We recently observed that more than one third of pediatric patients who presented with non‐A, non‐B fulminant liver failure (FLF) also developed aplastic anemia (AA) either before or shortly after liver transplantation. Factors involved in the suppression of bone marrow could be the same as those causing hepatic failure. We considered parvovirus B19 a candidate etiologic agent because of the known tropism of B19 for erythroid precursors. Archived liver and serum from six patients undergoing liver transplantation for non‐A, non‐B, non‐C FLF with associated AA were analyzed for the presence of B19 DNA and anti‐B19 serology. An age‐ and gendermatched control group (N = 44) was analyzed in parallel. B19 DNA studies and anti‐B19 serology were performed in a blinded fashion. B19 serologies were performed by antibody capture enzyme‐linked immunosorbent assay (ELISA). B19 DNA was detected after polymerase chain reaction (PCR) amplification of target B19 DNA sequences in liver and serum. Liver tissue showed evidence of B19 DNA in four of six (66%) patients with FLF and associated AA. Two of 4 patients with cryptogenic FLF but without AA had B19 DNA detected in the liver tissue. Of the 34 remaining controls, only 5 (15%) showed evidence of B19 DNA in liver tissue (66% vs. 15%, P = .016). B19 DNA was not detected in any of the test or control sera. This study provides evidence to support the role of parvovirus B19 in the development of FLF and associated AA. (Hepatology 1995; 22:1661‐1665).
Hepatology – Wiley
Published: Dec 1, 1995
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