Mr. Z. is a 24‐year‐old landscaper without significant medical history who presented with easy bruising and bleeding for several days. Three months prior to his presentation, he had complained of nausea, vomiting, and jaundice. His laboratory results from an outpatient clinic showed ALT of 1826, AST of 1530, and total bilirubin of 39.2, with negative hepatitis B and C and HIV serology. His symptoms resolved with supportive care. The patient began to notice swelling and easy bruising of his arms a few days before his admission, which was accompanied by gingival bleeding and hematochezia. He denied fever, chills, weight loss, or exposure to toxins but recalled taking hydroxyzine for pruritus when he had hepatitis. On physical examination, his maximum temperature was 37.8°C. Mucosal hemorrhagic bullae were seen, along with hematomas on both arms, and scattered ecchymoses on the torso and bilateral lower extremities. The significant laboratory results were: white blood cell count 1.1, hemoglobin 12.3, platelets 3, neutrophils 19%, lymphocytes 78%, bands 1%. Liver function tests were normal, as was PT/PTT. Hepatitis A IgM was negative, hepatitis B surface antigen and core antibody were negative, hepatitis C antibody was negative, ANA was negative, and CD55 and CD59 were normal. The peripheral smear showed normocytic and normochromic erythrocytes, leukopenia with predominant lymphocytes and occasional bands, and marked thrombocytopenia. The bone marrow aspiration and biopsy revealed a marrow devoid of almost all cellular elements. Flow cytometry showed a reduced CD4/CD8 T‐cell ratio and a left‐shifted myeloid maturation. Cytogenetic analysis was normal. The diagnosis of aplastic anemia (AA) was therefore made. Patient was transferred immediately to a tertiary‐care medical center for the management of his AA. He is currently receiving immunosuppressive regimens.
AA is characterized by diminished or absent hematopoietic cells in the bone marrow. The most common congenital AA is Fanconi anemia, whereas the majority cases of acquired AA remain idiopathic. Other etiologies of the acquired form include drugs, radiation, toxic chemicals, viral infections, and immune disorders. The incidence of AA is estimated to be 2–4 patients per million population per year. Hepatitis‐associated AA is an uncommon variant that often affects previously healthy adolescent boys and young men several weeks following an acute episode of hepatitis. Interestingly, most patients with hepatitis‐associated AA are serologically negative for hepatitis A, B, and C. The detection of hepatitis G viral RNA has been reported in some cases.
This case highlights the importance of early recognition of this rare condition and immediate referral, given the extremely grave prognosis if left untreated.
V. Zhu ‐ none
To cite this abstract:Zhu V. A 24‐Year‐Old Man with Hepatitis‐Associated Aplastic Anemia. Abstract published at Hospital Medicine 2011, May 10-13, Dallas, Texas. Abstract 1017. Journal of Hospital Medicine. 2011; 6 (suppl 2). https://www.shmabstracts.com/abstract/a-24yearold-man-with-hepatitisassociated-aplastic-anemia/. Accessed January 21, 2020.