Hepatitis A Virus-induced Severe Hemolysis Complicated by Severe Glucose-6-Phosphate Dehydrogenase Deficiency

Abstract

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an x-linked recessive genetic disorder with mutation in the G6PD gene. Defect in the enzyme G6PD causes red blood cells (RBCs) to breakdown prematurely causing hemolytic anemia. Hemolytic anemia is also a known hematological complication associated with viral hepatitis. In such patients, hemolysis may be more severe if there is any secondary injury to RBC in the form of membrane defect, oxidative stress, or enzyme deficiency like in G6PD deficiency. Here, we present a case of an adult, not previously diagnosed with G6PD deficiency, who presented with viral hepatitis, severe hemolysis, and multiorgan failure.

Keywords: Glucose-6-phosphate dehydrogenase deficiency; hemolytic anemia; hemoperfusion; hepatitis A; methemoglobinemia; multiorgan failure.

Figure 1

Serial ammonia, serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase levels, and effect of ammonia filters

Figure 2

Serial bilirubin and prothrombin levels and effect of bilirubin filter