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Article
April 15, 1992

Aplastic Anemia and Viral HepatitisNon-A, Non-B, Non-C?

Author Affiliations

From the Clinical Hematology Branch, National Heart, Lung, and Blood Institute, Bethesda, Md (Drs Hibbs, Rosenfeld, and Young); Department of Medicine III, University of Ulm, (Germany) (Dr Frickhofen); Division of Virology, Centers for Biologics Evaluation and Research, US Food and Drug Administration, Kensington, Md (Dr Feinstone); Division of Hematology/Oncology, Children's Medical Center, Japanese Red Cross, Nagoya (Japan) 1st Hospital (Dr Kojima); Bone Marrow Transplant Center, 2nd Hematology Division, San Martino Hospital, Genoa, Italy (Dr Bacigalupo); Division of Pediatric Hematology, Hospital San Gerardo, Milan, Italy (Dr Locasciulli); Department of Surgery, University of Pittsburgh (Pa) School of Medicine (Dr Tzakis); and Department of Transfusion Medicine, National Institutes of Health, Bethesda, Md (Dr Alter).

JAMA. 1992;267(15):2051-2054. doi:10.1001/jama.1992.03480150057037
Abstract

Objective.  —To test the hypothesis that the rare, often fatal, syndrome of hepatitis-associated aplasia is associated with hepatitis C virus infection.

Design.  —Case series.

Setting.  —Tertiary referral centers in the United States, Japan, Italy, and Germany.

Patients.  —Twenty-eight patients with onset of aplastic anemia within 90 days after seeking medical attention for jaundice, or having serum transaminase levels 150% or more of normal (hepatitis-associated aplasia patients) and three patients who developed aplastic anemia following liver transplantation for non-A, non-B hepatitis.

Outcome Measures.  —Presence of hepatitis C in serum, bone marrow, and liver samples, detected by the polymerase chain reaction; antibody testing; and percentage of activated peripheral cytotoxic T lymphocytes determined by immunophenotyping.

Results.  —Hepatitis ribonucleic acid was present in the serum samples of 10 (36%) patients with hepatitis-associated aplasia. However, hepatitis C virus viremia was associated with transfusions received after the onset of aplasia: seven (58%) of 12 patients with hepatitis-associated aplasia who had received 21 or more units of blood products at the time of serum sampling were viremic, compared with only three (19%) of 16 patients with hepatitis-associated aplasia who had received 20 or less units of blood products (P<.05). Hepatitis C virus was not found in blood and bone marrow samples of three National Institutes of Health case patients tested at the time of diagnosis. None of three livers from non-A, non-B hepatitis patients who developed aplastic anemia after liver transplantation contained hepatitis C virus ribonucleic acid. Activated CD8+ T lymphocytes were elevated three- to 20-fold early in the course of hepatitis-associated aplasia.

Conclusions.  —Our results implicate a novel, non-A, non-B, and non-C agent in both hepatitis-associated aplasia and fulminant hepatitis.(JAMA. 1992;267:2051-2054)

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