Background and study aim: Minimal hepatic encephalopathy is a term used to describe cirrhotic patients who are clinically normal but show abnormalities of neurophysiological variables and/or cognition. Implicated theories of pathogenesis are similar to those of overt hepatic encephalopathy. Hypozincaemia was studied as a theory for the pathogenesis of overt hepatic encephalopathy. The aim of the present study is to evaluate the role of hypozincaemia in development of minimal hepatic encephalopathy among HCV induced compensated cirrhotic patients.
Patients and Methods: 30 patients with HCV induced compensated liver cirrhosis with minimal hepatic encephalopathy were studied versus 30 patients with HCV induced compensated liver cirrhosis without minimal hepatic encephalopathy. Diagnosis of minimal hepatic encephalo-pathy was based on positivity of both Number Connection Tests A and B. Serum zinc was evaluated for all subjects. Zinc deficient minimal hepatic encephalopathy patients were supplemented with zinc sulphate heptahydrate 220 mg daily for 1 month before HCV treatment and scores of Number Connection Tests A and B were redetermined.
Results: Serum zinc is significantly lower in patients with minimal hepatic encephalopathy than in those without minimal hepatic encephalopathy. Scores of Number Connection Tests A and B among zinc deficient patients with minimal hepatic encephalopathy were significantly improved after zinc supplementation.
Conclusion: Zinc deficiency may play a role in development of minimal hepatic encephalopathy among patients with HCV induced compensated liver cirrhosis. Zinc supplementation is recommended for the treatment of minimal hepatic encephalopathyamong those patients.