Abstract

Editor, Viral hepatitis usually manifests as a self-limiting illness. However, in the presence of glucose-6-phosphate dehydrogenase (G6PD) deficiency, it may be complicated with renal failure, hemolysis, hepatic encephalopathy and even death. The incidence of G6PD deficiency in the general population in northern India ranges from 2.2 % to 14 % [1]. We retrospectively analyzed the clinical presentation and outcome of patients with G6PD deficiency and acute viral hepatitis. The case records of all patients admitted in our hospital with acute viral hepatitis between January 2007 and December 2010 and ten patients (mean age 16.1 years, M:F 4:1) with G6PD deficiency and acute viral hepatitis were identified. Fourteen patients (mean age 19.3 years, M:F 5:2) with acute viral hepatitis and without G6PD deficiency were randomly selected by draw of lots for comparison. Both the groups were analyzed on the basis of age, sex, etiology of hepatitis, peak bilirubin levels, peak creatinine levels, prothrombin time, requirement of hemodialysis, hospital stay and outcome. Seven patients in the study group had hepatitis A infection and three had hepatitis E infection. In the control group, eight patients had hepatitis A, five had hepatitis E and one had mixed hepatitis A and E infection. As noted from Table 1, the mean peak bilirubin was significantly higher in the study group (p<0.001). Peak creatinine value was not significantly increased when compared to the control group. The mean international normalized ratio and indirect bilirubin was significantly higher in the study group. The mean duration of stay was nearly two and a half times more in the study group than in the control group. Mild hemolysis is seen in acute viral hepatitis but is rarely of clinical significance [2]. When viral hepatitis occurs in G6PD deficient individuals, hemolysis may be severe [3]. Gotsman et al. reported a more severe initial presentation in patients with acute viral hepatitis A and G6PD deficiency though the clinical outcome was not affected [4]. Abid and Khan reported five patients with acute viral hepatitis E, severe intravascular hemolysis, hyperbilirubinemia and anemia. Two patients required hemodialysis and they advocated that measures to prevent renal failure should be taken in such patients [5]. Hemolysis may result from decreased levels of reduced glutathione in red blood cells [2], consequent to the accumulation of oxidants due to hepatic dysfunction. Renal tubular dysfunction occurs due to excess hematin and bilirubin which result in obstruction of renal tubules. Good hydration and avoiding nephrotoxic drugs helps in preventing renal failure. Tests for G6PD deficiency may be negative during the hemolytic phase and should be repeated after 8–10 weeks of recovery. Vitamin K should be avoided in these patients. Studies from various parts of India have recommended vaccination against hepatitis A and B in communities with high prevalence of G6PD deficiency [6, 7].

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