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Research Article Free access | 10.1172/JCI114268

Biochemical and clinical response of fulminant viral hepatitis to administration of prostaglandin E. A preliminary report.

S B Sinclair, P D Greig, L M Blendis, M Abecassis, E A Roberts, M J Phillips, R Cameron, and G A Levy

Liver Disease Program, University of Toronto, Ontario, Canada.

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Liver Disease Program, University of Toronto, Ontario, Canada.

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Liver Disease Program, University of Toronto, Ontario, Canada.

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Liver Disease Program, University of Toronto, Ontario, Canada.

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Liver Disease Program, University of Toronto, Ontario, Canada.

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Liver Disease Program, University of Toronto, Ontario, Canada.

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Liver Disease Program, University of Toronto, Ontario, Canada.

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Liver Disease Program, University of Toronto, Ontario, Canada.

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First published October 1, 1989 - More info

Published in Volume 84, Issue 4 (October 1, 1989)
J Clin Invest. 1989;84(4):1063–1069. doi:10.1172/JCI114268.
Copyright © 1989, The American Society for Clinical Investigation.

Published October 1, 1989
Abstract

The effect of PG on patients with fulminant and subfulminant viral hepatitis (FHF) was studied. 17 patients presented with FHF secondary to hepatitis A (n = 3), hepatitis B (n = 6), and non-A, non-B (NANB) hepatitis (n = 8). 14 of the 17 patients had stage III or IV hepatic encephalopathy (HE). At presentation the mean aspartate transaminase (AST) was 1,844 +/- 1,246 U/liter, bilirubin 232 +/- 135 mumol/liter, prothrombin time (PT) 34 +/- 18, partial thromboplastin time (PTT) 73 +/- 26 s, and coagulation Factors V and VII 8 +/- 4 and 9 +/- 5%, respectively. Intravenous PGE1 was initiated 24-48 h later after a rise in AST (2,195 +/- 1,810), bilirubin (341 +/- 148), PT (36 +/- 15), and PTT (75 +/- 18). 12 of 17 responded rapidly with a decrease in AST from 1,540 +/- 833 to 188 +/- 324 U/liter. Improvement in hepatic synthetic function was indicated by a decrease in PT from 27 +/- 7 to 12 +/- 1 s and PTT from 61 +/- 10 to 31 +/- 2 s, and an increase in Factor V from 9 +/- 4 to 69 +/- 18% and Factor VII from 11 +/- 5 to 71 +/- 20%. Five responders with NANB hepatitis relapsed upon discontinuation of therapy, with recurrence of HE and increases in AST and PT, and improvement was observed upon retreatment. After 4 wk of intravenous therapy oral PGE2 was substituted. Two patients with NANB hepatitis recovered completely and remained in remission 6 and 12 mo after cessation of therapy. Two additional patients continued in remission after 2 and 6 mo of PGE2. No relapses were seen in the patients with hepatitis A virus and hepatitis B virus infection. Liver biopsies in all 12 surviving patients returned to normal. In the five nonresponders an improvement in hepatic function was indicated by a fall in AST (3,767 +/- 2,611 to 2,142 +/- 2,040 U/liter), PT (52 +/- 25 to 33 +/- 18 s), and PTT (103 +/- 29 to 77 +/- 44 s), but all deteriorated and died of cerebral edema (n = 3) or underwent liver transplantation (n = 2). These results suggest efficacy of PGE for FHF, and further investigation is warranted.

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