Hepatocellular failure

A 25-year-old woman developed abdominal pain, jaundice, and vomiting 5 days after consuming ecstasy. She had hepatocellular failure with a prothrombin ratio of 6.5, cytolysis, cholestasis, renal insufficiency, and encephalopathy. She had a liver transplant 2 days later and recovered fully. 

Caballero F, Lopez-Navidad A, Cotorruelo J, Txoperena G. Ecstasy-induced brain death and acute hepatocellular failure multiorgan donor and liver transplantation. Transplantation 2002 74(4) 532-7. 

Acute hepatocellular failure Allopurinol, aspirin, cocaine, cyclophosphamide, dantrolene, halothane, isoniazid, ecstasy, methyldopa, NSAIDs... 

Akhtar, A.J. Conjunctival edema. A marker of increased mortality in patients with advanced hepatic encephalopathy and hepatocellular failure. Dig. Dis. Sci. 2002 47 373-375... 

The place of dye tests in the investigation of the jaundiced patient is another aspect on which further studies are required. Biliary obstruction itself causes dye to be retained in plasma so that in a jaundiced patient it is not known to what extent a high dye retention value is due to biliary obstruction or to hepatocellular impairment. It is possible, however, that mathematical analysis of plasma dye disappearance curves may allow the two components to be separately assessed. With BSP, measurement of dye conjugates in plasma offer another means of separating the effects of biliary obstruction from those of hepatocellular failure, although results to date have not been promising in the assessment of individual patients. 

A third group of toxins are those which give rise to acute hepatocellular failure only in certain individuals who are susceptible. Important examples include sodium valproate, an anticonvulsant drug which gives rise to toxicity in some children, and halothane, an anaesthetic agent. 

Severe cases of acute liver damage may progress to hepatocellular failure. 

Extrahepatic biliary obstruction occurs due to a myriad of benign and malignant etiologies. The resulting cholestasis may lead to malabsorption, coagulopathy, pruritus, hepatocellular failure, renal dysfunction. 

There appear to be two clinical presentations of Impila poisoning. The most common is one in which severe hepatocellular failure predominates. In many of these cases, signs of renal failure accompany the hepatic necrosis [33]. The second and less common clinical presentation of Impila poisoning is where renal failure [7] is an early finding and precedes the development of hepatic failure [8]. 

IV colchicine should be avoided because it is associated with serious adverse effects (e.g., bone marrow suppression, tissue necrosis from local extravasation, disseminated intravascular coagulation, hepatocellular toxicity, and renal failure). If considered necessary, the recommended initial IV dose is 2 mg (if renal function is normal) diluted in 10 to 20 mL of normal saline administered slowly over 10 to 20 minutes in a secure, free-flowing IV line to avoid extravasation. This may be followed by two additional doses of 1 mg each at 6-hour intervals, with the total dose not exceeding 4 mg. After a full IV course, patients should not receive colchicine by any route for at least 7 days. 

Hepatotoxicity Naltrexone has the capacity to cause direct hepatocellular injury when given in excessive doses. It is contraindicated in acute hepatitis or liver failure, and its use in patients with active liver disease must be carefully considered in light of its hepatotoxic effects. 

Discontinue nefazodone if clinical signs or symptoms suggest liver failure. Patients who develop evidence of hepatocellular injury such as increased serum AST or serum ALT levels at least 3 times the upper limit of normal while on nefazodone should be withdrawn from the drug. These patients should be presumed to be at increased risk for liver injury if nefazodone is reintroduced. Accordingly, do not consider such patients for retreatment. 

No evidence of another cause of hepatocellular injury, such as viral hepatitis, marked hypotension, or congestive heart failure. 

Cholestatic jaundice, hepatocellular neoplasms, peliosis hepatis, edema with or without congestive heart failure, and suppression of clotting factors II, V, VII, andX have been reported. 

The mercury ion is capable of causing local or systemic toxicity. For local irritation, they are combined with theophylline in an attempt to diminish the irritative toxicity at the site of injection. IV administration may lead to ventricular arrhythmias. They cause hepatocellular damage and even precipitate hepatic failure. They can also lead to low salt syndrome, hypochloraemic alkalosis and potassium depletion. 

Hepatic peroxisome proliferation has not been evaluated in studies of human subjects or systems treated with cinnamyl anthranilate. However, interspecies comparisons with other peroxisome proliferators, along with the role of PPARa in this response, indicate that humans can reasonably be predicted to be refractory to induction of peroxisome proliferation and hepatocellular proliferation by cinnamyl anthranilate. This conclusion is further supported by the failure to detect intact cinnamyl anthranilate in the urine of human volunteers given large single doses. 

A 37-year-old woman with refractory idiopathic thrombocytopenic purpura, who had responded dramatically to danazol 600 mg/day after the failure of other forms of treatment, developed a multinodular well-differentiated trabeculovesicular hepatocellular tumor after 5 years. There were no metastases and no invasion of the lymph nodes, and after chemoembolization she received an orthoptic liver transplant. A year later she remained in good condition. 

GGT is fouud particularly iu hepatocytes aud biliary epithelial cells. GGT serum levels may be high iu liver disease, but it is particularly a feature of biliary outflow obstruction more so than hepatocellular damage. GGT serum measuremeut provides a very sensitive indicator of the presence or absence of hepatobiliary disease. However, raised GGT levels have also been reported in a variety of other clinical conditions, including pancreatic disease, myocardial infarction, chronic obstructive pulmonary disease, renal failure, diabetes, obesity and alcoholism. It is also a sensitive indicator of liver damage through alcohol iugestion. 

Liver disease is now recognised as a major complication of type 2 diabetes. Diabetes mellitus can lead to metabolic changes that alter normal hepatic and biliary function and structure. Type 2 diabetes is associated with an increased risk of a range of hepatobiliary diseases, including non-alcoholic fatty liver disease, cirrhosis, acute liver failure, hepatocellular carcinoma and cholelithiasis [22]. 

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