Liver failure, acute

Acid-base imbalance Acute liver failure Amphetamines Anaphylaxis Autoimmune diseases Cholestasis Chronic inflammatory diseases... 

Type A HE is induced by acute liver failure, Type B results from portal-systemic bypass without intrinsic liver disease, and Type C occurs with cirrhosis. HE may be classified as episodic, persistent, or minimal. 

The reactions of nucleophiles with benzoquinone and related compounds can also be viewed as Michael reactions. Benzoquinone is one of the reactive metabolites of benzene, a solvent also associated with aplastic anemia (Fig. 8.14). A similar reactive metabolite is responsible for the hepatotoxicity of acetaminophen (Fig. 4.71), the most common cause of acute liver failure however, most of this reactive metabolite is detoxified by reaction with glutathione, and it is only when glutathione is depleted to approximately 10% of the normal level that significant toxicity ensues. 

Its use was associated with a markedly increased risk of acute idiopathic liver injury and acute liver failure [50]. 

Graham, D.J., Drinkard, C.R. and Shatin, D. (2003) Incidence of idiopathic acute liver failure and hospitalized liver injury in patients treated with troglitazone. The American Journal of Gastroenterology, 98, 175—179. 

The reader should note the emphasis in the above paragraphs drug-induced hepatotoxicity is the leading cause of acute liver failure and the number one reason for regulatory actions against drugs in the United States ... 

Hepatotoxicity Severe hepatic reactions, including acute liver failure, jaundice, hepatitis, and cholestasis, have been reported rarely in postmarketing data in patients receiving infliximab. Autoimmune hepatitis has been diagnosed in some of... 

Hepatitis A is common, particularly in areas of poor sanitation, and is transmitted by food or drink contaminated by a sulferer/carrier. Clinical symptoms include jaundice, and are usually mild. A full recovery is normally recorded. Hepatitis B is transmitted via infected blood. Symptoms of acute hepatitis B include fever, chill, weakness and jaundice. Most sufferers recover from such infection, although acute liver failure and death sometimes occur 5-10% of sufferers go on to develop chronic hepatitis B. Acute hepatitis C is usually mild and asymptomatic. However, up to 90% of infected persons go on to develop a chronic form of the condition. Hepatitis D is unusual in that it requires the presence of hepatitis B in order to replicate. It thus occurs in some persons concomitantly infected with hepatitis B virus. Its clinical symptoms are usually severe, and can occur in acute or chronic form. 

Acute liver failure, beginning within one or two days of overdosage, can lead to encephalopathy, haemorrhage, oedema and death. Prolongation of prothrombin time is proportional to the degree of liver injury and is the best guide to severity of liver injury. Peak toxicity is seen 3 days after the overdose is taken. 

Corticosteroids have no value in supportive therapy. Acute liver failure is the main problem and specific features noted below require treatment ... 

There appears to be little difference between benzodiazepines and kava extract in anxiolytic activity. However, kava extracts seem to have fewer side effects. Two studies with more than 3000 patients each found unwanted events in about 2% of patients during treatment with kava extract. The more frequently reported side effects were gastrointestinal complaints, allergic skin reactions, headache, and photosensitivity (Pittler and Ernst, 2000). There have been isolated reports of hepatotoxicity and acute liver failure (Escher et ah, 2001). Kava may potentiate the sedative effects of other medications including barbiturates and benzodiazepines. Kava can also cause behavioral disinhibition in a minority of individuals, including children. The most common problem, which is usually associated with persistent and excessive usage, is a scaly skin rash called kava dermopathy, which is reversible. 

Kortsalioudaki, C., Taylor, R. M., Cheeseman, P., Bansal, S., Mieli-Vergani, G., and Dhawan, A. (2008). Safety and efficacy of N-acetylcysteine in children with non-acet-ammophen-induced acute liver failure. Liver Transpl. 14(1), 25-30. 

It is used in burns, shock, in patients of acute liver failure and on dialysis. 

Six unselected patients (four women), mean age 27 years, with acute liver failure and grade IV hepatic encephalopathy received terlipressin 0.005 mg/kg as a single intravenous bolus (16). There was an increase in cerebral blood flow 1 hour after the bolus, which returned to baseline at 5 hours, and an increase in intracranial pressure at 1 hour, which returned to baseline at 2 hours. The authors speculated that terlipressin could have a deleterious effect on cerebral hemodynamics in patients with severe hepatic encephalopathy. 

Shawcross DL, Davies NA, Mookcrjcc RP, Hayes PC, Williams R, Lee A, Jalan R. Worsening of cerebral hyperemia by the administration of terlipressin in acute liver failure with severe encephalopathy. Hepatology 2004 39 471-5. 

All cases of acute liver failure related to the use of lovastatin have been reviewed, and probably the frequency is similar to the background rate. This suggests that periodic monitoring of alanine transaminase in these patients would be burdensome and expensive (24). 

Suhler, E., W. Lin, H.L. Yin, and W.M. Lee. 1997. Decreased plasma gelsolin concentrations in acute liver failure, myocardial infarction, septic shock, and myonecrosis. Crit Care Med. 25 594—8. 

Lophyrotomin leads to fatal intoxications in cattle and sheep, with muscle twitching, refusal of food, and acute liver failure. 

Jalan R., Damink S. W., Deutz N. E., Lee A., and Hayes P. C. (1999) Moderate hypothermia for uncontrolled intracranial hypertension in acute liver failure. I/meet 354, 1164-1168. 

Belanger M, Butterworth RF. Acute liver failure a critical appraisal of available animal models. Metab Brain Dis 2005 20 409-23. 

A 52-year-old man with a 10-day history of fatigue and jaundice had been taking nefazodone (300 mg/day) for depression for about 6 weeks. Biochemical investigations showed acute liver failure. Infective hepatitis and immune disorders were excluded. He failed to respond to medical treatment, and hepatic transplantation was performed. Histological examination of the liver showed parenchymal necrosis, particularly in centrilobular areas, together with lymphocytic infiltration (10). 

Lucena MI, Andrade RJ, Gomez-Outes A, Rubio M, Cabello MR. Acute liver failure after treatment with nefazodone. Dig Dis Sci 1999 44(12) 2577-9. 

Olanzapine caused increased transaminases in a 38-year-old man with hereditary coproporphyria the enzyme changes were not associated with symptoms or evidence of either acute liver failure or exacerbation of his porphyria (230). 

Drug hepatotoxicity is a common cause of acute liver failure, with an incidence of 1 in 10 000-100 000. 

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