Abstract
In a retrospective long-term follow-up study the clinical course of liver disease was examined in renal allograft recipients with hepatitis C virus (HCV) infection and negative hepatitis B surface antigen under immunosuppressive therapy. We compared 42 anti-HCV antibody (anti-HCV) positive patients (study group) to 213 anti-HCV negative patients (control group). All patients received immunosuppressive therapy. Measurements were made of the following: aminotransferases, bilirubin, albumin, gammaglobulins, ascites, spleen diameter, HCV RNA, and anti-HCV antibody. We found all but four anti-HCV positive patients to be HCV RNA positive prior to transplantation. There were no differences in overall mortality or mortality secondary to liver disease or sepsis. Normal liver enzymes were found in 13 (31%) anti-HCV positive and in 137 (64%) anti-HCV negative patients during the whole mean observation period of 65 months (range 10–215). Aminotransferase activity decreased in anti-HCV positive and negative patients during the observation period. Liver function with regard to synthesis and excretion was normal in anti-HCV negative and anti-HCV positive patients. No signs of portal hypertension were observed in the anti-HCV positive group. Neither the different immunosuppressive regimens nor the antirejection therapy led to differences between anti-HCV positive and negative groups with respect to liver function and did not alter the clinical course. We conclude that HCV infection in patients under immunosuppressive therapy causes only a mild liver disease, as determined by clinicochemical and clinical parameters, and that mortality rate is not increased.
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Abbreviations
- ALT :
-
Alanine aminotransferase
- AST :
-
Aspartate aminotransferase
- CMV :
-
Cytomegalovirus
- EBV :
-
Epstein-Barr virus
- ELISA :
-
Enzyme-linked immunosorbent assay
- HBsAg :
-
Hepatitis B surface antigen
- HCV :
-
Hepatitis C virus
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Grotz, W.H., Peters, T.H., Schlayer, H.J. et al. Immunosuppressive therapy and hepatitis C virus infection: the clinical course of liver disease. J Mol Med 74, 407–412 (1996). https://doi.org/10.1007/BF00210635
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DOI: https://doi.org/10.1007/BF00210635