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Results for “Hepatic Insufficiency”

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At least 19 recordsLinked to original sources
PubMed1977

[Therapy of hepatic insufficiency].

Hepatic insufficiency is generally caused by active liver cirrhosis with portal hypertension. The final stage is the exogenous hepatic coma. Much rarer is the endogenous hepatic coma caused by fulminant acute hepatitis or severe intoxications. In the treatment of hepatic insufficiency it is first necessary to eliminate all exacerbating factors such as too high protein-intake, gastrointestinal bleedings, abuse of alcohol and diuretics. Because hepatic encephalopathy is mainly produced by toxic intestinal protein metabolites no protein should be adminstered at the beginining of the disease. The production of toxic protein metabolites in the gut can be diminished as well by enemas with sodium acetate buffer (pH 4, 5) as by neomycin (6-8 gm daily). Because long-term treatment with neomycin reduces also the physiological intestinal bacteria combination with lactulose (70-100 gm daily) is better. Treatment with lactulose reduces not only significantly hyperammoniemia but also increases serum phenols. The same effect have so-called ammonia reducing amino acids such as arginine, ornithine and glutamic acid. In endogenous hepatic coma blood exchange transfusions, liver perfusions and charcoal perfusions are necessary. Nevertheless, the prognosis of hepatic insufficiency caused by fulminant hepatitis is very poor in the final stage of the disease. Therefore early diagnosis and treatment in special departments with intensive care is necessary.

Alcoholism↗
PubMed1989

Steady-state intravenous pharmacokinetics of pirenzepine in patients with hepatic insufficiency and combined renal- and hepatic insufficiency.

The steady-state intravenous pharmacokinetics of pirenzepine has been investigated in patients with chronic liver disease and others with combined chronic liver disease and renal insufficiency. The plasma clearance (CL) of Pirenzepine, steady-state plasma concentration Cmin(ss) and dominant half life t1/2 gamma were not significantly altered in the chronic liver disease group. In patients with renal and hepatic insufficiency, CL was reduced, t1/2 gamma was prolonged from 11.1 to 19.4 h and Cmin(ss) was elevated from 36 ng/ml to 66 ng/ml compared to healthy controls. Plasma concentrations remained in the therapeutic range and the dosage regimen was well tolerated. Adjustment of the dose of pirenzepine need be considered only in cases of severe impairment of both renal and hepatic elimination.

Adult↗
PubMed1977

[Hepatic insufficiency - clinical picture].

Hepatic insufficiency results from extreme derangement of liver cell function. Pathophysiology and clinical picture of this syndrome are briefly discussed; the latter correlate rather poorly with laboratory data - the poorest correlation existing between clinical picture and bioptic findings. Acute hepatic insufficiency may occur in the course of every pathological process involving the liver, it does however arise most often in severe viral hepatitis with widespread disintegration of liver cells and in toxic liver damage. Chronic hepatic insufficiency is typical for the final stages of cirrhosis of the liver. Measurement of coagulation factors has proved to be the best prognostic parameter in hepatic failure.

Acidosis↗
PubMed2003

Diurnal locomotor activity and oxidative metabolism of the suprachiasmatic nucleus in two models of hepatic insufficiency.

Subjects with hepatic cirrhosis develop alterations of several rhythmic behavioural and biochemical patterns. Since most cirrhotic patients combine portal hypertension and hepatic impairment, our work aims to assess the extent to which rhythmical changes can be due to hepatic insufficiency or portal hypertension. This was done using two experimental models in rats, portacaval shunt model (PC) and portal hypertension by a triple stenosing ligature of the portal vein (PH). We assess diurnal locomotor activity and determine the oxidative metabolism of the suprachiasmatic nucleus (SCN) by histochemical determination of cytochrome oxidase (COX). The results show that animals with PC have altered diurnal locomotor rhythm compared to control and PH rats (p<0.001). They also present lower COX activity in the SCN (p<0.05). We conclude that rhythmic alterations are due to hepatic insufficiency and not to portal hypertension.

Animals↗
PubMed1996

Pharmacokinetics of ondansetron in patients with hepatic insufficiency.

Ondansetron is primarily eliminated via hepatic metabolism; thus, liver disease may affect its clearance. The pharmacokinetics of ondansetron in patients with different degrees of hepatic insufficiency (N = 12 with hepatic impairment, as categorized by Pugh's classification method) were assessed and the results compared with results for age- and gender-matched control subjects with normal liver function (n = 12). A secondary objective was to correlate the Pugh method of assessing hepatic impairment and quantitative metabolic markers used to assess hepatic function (antipyrine clearance and indocyanine green clearance) with changes in the pharmacokinetics of ondansetron. This was an open-label study in which 8 mg ondansetron was given orally and intravenously, following a randomized crossover design. Clearance of ondansetron was lower among patients with hepatic impairment that control subjects. After a single, oral dose of ondansetron, mean absolute bioavailability increased markedly with increased hepatic insufficiency (approaching 100% in the group with severe hepatic impairment versus 66% for control subjects). These data suggest that there is a reduced first-pass effect in patients with liver disease resulting in a higher AUC0-infinity. A correlation existed between clearance of ondansetron and decreased antipyrine clearance; a smaller correlation existed between ondansetron clearance and indocyanine green clearance. Mean percent of ondansetron bound to plasma proteins was significantly lower in patients with liver disease than in control subjects. None of the patients experienced any severe adverse reactions attributed to ondansetron. A reduction in the clearance of ondansetron is associated with increasing degrees of hepatic insufficiency; therefore, patients with severe hepatic impairment (Pugh score of > 9) should have their daily dose of ondansetron limited to 8 mg (or 0.15 mg/kg).

Administration, Oral↗
PubMed2006

[Clinical study on severe acute pancreatitis complicated by hepatic insufficiency].

OBJECTIVE: To investigate the pathogenic factors of severe acute pancreatitis (SAP) complicated by hepatic insufficiency, the prognosis and the effective preventive and therapeutic interventions. METHODS: One hundred and fifty-two patients with SAP (from January 2003 to June 2004) were divided into 2 groups, SAP with hepatic insufficiency group and SAP without hepatic insufficiency group. The related factors such as causes of disease, serum biochemical criteria, complications, mortality and course of disease were observed. RESULTS: The concentrations of serum amylase, creatinine and lactate dehydrogenase were all much higher in the SAP with hepatic insufficiency group than those in the SAP without hepatic insufficiency group (P<0.05). The incidences of complications such as acute renal failure, heart failure, gastrointestinal hemorrhage and infection were also higher in the SAP with hepatic insufficiency group than those in the SAP without hepatic insufficiency group (P<0.05). There was no significant difference in mortality between these two groups, but the course of disease in SAP with hepatic insufficiency group was longer than that in the other group (P<0.05). CONCLUSION: The causes of SAP complicated by hepatic insufficiency are related to the imbalance of internal environment and the characteristics of the liver function. To control the biliary tract diseases, intervene with traditional Chinese medicine, recover the intestinal function in time, reduce the damage of pancreatic enzyme, maintain the stability of internal environment and avoid using drugs that can induce liver injury are all important aspects of reducing the incidence of hepatic insufficiency.

Adult↗
PubMed1983

Mezlocillin kinetics in hepatic insufficiency.

To establish elimination kinetics of mezlocillin in patients with hepatic insufficiency, we gave eight normal subjects and four patients with hepatic insufficiency and normal renal function a single 3-gm dose of mezlocillin by intravenous infusion. Subjects with hepatic insufficiency all had serum bilirubins levels of above 3 mg/dl, prothrombin times more than 2 sec longer than control, and creatinine clearances above 60 ml/min. Mezlocillin concentrations were determined by microbiologic assay. Kinetic analysis was by model-independent methods. Elimination half-life was 0.96 hr for subjects with normal liver function and 2.62 hr for patients with hepatic insufficiency. Mean total body clearance for normal subjects was 247 ml/min, while in patients with hepatic insufficiency it was 125.4 ml/min. We conclude that hepatic insufficiency prolongs mezlocillin elimination and suggest that therapeutic guidelines be set up.

Adult↗