Purpose: Background: Liver diseases are common after bone marrow transplant, the most common being graft versus host disease (GVHD) and hepatotoxicity due to drugs. Viral hepatitides are less common, usually caused by reactivation of or new infection with hepatitis B, C or herpesviruses. There are few descriptions of Coxsackie hepatitis in the literature. We report a patient who developed submassive Coxsackie hepatitis eight months following allogeneic stem cell transplantation. Case Report: A 54 year-old male with non-Hodgkin's lymphoma underwent allogeneic stem cell transplantation after failing chemotherapy. Immunosuppressive drugs and prophylactic antimicrobials and antivirals, including acyclovir, had been discontinued for two months when he developed flu-like symptoms, loose stools, painful oral apthous ulcers, jaundice, a maculopapular rash on the chest and abdomen, and nontender hepatomegaly. Serum alanine (ALT) and aspartate (AST) aminotransferases were elevated (1108 U/L and 1160 U/L, respectively); total bilirubin was 10.8 mg/dL and alkaline phosphatase was 402 U/L. A liver biopsy showed submassive hepatic necrosis with viral features, but no GVHD. Herpes simplex virus (HSV) and Coxsackie virus hepatitis were suspected based on clinical findings and recent discontinuation of prophylactic antivirals. Acyclovir treatment was restarted. Hepatitis A, B and C serologies and antibody titers were drawn for HSV, human herpesvirus (HHV)-6, HHV-8, adenovirus, Epstein Barr virus, cytomegalovirus, HIV, toxoplasma, and Coxsackie viruses. Weekly measurement of ALT, AST, bilirubin and alkaline phosphatase showed a gradual decline; his apthous ulcers healed. A Coxsackie A9 antibody titer was 1:256, Coxsackie B antibody titer was 1:160, and HHV-6 IgG titer was 1:43. Repeat titers after two weeks of acyclovir treatment showed no change in the Coxsackie B and HHV-6 titers, but the Coxsackie A9 titer declined to 1:64. At this point, the diagnosis of Coxsackie A9 hepatitis was confirmed. Viral suppression treatment with acyclovir was continued. Liver chemistries normalized over 12 weeks. Discussion: Coxsackie virus infections in patients undergoing bone marrow transplantation vary in severity from mild viral enteritis to severe fatal myocarditis. Hepatic involvement with Coxsackie infection has been reported, however, submassive hepatic necrosis has not been documented previously in a stem cell transplant recipient. This case illustrates the importance of considering Coxsackie viruses as etiologic agents when evaluating a patient with hepatitis after a bone marrow transplant. Treatment remains largely supportive but acyclovir can be used to prevent fulminant transformation of the disease.