Early investigations suggested the utility of routine monitoring of se
rum biochemistry to identify patients at risk for rare, idiosyncratic
acute liver failure and other forms of serious hepatotoxicity associat
ed with the use of anticonvulsants. Such monitoring became the standar
d recommendation. Clinical examination and serum biochemistry screenin
g 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 failu
re such as valproic acid (sodium valproate) or felbamate, and those at
increased risk for acute hepatic failure should receive these drugs o
nly after careful consideration of all the circumstances. The availabl
e scientific evidence, however, does not support indiscriminate and re
peated serum biochemistry monitoring for patients receiving anticonvul
sants, mainly because moderate elevations of transaminase and alkaline
phosphatase levels are common in asymptomatic patients receiving thes
e drugs, and serum biochemistry changes are not always present in the
early course of acute anticonvulsant-associated hepatic failure. Caref
ul history-taking and notification of patients, caregivers and physici
ans of high risk groups and the warning symptoms and signs of incipien
t hepatic failure, such as decreased alertness,jaundice, vomiting, hae
morrhage, increased frequency of seizures, anorexia and oedema, especi
ally during the first 6 months of treatment, are the best methods for
early detection.