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Prednisolone in HBsAg‐positive chronic active hepatitis: Histologic evaluation in a controlled prospective study

Prednisolone in HBsAg‐positive chronic active hepatitis: Histologic evaluation in a controlled... To study the value of corticosteroids in HBsAg‐positive chronic active hepatitis, 18 pairs of liver histology comprising 36 liver biopsies from a prospective, randomized, controlled trial were evaluated. The median interval between the initial and follow‐up histology was 8 1/2 months in 8 patients given prednisolone and 8 1/4 months in 10 patients given placebo tablets. Following medication, there was significantly greater erosion of the limiting plate in the prenisolone group (p = 0.039) accompanied by a larger quantity of HBsAg (p = 0.045) and HBcAg (p = 0.006) in the liver. We conclude that prednisolone causes immunosuppression permitting enhanced viral multiplication and leads to increased erosion of the limiting plate. Our result also indicates that progression to cirrhosis is unhalted by prednisolone therapy. The histologic findings support clinico‐biochemical conclusion that the use of prednisolone is deleterious to patients with HBsAg‐positive chronic active hepatitis. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Hepatology Wolters Kluwer Health

Prednisolone in HBsAg‐positive chronic active hepatitis: Histologic evaluation in a controlled prospective study

Hepatology , Volume 2 (6) – Nov 1, 1982

Prednisolone in HBsAg‐positive chronic active hepatitis: Histologic evaluation in a controlled prospective study

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References (23)

Publisher
Wolters Kluwer Health
Copyright
Copyright © 1982 American Association for the Study of Liver Diseases
ISSN
0270-9139
eISSN
1527-3350
DOI
10.1002/hep.1840020605
Publisher site
See Article on Publisher Site

Abstract

To study the value of corticosteroids in HBsAg‐positive chronic active hepatitis, 18 pairs of liver histology comprising 36 liver biopsies from a prospective, randomized, controlled trial were evaluated. The median interval between the initial and follow‐up histology was 8 1/2 months in 8 patients given prednisolone and 8 1/4 months in 10 patients given placebo tablets. Following medication, there was significantly greater erosion of the limiting plate in the prenisolone group (p = 0.039) accompanied by a larger quantity of HBsAg (p = 0.045) and HBcAg (p = 0.006) in the liver. We conclude that prednisolone causes immunosuppression permitting enhanced viral multiplication and leads to increased erosion of the limiting plate. Our result also indicates that progression to cirrhosis is unhalted by prednisolone therapy. The histologic findings support clinico‐biochemical conclusion that the use of prednisolone is deleterious to patients with HBsAg‐positive chronic active hepatitis.

Journal

HepatologyWolters Kluwer Health

Published: Nov 1, 1982

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