Severe hyperbilirubinemia due to acute hepatitis A superimposed on a chronic hepatitis B carrier with glucose-6-phosphate dehydrogenase deficiency.

Taiwan is an endemic area for hepatitis A and B virus infections; nearly 90% of adults have serological markers for either virus. Glucose-6-phosphate dehydrogenase (G6PD) deficiency is also common, ranging from 2% to 10%. We report the case of a 36-yr-old chronic HBV male carrier with G6PD deficiency who developed acute viral hepatitis A with severe hyperbilirubinemia and intravascular hemolysis. The hemolysis was in all likelihood the result of recent exposure to sulfa drugs. Fulminant hepatitis was the initial impression, because the peak serum total bilirubin concentration was alarmingly high, at 85.4 mg/dl. Exchange plasmapheresis was fresh frozen plasma was performed, and various laboratory studies gradually returned to near normal laboratory studies gradually returned to near normal over the next 3 wk. The patient made an uneventful recovery 1 month after admission.