THE CLINICAL AND PATHOLOGICAL COURSE OF HEPATITIS B LIVER DISEASE IN RENAL TRANSPLANT RECIPIENTS
- 1 May 1984
- journal article
- research article
- Published by Wolters Kluwer Health in Transplantation
- Vol. 37 (5) , 461-466
- https://doi.org/10.1097/00007890-198405000-00008
Abstract
A prospective study of the clinical and pathological sequelae of hepatitis B (HB) disease in 22 immunosuppressed renal transplant patients is reported. All patients had allografts that functioned for > 1 yr, and all were hepatitis B surface antigen (HBsAg)-positive following transplantation. None of the 18 patients who had serial HBsAg tests converted to HBsAg negative. Serial liver biopsies were performed in 19 patients and one liver biopsy was available in the remaining three patients. Follow-up ranged from 12 to 93 mo. Seven patients ultimately developed cirrhosis, 6 developed chronic active hepatitis, 5 developed chronic persistent hepatitis, and in 4 the presence of HB virus in hepatocytes was the sole morphologic alteration. The initial liver biopsy was not an accurate predictor of ultimate severity of liver disease because 5 of the 12 patients with virus only or chronic persistent hepatitis subsequently developed chronic active hepatitis or cirrhosis. Clinical liver dysfunction occurred in 8 patients, all of whom had chronic active hepatitis or cirrhosis. Three patients died with hepatic failure and 2 with hepatoma. The risk of death from liver disease in BGsAg-positive renal transplant patients was 5% per patient-year. For comparison, 10 HBsAg-positive patients whose renal failure had been treated by hemodialysis were also studied over a comparable period. Biochemical evidence of persistent liver dysfunction recurred in 1 patient only; 4 patients converted to the HBsAg-negative state; and no patient has died from complications of liver disease. Evidently, in the immunosuppressed renal transplant patient HB infection often results in the development of chronic active hepatitis, leading to cirrhosis and death from hepatoma and hepatic failure.This publication has 12 references indexed in Scilit:
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