Hepatocyte dysfunction and hepatic encephalopathy in Plasmodium falciparum malaria.

Background: According to the WHO, signs of hepatic dysfunction are unusual, and hepatic encephalopathy is never seen in malaria. However, in recent years, isolated cases have been reported from different parts of world.
Aim: To identify the evidence for hepatocyte dysfunction and/or encephalopathy in jaundiced patients with falciparum malaria.
Design: Prospective observational study.
Methods: We studied 86 adult patients of both sexes who had malaria with jaundice (serum bilirubin > 3 mg%). The main outcome measures were: flapping tremor, deranged psychometric test, level of consciousness, serum bilirubin level, serum aspartate transaminase (AST) and alanine transaminase (ALT) levels, blood ammonia level, viral markers for hepatitis, ultrasonography of liver and gall bladder and electroencephalography (EEG).
Results: The range of serum bilirubin was 3-48.2 mg% (mean +/- SD 10.44 +/- 8.71 mg%). The ranges of AST and ALT levels were 40-1120 IU/l (294.47 +/- 250.67 IU/l) and 40-1245 IU/l (371.12 +/- 296.76 IU/l), respectively. Evidence of hepatic encephalopathy was seen in 15 patients. Asterexis was observed in 9 patients, impaired psychometric tests in 12 and altered mental state in 13. Arterial blood ammonia level was 120-427 meq/l (310 +/- 98.39 meq/l). EEG findings included presence of large bilateral synchronous slow waves, pseudo burst suppression and triphasic waves. Four patients died due to multiple organ dysfunction; the others made rapid recoveries.
Discussion: There is strong evidence of hepatocyte dysfunction and hepatic encephalopathy in some of these patients, with no obvious non-malarial explanation. Current guidelines may need to be revised.