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Long‐term mortality and morbidity of transfusion‐associated non‐A, non‐B, and type C hepatitis: A National Heart, Lung, and Blood Institute collaborative study
Author(s) -
Seeff Leonard B.,
Hollinger F. Blaine,
Alter Harvey J.,
Wright Elizabeth C.,
Cain Casey M. B.,
Buskell Zelma J.,
Ishak Kamal G.,
Iber Frank L.,
Toro Doris,
Samanta Arun,
Koretz Ronald L.,
Perrillo Robert P.
Publication year - 2001
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1053/jhep.2001.21905
Subject(s) - medicine , term (time) , intensive care medicine , blood transfusion , hepatitis , lung , hepatitis c , emergency medicine , pediatrics , cardiology , quantum mechanics , physics
Abstract Persons with non‐A, non‐B hepatitis (cases) identified in 5 transfusion studies in the early 1970s have been followed ever since and compared for outcome with matched, transfused, non‐hepatitis controls from the same studies. Previously, we reported no difference in all‐cause mortality but slightly increased liver‐related mortality between these cohorts after 18 years follow‐up. We now present mortality and morbidity data after approximately 25 years of follow‐up, restricted to the 3 studies with archived original sera. All‐cause mortality was 67% among 222 hepatitis C‐related cases and 65% among 377 controls ( P = NS). Liver‐related mortality was 4.1% and 1.3%, respectively ( P = .05). Of 129 living persons with previously diagnosed transfusion‐associated hepatitis (TAH), 90 (70%) had proven TAH‐C, and 39 (30%), non‐A‐G hepatitis. Follow‐up of the 90 TAH‐C cases revealed viremia with chronic hepatitis in 38%, viremia without chronic hepatitis in 39%, anti‐HCV without viremia in 17%, and no residual HCV markers in 7%. Thirty‐five percent of 20 TAH‐C patients biopsied for biochemically defined chronic hepatitis displayed cirrhosis, representing 17% of all those originally HCV‐infected. Clinically evident liver disease was observed in 86% with cirrhosis but in only 23% with chronic hepatitis alone. Thirty percent of non‐A, non‐B hepatitis cases were unrelated to hepatitis viruses A,B,C, and G, suggesting another unidentified agent. In conclusion, all‐cause mortality approximately 25 years after acute TAH‐C is high but is no different between cases and controls. Liver‐related mortality attributable to chronic hepatitis C, though low (<3%), is significantly higher among the cases. Among living patients originally HCV‐infected, 23% have spontaneously lost HCV RNA.