Autoimmune Hemolytic Anemia in Treatment-Naïve Chronic Hepatitis C Infection

Abstract

Purpose: Hepatitis C Virus (HCV) is a blood borne pathogen that infects the liver and is associated with great morbidity. Chronic HCV infection can lead to cirrhosis, hepatocellular carcinoma, and ultimately liver failure. Less commonly known extrahepatic manifestations of HCV exist as numerous studies have been published demonstrating Autoimmune Hemolytic Anemia (AIHA) in chronic Hepatitis C patients receiving Ribavarin or Interferon. On the contrary, there is minimal literature demonstrating AIHA in treatment-naive chronic hepatitis. Case Presentation: A 53-year-old man with chronic Hepatitis C infection presented with 7 days of sharp right upper quadrant abdominal pain complicated by rapidly increasing abdominal girth, nausea, vomiting, weakness, fever and jaundice. His HCV course was complicated by cirrhosis, esophageal varices, portal hypertensive gastropathy and spontaneous bacterial peritonitis. Physical examination: Jaundiced sleepy male with normal vital signs. Scleral icterus, distended abdomen tender to palpation in the right upper quadrant, gynecomastia, diffuse spider angiomata on anterior chest, and +2 bilateral pitting edema up to the knees. No asterixis, palmar erythema, or caput medusae. Laboratory data: WBC 5700/UL, Hemoglobin 8.3 g/dl, MCV 112.4, platelets 47,000/UL. Indirect bilirubin of 14.3 mg/dl was worrisome for hemolytic anemia. Reticulocyte count 9.6% and direct Coomb's test antibody positive. Peripheral smear showed increased spherocytes, polychromasia, and thrombocytopenia consistent with AIHA. Workup: Etiologies of AIHA include malignancy, SLE, Ribavarin and Interferon. MRI and CT abdomen with contrast illustrated cirrhosis, but did not depict neoplastic lesions or lymphadenopathy. Chest CT and x-ray demonstrated no neoplasms, mediastinal or axillary lymphadenopathy, and no changes of the bony thorax consistent with a cancerous process. Bone marrow biopsy demonstrated erythroid hyperplasia with cell lines. No tumor or lymphoma was noted. Thus, malignancy was ruled out as an etiology of AIHA. SLE was subsequently ruled out with a negative ANA panel, and iatrogenic etiology was non-contributory as the patient had never received Ribavarin or Interferon. Conclusion: We present a rare case of AIHA infection where conceivably all etiologies of AIHA were thoroughly ruled out - demonstrating HCV as a unique and novel cause of AIHA. This is of great interest in idiopathic AIHA, as physicians we can look to HCV as an underlying source of AIHA. More recently, HCV is becoming an epidemic in the United States. Thus, unprecedented medical conditions associated with HCV are of great interest.