Hepatitis alcohol

Liver diseases Alcoholic hepatitis (A), hepatitis B and C (A), non-alcoholic steatohepatitis (A), liver transplantation (A), Wilson s disease (A)... 

Apart from these two Vertex compounds, only one other caspase inhibitor, BDN-6556, has been used in clinical trials. This compound belongs to the class of oxamyl dipeptides and was originally developed by Idun Pharmaceuticals (taken over by Pfizer). It is the only pan-caspase inhibitor that has been evaluated in humans. BDN-6556 displays inhibitory activity against all tested human caspases. It is also an irreversible, caspase-specific inhibitor that does not inhibit other major classes of proteases, or other enzymes or receptors. The therapeutic potential of BDN-6556 was first evaluated in several animal models of liver disease because numerous publications suggested that apoptosis contributes substantially to the development of some hepatic diseases, such as alcoholic hepatitis, hepatitis B and C (HBV, HCV), non-alcoholic steato-hepatitis (NASH), and ischemia/reperfusion injury associated with liver transplant. Accordingly, BDN-6556 was tested in a phase I study. The drug was safe and... 

Lunel, F., Descamps-Latscha, B., Descamps, D., Le Char-pentier, Y., Grippon, P., Valla, D., Cadranel, J-F, Trum, J. and Opolon, P. (1990). Predictive value of whole blood chemiluminescence in patients with alcoholic hepatitis. Hepatology 12, 264-272. 

Corticosteroid therapy for patients with alcoholic hepatitis (steatonecrosis) with or without hepatic encephalopathy... 

Progression of alcoholic liver disease moves through several distinct phases from development of fatty liver to the development of alcoholic hepatitis and cirrhosis. Fatty liver and alcoholic hepatitis may be reversible with cessation of alcohol intake, but cirrhosis itself is irreversible. Although the scarring of cirrhosis is permanent, maintaining abstinence from alcohol can still decrease complications and slow development to end-stage liver disease.22 Continuing to imbibe speeds the advancement of liver dysfunction and its complications. 

Lp(a) is synthesized mainly, probably only, in the liver. This is supported by the fact that patients with hepatic dysfunction due to cirrhosis and alcoholic hepatitis exhibit low plasma Lp(a) concentrations (F6, G22, U10). 

Animals exposed to 2100 ppm for 1-3 hours exhibited restlessness, mucous membrane irritation, and drowsiness. Rats exposed to 1500 ppm for 8 hours survived. Injection of 3 ml/kg or intragastric administration of 5 ml/ kg diacetone alcohol in rabbits caused respiratory depression, narcosis, and death. A temporary decrease in the number of erythrocytes in the blood of rats was observed for IM- days after intragastric administration of 2 ml/kg of diacetone alcohol hepatic lesions characterized by vacuolization and granulation of the parenchymal cells were noted, but recovery was complete in 7 days. ... 

Adverse reactions may include acneiform eruptions allergic dermatitis arthropathy multiple cases of cholestatic and fulminant hepatitis drowsiness fatigue headache hepatotoxicity resembling viral or alcoholic hepatitis impotence metallic or garlic-like aftertaste peripheral neuropathy polyneuritis optic or retrobulbar neuritis restlessness occasional skin eruptions. 

Alcohol has a range of effects for some, desirable acute effects unwanted effects on the developing fetus and with long-term consumption, effects on the liver and other organs. In the US, over 2 million people experience alcohol related liver disease. Effects on the liver are dose related the more you consume the greater the effects. Early on there is an accumulation of fat in the liver as a result of the metabolism of alcohol. Some heavy drinkers develop an inflammation (alcoholic hepatitis) of the liver. Metabolites of alcohol, produced by the liver, are toxic to the liver cells. 

For alcoholic hepatitis is no specific treatment beyond alcohol withdrawal. Corticosteroids have no value. Fatty change in the liver is common, but should not be confused with fatty change associated with non-alcoholic disease, notably diabetes melli-tus. 

Pharmacokinetics Poorly absorbed from the G1 tract. Protein binding greater than 98%. Metabolized in the liver. Minimally eliminated in urine. Plasma levels are markedly increased in chronic alcoholic hepatic disease, but are unaffected by renal disease. Half-life 14 hr. 

Pharmacokinetics Well absorbed from theGl tract minimally absorbed after topical application. Protein binding less than 20%. Widely distributed crosses blood-brain barrier. Metabolized in the liver to active metabolite. Primarily excreted in urine partially eliminated in feces. Removed by hemodialysis. Half-life 8 hr (increased in alcoholic hepatic disease). 

Unlabeled Uses AIDS wasting syndrome, alcoholic hepatitis, burns. Turner syndrome... 

Liver disease is the most common medical complication of alcohol abuse an estimated 15-30% of chronic heavy drinkers eventually develop severe liver disease. Alcoholic fatty liver, a reversible condition, may progress to alcoholic hepatitis and finally to cirrhosis and liver failure. In the United States, chronic alcohol abuse is the leading cause of liver cirrhosis and of the need for liver transplantation. The risk of developing liver disease is related both to the average amount of daily consumption and to the duration of alcohol abuse. Women appear to be more susceptible to alcohol hepatotoxicity than men. Concurrent infection with hepatitis or C virus increases the risk of severe liver disease. 

Biguanide drugs are contraindicated in patients with renal disease, alcoholism, hepatic disease, or conditions predisposing to tissue anoxia (eg, chronic cardiopulmonary dysfunction) because of an increased risk of lactic acidosis induced by biguanide drugs. 

Fulminant liver failure results from massive necrosis of liver tissue. Diminution of mental function results, and this often leads to coma. The body undergoes a buildup of toxic products, alteration of its acid balance, and a decrease in cerebral blood flow. Impaired blood coagulation and intestinal bleeding occur as well. Other malfunctions and diseases of the liver include viral infections and alcoholic hepatitis. In 1999, of the 14,707 individuals on a waiting list for transplants, 4,498 received transplants and 1,709 died while waiting. As of February 2002, 18,434 people awaited liver transplants. 

Other malfunctions and diseases of the liver include viral infections and alcoholic hepatitis. In 1999, of the 14,707 individuals who were on the waiting list for liver transplants, 4,498 received transplants and 1,709 died. As of February 2002,18,434 people awaited liver transplants. 

Acquired hyperammonemia Liver disease is a common cause of hyperammonemia in adults. It may be a result of an acute po cess, for example, viral hepatitis, ischemia, or hepatotoxins. Cirrhosis of the liver caused by alcoholism, hepatitis, or biiary obstruction may result in formation of collateral circulation around the liver. As a result, portal blood is shunted directly rto the systemic circulation and does not have access to the ter. The detoxification of ammonia (that is, its conversion to urea) is, therefore, severely impaired, leading to elevated levels of cicu lating ammonia. 

Korula J. Tuberculous peritonitis complicating corticosteroid therapy for acute alcoholic hepatitis. Dig Dis Sci 1995 40(10) 2119-20. 

A 50-year-old obese woman taking glipizide 5 mg/day who had been drinking a bottle of rum daily for 2 months developed an acute hepatitis and died (115). The viral hepatitis profile was negative. At autopsy the liver weighed 1800 g and there was focal necrosis without evidence of autoimmune or alcoholic hepatitis. There was no brain edema. 

Milk thistle has been used to treat acute and chronic viral hepatitis, alcoholic liver disease, and toxin-induced liver injury in human patients. Milk thistle has most often been studied in the treatment of alcoholic hepatitis and cirrhosis. In both of these disorders, outcomes have been mixed and reports include significant reductions in markers of liver dysfunction and in mortality, as well as no effect. In acute viral hepatitis, studies have generally involved small sample sizes and have shown mixed outcomes of improved liver function (eg, aminotransferase values, bilirubin, prothrombin time) or no effect. Studies in chronic viral hepatitis and toxin-induced injury have also been of small size but have reported mostly favorable results. Parenteral silybin is marketed and used in Europe as an antidote in Amanitaphalloides mushroom poisoning, based on favorable outcomes reported in case-control studies. 

Lee TD, Sadda MR, Mendler MJ, et al. Abnormal hepatic methionine and glutathione metabolism in patients with alcoholic hepatitis. Alcohol Clin Exp Res 2004 28 173-181. 

A.L. Baker, et al., A randomized clinical trail of insulin and glucagons infusion for treatment of alcoholic hepatitis Progress report in 50 patients. Gastroenterology 80 1410-1414, 1981. 

Carithers RL, Herlong HF, Diehl AM et al. (1989) Methyl-prednisolone therapy in patients with severe alcoholic hepatitis. Ann Intern Med 110 685-690... 

Maddrey WC, Boitnott JK, Bedine MS et al. (1978) Corticosteroid therapy of alcoholic hepatitis. Gastroenterology 75 193-199... 

Hurtova M, Duclos-Vallee JC, Saliba F, Emile JF, Bemelmans M, Castaing D, Samuel D. Liver transplantation for fulminant hepatic failure due to cocaine intoxication in an alcoholic hepatitis C virus-infected patient. Transplantation 2002 73(l) 157-8. 

A 39-year-old man died suddenly 1 hour after taking a single oral dose of haloperidol 5 mg (14). He had myasthenia, alcoholic hepatitis, and electrolyte abnormalities due to inadequate nutritional state. His electrocardiogram showed prolongation of the QTC interval (460 ms). Autopsy showed a cardiomyopathy but no explanation for sudden death. 

Alcoholic liver disease Develops in 15% of individuals who drink heavily for more than a decade. Patients may also have concurrent alcoholic hepatitis with fever, hepatomegaly, janndice and anorexia. AST and ALT are both elevated bnt less than 300 IU/1, with a AST ALT ratio >2.0, a valne rarely seen in other liver diseases. 

There are three main histological stages of alcoholic liver disease, as highlighted in Figure 3.3 stage 1, steatosis (fatty infiltration of the hepatocyte) stage 2, alcoholic hepatitis and stage 3, fibrosis and cirrhosis. 

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