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Blood, Vol. 94 No. 4 (August 15), 1999:
pp. 1460-1464
From the Center for Liver Diseases, Albert Einstein Medical Center,
Philadelphia, PA; the Department of Transfusion Medicine and Clinical
Center, Liver Diseases Section, NIDDK, National Institutes of Health,
Bethesda, MD; the Gastrointestinal Unit, Massachusetts General
Hospital, Boston, MA; and the Center for Liver Diseases, University of
Miami, Miami, FL.
Excluding acute hepatic failure caused by drugs, the etiology of
fulminant hepatitis (FH) remains unknown in many patients. There are
conflicting data about a possible pathogenic role for the hepatitis G
virus (HGV) in patients with cryptogenic fulminant hepatitis (non-A-E
FH). We investigated the presence of circulating HGV in 36 patients
with well-documented non-A-E fulminant and 5 patients with
subfulminant hepatitis from 3 geographic locations in the United
States. Serum HGV RNA was determined by reverse transcriptase-polymerase chain reaction using primers from
the NS5 region of the HGV genome. HGV RNA was also measured before and
after liver transplantation in 5 patients and at different time points
in 7 patients. Serum samples were recoded and reanalyzed for HGV RNA
using different primer sets to assess the validity of the HGV RNA
assay. HGV was present in serum of 14 of the 36 patients (38.8%) with
non-A-E fulminant hepatitis. Twenty percent of patients from the
Northeast, 11% of the patients from the Southeast, and 50% from the
Mid-Atlantic regions of the United States had circulating HGV RNA. The
use of therapeutic blood products was significantly associated with the
presence of serum HGV RNA (P < .02). Retesting for HGV RNA
with different primers was positive in all but 1 case. HGV RNA is not
causally related to non-A-E fulminant hepatitis. The finding of HGV
RNA in serum from these patients is likely related to the
administration of blood product transfusion after the onset of
fulminant hepatitis.
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