S3531 Acute Hepatitis a Causing Severe Hemolysis and Renal Failure in a Glucose-6-Phosphate Dehydrogenase Deficient Patient

Abstract

INTRODUCTION: Hepatitis A virus infections are usually self-limited illness that rarely causes fulminant liver failure. Hemolysis is a known complication of viral hepatitis and is typically mild. Severe hemolysis is uncommon; however, it has been reported in patients with Glucose-6-phosphate dehydrogenase (G6PD) deficiency. We report the first case in the United States with undiagnosed G6PD deficiency who presented with hyperbilirubinemia, severe hemolysis, and renal failure due to acute hepatitis A infection. CASE DESCRIPTION/METHODS: A 55-year-old male with a past medical history significant for HIV, presented with complaints of jaundice, fatigue, weakness, and abdominal pain for two weeks. The patient denies any history of alcohol, illicit drug use, or family history of liver disease. On examination, he was hemodynamically stable with scleral icterus. On admission laboratory test showed creatinine 6.38 mg/dL (0.7–1.3) , BUN 48 mg/dL (7–18), total bilirubin 51.8 mg/dL (0.2–1), direct bilirubin 40.4 mg/dL (< =0.2), Lactate dehydrogenase 2678 unit/L (87–241), Haptoglobin < 7.7 mg/dL, Alkaline phosphatase 195 unit/L, AST 4,216 unit/L (15–37), ALT 6,244 unit/L (16–61), Lactic acid 5.5 mmol/L(0.4–2), WBC 16.6 thou/mcL (4.2–10.2), Hemoglobin 7.5 g/dL (12.8–16.4), Platelet 344 thou/mcL (150–400), and INR 1.6 (0.8–1). His combs test was negative. He underwent extensive workup for etiology for his jaundice, including viral hepatitis (HSV, EBV, CMV, HAV, HBV, HCV, HEV), Autoimmune (ANA, SMA, AMA, Immunoglobins), obstructive process (CT abdomen/pelvis). All these tests were negative except for a positive for Hepatitis A IgM. His peripheral blood smear showed hemolysis. He was treated empirically with antibiotics, intravenous fluids, and hemodialysis for renal failure. He underwent liver and kidney biopsies, which showed cholestatic hepatitis and acute tubular injury with bile and hemoglobin casts, respectively (Figures 1 and 2). His G6PD level was low 6.2 U/g Hgb (7–20.5), confirming the diagnosis. With supportive measures, the patient clinically improved, and he was discharged home on day 25 with a total bilirubin of 13 (Figure 3). DISCUSSION: Our patient had acute hepatitis A, which precipitated hemolysis and renal failure in the setting of undiagnosed G6PD deficiency. In conclusion, intravascular hemolysis due to G6PD deficiency should be considered in patients with acute hepatitis A infection who presenting with marked hyperbilirubinemia and renal failure.Figure 1.: A. Liver biopsy (H&E, x40) shows bridging necrosis and collapse of parenchyma with cholestasis and sparse inflammatory infiltrate rich in lymphocytes and plasma cells (B. inset x200). C. A trichrome stain (x20) shows lack of fibrosis supporting acute nature of the illness.Figure 2.: A. Renal biopsy shows tubular casts comprising of hemoglobin (hemoglobin immunostained in B) and bile pigment (Fauchet stain in C). Glomeruli and vasculature were within normal limits.Figure 3.: Changes in liver tests during hospitalization are plotted from admission at day 1 to day 25.