Case Presentation: Hepatitis B is a viral infection that attacks the liver and can cause both acute and chronic disease. The WHO estimates 1.5 million new infections each year. Most people remain asymptomatic. However, some people have acute illness that lasts several weeks, which can be complicated by acute liver failure. Glucose-6-phosphate dehydrogenase (G6PD) deficiency is x-linked and is the most common human enzymopathy. It affects an estimated 400 million people worldwide, is more common in males, and is mostly diagnosed in infants.
Discussion: A 73-year-old male presented with lethargy, loss of appetite, scleral icterus, and dark colored urine. On examination, vitals were within normal range. Diffuse jaundice was present, along with hepatomegaly. The patient was alert and oriented. Notable labs included AST 3017 unit/L, ALT 2712 Unit/L, BUN 74 mg/dL, Cr 3.6 mg/dL, total bilirubin 72.4 mg/dL, direct bilirubin 41.8 mg/dL, indirect bilirubin 30.6 mg/dL, hemoglobin 12.9 g/dL, white count 17,000 per microliter and platelet count of 173,000 per microliter. Prothrombin time was 19.2 seconds and INR (International Normalized Ratio) was 1.73. Imaging including CT abdomen did not show any abnormalities.The hepatitis panel was positive for Hepatitis B Core Antibody Total, Hepatitis B Core Antibody IgM, and Hepatitis B Surface Antibody, log 10 HBV IU/mL 2914. Hematological work up was pursued, which was concerning for LDH 4875, ferritin > 7500, reticulocyte percent 20.95%, absolute reticulocyte count 0.5129, and haptoglobin < 10. Coomb’s test was negative. Peripheral smear showed macrocytic anemia and no schistocytes. Erythrocyte G6PD level was performed which was low at 60 U/10E12 RBC despite acute hemolysis. The patient was started on hemodialysis due to electrolyte derangement and oliguria. He was also given intravenous fluids and started on Entecavir for acute complicated hepatitis B infection. A renal biopsy was suggestive of acute tubular injury with bilirubin and hemoglobin casts. The patient’s liver function, hemolysis labs, and renal function continued to improve, and he no longer required hemodialysis after several weeks of treatment.
Conclusions: Hemolytic anemia has been associated with viral hepatitis, but the degree is usually mild to moderate. In cases of severe intravascular hemolysis, underlying diagnoses such as hepatitis and G6PD deficiency should be sought out. Our case is unique in that this patient had no prior diagnosis of G6PD deficiency at his age. Additionally, the resulting cast nephropathy from hemolysis caused acute renal failure requiring hemodialysis. It is the first reported case of severe hemolysis and renal failure precipitated by acute hepatitis B in a patient with undiagnosed G6PD deficiency. Treatment with Entecavir resulted in marked improvement in clinical manifestations as well as laboratory tests. After about 6 weeks of dialysis, the patient made a full recovery. When severe hemolysis is present, hepatitis B should be a differential diagnosis as well as G6PD deficiency. Early recognition and treatment is key to preventing further complications. Prompt treatment of complicated hepatitis B with anti-viral therapy as well as supportive treatment for hemolysis is critical to early recovery and preventing life threatening organ failure.