We read with interest the paper of Martin et al. (1) published in a recent issue of this journal. In this study, 28 patients did not have hepatitis C virus (HCV) antibodies by ELISA (Ortho Diagnostics, Raritan, NJ) before liver transplantation, and none of them developed HCV antibodies or clinically overt hepatitis C afterwards. Certainly, as the authors stated, the development of more sensitive techniques to detect HCV infection in patients with allografts may establish whether anti-HCV seronegative cases of HCV infection occur. However, even if underestimated in the study of Martin et al., the prevalence of hepatitis C appears very low if compared with the high number of blood products received.
We attempted to evaluate the prevalence of HCV infection in patients undergoing allogeneic bone marrow transplantation (BMT), which is, as in liver transplantation, associated with high blood derivative requirements. Forty-eight patients underwent 52 BMTs from May 1984 t o July 1989. Serum samples drawn before and after the BMTs were kept frozen until HCV antibodies were tested with ELISA in 43 of these patients who underwent 46 BMTs for chronic myeloid leukemia (9 patients), acute lymphocytic leukemia (10 patients), acute myeloid leukemia (10 patients), multiple myeloma (5 patients), lymphoma (4 patients) and miscellaneous disorders (5 patients). HCV antibodies were not detected either before or after BMT in the 18 patients who died within 3 mo after BMT. Serum abnormalities of liver function tests were noted in 12 of these patients and were attributed to acute graft vs. host disease (GVHD) or veno-occlusive disease but not to a likely HCV infection. Twenty-eight patients survived more than 3 mo after BMT; none had HCV antibodies before BMT. After BMT, HCV antibodies were detected in 3 of these 28 patients (10.7% prevalence). In these three patients, HCV seropositivity developed 1 mo, 6 mo and 12 mo, respectively, after BMT. A liver biopsy was performed in the second patient and showed lymphocytic inflammatory infiltrate with biliary neocanaliculi and mild steatosis with no clinical signs of GVHD and no biological signs of cytomegalovirus infection. All three patients experienced fluctuating cytolysis during follow-up. High HCV antibody levels were still observed 5 yr, 5 yr and 3 yr, respectively, after BMT, whereas only two of them had elevated transaminases at the end of follow-up. These three patients were positive with second gen-