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)

Benzoate-metabolizing capacity was studied in control subjects and in liver disease patients after intra-venous loading of 15 mg benzoate per kg of body weight. In the 7 control subjects, the mean level (+/- SEM) of Cmax for serum benzoate was 104.1 +/- 6.8 micrograms/ml, AUC was 2.57 +/- 0.32 mg.min/ml, MRT was 21.5 +/- 1.5 min and T1/2 was 15.5 +/- 1.3 min. For serum hippurate, on the other hand, Tmax was 27.9 +/- 6.0 min, Cmax was 33.4 +/- 2.1 micrograms/ml, AUC was 1.96 +/- 0.13 mg.min/ml, MRT was 39.6 +/- 2.9 min and T1/2 was 30.7 +/- 2.4 min. In 12 patients with chronic hepatitis, Cmax, AUC, MRT and T1/2 for benzoate and Tmax, MRT and T1/2 for hippurate remained at control levels, but Cmax and AUC for hippurate were slightly decreased compared to controls. However, in 18 patients with liver cirrhosis, Cmax and AUC for benzoate were in the control range but MRT and T1/2 were significantly delayed (p less than 0.01 for both). Moreover, the MRT value was increased in proportion to the severity of liver disease (p less than 0.01). AUC for hippurate was not changed to any extent, and Tmax, MRT and T1/2 were slightly delayed, while Cmax was significantly reduced. AUC, MRT and T1/2 for benzoate and Tmax, MRT and T1/2 for hippurate showed significant correlation with serum albumin levels, prothrombin time and indocyanine green clearance rate. These results suggest that benzoate-metabolizing capacity, especially as indicated by the MRT value for serum benzoate, appears to be a better index than the indocyanine green clearance rate for determining hepatic functional reserve in chronic liver disease.
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PMID:Clinical significance of benzoate-metabolizing capacity in patients with chronic liver disease: pharmacokinetic analysis. 151 61

Three different studies were conducted to assess the pharmacokinetics of moclobemide in subjects with conditions complicating dose determination. The first examined the absorption and disposition of moclobemide in an elderly population and compared these with results obtained in a group of normal young subjects. No significant differences were found between the groups in the intravenous (i.v.) parameters of disposition, and no differences with regard to disposition of the metabolite, Ro 12-8095. In addition, the minimum steady-state concentrations of moclobemide and the main plasma metabolite did not differ between the elderly and younger patients. In the second study, clearance tests in patients with cirrhosis of the liver confirmed that hepatic function is drastically reduced in this group of patients; it is therefore possible that moclobemide absorption and distribution might be influenced. In only 3 of the 12 patients investigated, slowly declining plasma concentrations after administration pointed to a severely limited elimination capacity for moclobemide. In the remaining 9 subjects, average values of several parameters changed significantly (t 1/2 beta, MRT and C1), whereas Vss and renal clearance were not significantly altered. In patients with kidney dysfunction, there were no differences in kinetics between patients undergoing hemodialysis and those who were not. Compared with normal healthy volunteers, no differences were found for renal patients, with the exception of the mean absorption time, which was significantly prolonged. From these studies it can be concluded that, pharmacokinetically, neither age nor renal impairment require adjusting the dosage of moclobemide. Patients with liver cirrhosis, however, need to have the usual dose reduced to one half or one third, or else the dosage intervals can be increased to prevent cumulation.
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PMID:Absorption and disposition of moclobemide in patients with advanced age or reduced liver or kidney function. 224 88

Pharmacokinetics of ornidazole, a nitroimidazole derivative, was investigated after intravenous injection in 3 groups of 10 patients with different hepatic diseases: hepatitis, noncholestatic cirrhosis and extrahepatic cholestasis. Plasma concentrations of ornidazole and its two major hydroxylated metabolites, M1 [alpha-(chloromethyl)-2-hydroxymethyl-5-nitroimidazole-1-ethanol] and M4 [3-(2-methyl-5-nitroimidazole 1-yl)-1,2-propane diol] were measured by HPLC assay. As a consequence of a decreased clearance (26% to 48%), the half-life and MRT are increased in all patients by 19% to 38% when compared with healthy volunteers. No clear difference could be established between the different groups. The volume of distribution remains the same in all patients and controls except those suffering from cancer. As previously shown in patients with severe liver cirrhosis, both metabolites accumulate in plasma as a result of decreased elimination; formation is no longer the rate-limiting step of their kinetics. This metabolite accumulation is in part due to decreased biliary excretion and to hepatocellular failure.
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PMID:Pharmacokinetics of ornidazole in patients with acute viral hepatitis, alcoholic cirrhosis, and extrahepatic cholestasis. 270 94

The advent of new imaging modalities such as CT-AP and MRT has markedly improved the diagnosis and staging of primary liver tumors and will change the diagnostic impact of laparoscopy. Diagnostic laparoscopy in this retrospective study was not found to add information in regard to tumor staging and resectability, and there was no clear benefit by avoiding diagnostic laparotomies when all imaging and biopsy techniques available were used preoperatively. Therefore, we advocate the use of diagnostic laparoscopy only in selected cases suspicious for superficial small tumor lesions and cirrhosis with impact on the treatment modality.
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PMID:[Value of diagnostic laparoscopy in primary malignant liver tumors]. 993 73

Ultrasound is unquestionably of great importance in the diagnosis of liver diseases due to the technical improvements of the last years. Indications for an ultrasound examination are the primary diagnosis of chronic liver disease and the screening for hepatocellular carcinoma. Apart from the diagnosis of portal hypertension in liver cirrhosis a portal vein thrombosis should be detected or excluded in cases of new or refractory ascites. The Budd-Chiari syndrome is another rare but important indication. There is a considerable improvement in the differential diagnosis of focal liver lesions especially due to contrast-enhanced sonography. Using phase-inversion harmonic sonography it is possible to detect tumor vascularity in a very sensitive manner. The accuracy of contrast-enhanced sonography is comparable with helical-CT or MRT, and contrast-enhanced sonography is very useful in the evaluation of response to ablation therapy of hepatocellular carcinoma.
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PMID:[Value of ultrasound and doppler sonography in chronic hepatitis and liver cirrhosis]. 1590 Aug 27

Nodular regenerative hyperplasia (NRH) is characterized by a non-cirrhotic micronodular transformation of the liver parenchyma. It is based on the obliteration of small portal veins. Macroregenerative nodules (MRN) develop in areas of favourable blood flow in otherwise hypoperfused liver tissue. Hypoperfusion is caused by obliteration of liver veins and/or large portal veins with the subsequent atrophy or extinction of parenchyma. The hyperperfused and sometimes rapidly growing MRN might simulate a malignant tumor in CT and MRT. Morphologically, MRN resemble FNH. In contrast to hepatocellular adenoma, they show a more or less nodular architecture with fibrous septa and ductular structures. NRH and cases of MRN without cirrhosis can indicate an extrahepatic/systemic disease causing altered liver perfusion. MRN in liver cirrhosis must be differentiated from dysplastic nodules and highly differentiated hepatocellular carcinoma by cytological and microarchitectural criteria. Focal nodular hyperplasia (FNH) can imitate liver cirrhosis, steatohepatitis, cholangitis or chronic hepatitis, if biopsy material does not include normal perilesional liver tissue. Telangiectatic FNH might resemble classic hepatocellular adenoma. Neoductular structures and septation argue for this rare subtype of FNH. Neoductular transformation of hypoperfused liver parenchyma might imitate cholangioma or cholangiocarcinoma.
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PMID:[Nodular lesions of liver parenchyma caused by pathological vascularisation/perfusion]. 1677 11