Abstract

Early investigations suggested the utility of routine monitoring of serum biochemistry to identify patients at risk for rare, idiosyncratic acute liver failure and other forms of serious hepatotoxicity associated with the use of anticonvulsants. Such monitoring became the standard recommendation. Clinical examination and serum biochemistry screening are standard practice before starting a patient on anticonvulsants. Patients with aggravated hepatic dysfunction or overt hepatic disease should not receive anticonvulsants associated with acute hepatic failure such as valproic acid (sodium valproate) or felbamate, and those at increased risk for acute hepatic failure should receive these drugs only after careful consideration of all the circumstances. The available scientific evidence, however, does not support indiscriminate and repeated serum biochemistry monitoring for patients receiving anticonvulsants, mainly because moderate elevations of transaminase and alkaline phosphatase levels are common in asymptomatic patients receiving these drugs, and serum biochemistry changes are not always present in the early course of acute anticonvulsant-associated hepatic failure. Careful history-taking and notification of patients, caregivers and physicians of high risk groups and the warning symptoms and signs of incipient hepatic failure, such as decreased alertness, jaundice, vomiting, haemorrhage, increased frequency of seizures, anorexia and oedema, especially during the first 6 months of treatment, are the best methods for early detection.

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