the mucous coat of the esophagus, stomach and duodenum are comparable in patients with liver diseases and in the population (without chronic hepatic diseases). The simultaneous application of Nexium and modern hepatotropic drugs does not cause the development of hepatotoxic reactions.
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PMID:[Experience of application of Esomeprazole in patients with chronic hepatic diseases associated with acid-dependent diseases]. 1546 17

We report different effects of administration of proton pump inhibitors on tacrolimus blood concentration in two living-donor liver transplant patients. In case 1, a 51-year-old man with liver cirrhosis due to hepatitis C virus underwent living-donor liver transplantation, and tacrolimus was orally administered. Omeprazole (40 mg/day) was introduced intravenously between postoperative days 5 and 6, and oral lansoprazole (30 mg/day) was introduced from day 6, leading to an increase in the concentration/dose ratio of tacrolimus from day 10. In case 2, a 41-year-old living-donor liver transplant woman received tacrolimus, and co-administered with omeprazole (40 mg/day) intravenously during 7 days immediately after surgery. During this period, trough concentration of tacrolimus was high, but the concentration/dose ratio of tacrolimus was gradually decreasing with time. Switched to rabeprazole (10 mg/day) orally on the postoperative 8th day, the concentration/dose ratio of tacrolimus remained low, indicating little drug-drug interaction between tacrolimus and rabeprazole. In both cases, the genotypes of CYP2C19 and CYP3A5 were defective both in the graft liver and in the native intestine. A drug-drug interaction between rabeprazole and tacrolimus was not observed in this case study presented, suggesting that this combination could be safely used in tacrolimus therapy after liver transplantation.
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PMID:Interaction between tacrolimus and lansoprazole, but not rabeprazole in living-donor liver transplant patients with defects of CYP2C19 and CYP3A5. 1844 94