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A Sallow Infant

A6-month-old previously healthy female was found to be anemic during her well-child check. She was started on iron supplementation and scheduled for a return visit. Three weeks later she was noted to be jaundiced with persistence of her anemia, prompting referral to gastroenterology. Further history revealed no known exposure to hepatitis, toxins, or medications. There had been no preceding illnesses or fever. Her immunizations were up to date, including the hepatitis B virus, vaccine series. Medical history was significant for jaundice at 1 week of age, attributed to breast-feeding. Family history was negative for anemia, early cholelithiasis, splenectomy, cystic fibrosis, systemic lupus erythematosis, Wilson’s disease, and α-1-antitrypsin deficiency. Physical examination revealed a pale, jaundiced, irritable female. Vital signs were significant for mild tachycardia. There was no cardiac murmur and the lungs were clear to auscultation. Hepatomegaly was present, but no spleen was palpable. There were no cutaneous signs of chronic liver disease, such as palmar erythema, spider angiomas, or xanthomas. At the time of evaluation, she was found to have a normal platelet count (474 × 103), leukocytosis (18,300), and normochromic, normocytic anemia (hematocrit = 22.9%; hemoglobin = 8.1 g/dL; MCV = 96.6 fl). A blood smear showed anisocytosis, poikilocytosis, schistocytosis, teardrop cells, and polychromasia, consistent with a hemolytic process. A direct Coombs test was positive (poly-Coombs (3+), antiIgG (3+), and anti-C3 (2+)). A liver panel showed elevated serum transaminases (alanine aminotransferase = 5663 U/L; aspartate aminotransferase = 4567 U/L) and bilirubin (total = 10.1 mg/dL, direct = 6.1 mg/dL); total protein (7.5 g/dL) and albumin (4.5 g/dL) levels were normal. The prothrombin time and partial thromboplastin time were normal. Abdominal ultrasound showed a normal gallbladder without stones or sludge; mild splenomegaly; and a normal sized liver, with a diffuse heterogeneous pattern consistent with hepatocellular injury. Serology for hepatropic viruses (hepatitis A virus, hepatitis B virus, and hepatitis C virus), cytomegalovirus, parvo-B19, and Ebstein-Barr virus was negative. A presumptive diagnosis of autoimmune hepatitis and autoimmune anemia was made. Serology for anti -smooth muscle antibody, anti-nuclear antibody, and anti–liver/kidney microsomal antibody was obtained (all eventually returning negative) and intravenous steroids were begun (solumedrol, 2 mg/kg/ day). Because of poor venous access, a percutaneous intracardiac catheter (PICC) was placed. A rapid response to steroids was noted with a marked decrease in aminotransferase levels. She was converted to oral prednisone (2 mg/kg/day) and discharged home after 1 week. A liver biopsy was not performed because of the potential need for a transfusion and the difficulty in finding antibody-negative blood. Before her scheduled follow-up visit, she pre-