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Prepublished online as a Blood First Edition Paper on April 17, 2002; DOI 10.1182/blood-2002-01-0226.
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Blood, 1 June 2002, Vol. 99, No. 11, pp. 4240-4242
BRIEF REPORT
Prospective study of hepatitis C viral infection as a risk
factor for subsequent B-cell neoplasia
Charles S. Rabkin,
Beatriz
H. Tess,
Roberta E. Christianson,
William E. Wright,
David J. Waters,
Harvey J. Alter, and
Bea J. van den Berg
From the Division of Cancer Epidemiology and Genetics,
National Cancer Institute, Bethesda, MD; Child Health and Development
Studies, Berkeley, CA; Cancer Surveillance Section, California
Department of Health Services, Sacramento; Science Applications
International Corporation, Frederick, MD; Department of Transfusion
Medicine, National Institutes of Health Clinical Center, Bethesda, MD.
Several case-control studies have found increased prevalence of
hepatitis C virus (HCV) in patients with non-Hodgkin lymphoma (NHL) and
other B-cell lymphoproliferative disorders. We examined whether HCV
infection preceded the development of these neoplasms in a prospective
cohort study of 48 420 individuals in northern California. Stored sera
from 95 subjects with NHL (n = 57), multiple myeloma (n = 24), or
Hodgkin disease (n = 14) diagnosed a mean of 21 years after
phlebotomy were screened for antibodies to HCV as well as viral RNA,
based on previous reports of antibody-negative viremia. Sera from 4 cases and one of 95 age-, sex-, and race-matched controls were
repeatedly reactive by enzyme immunoassay, but none were confirmed by
recombinant immunoblot assay; none of the case sera had HCV RNA
by reverse transcription- polymerase chain reaction. Although
acquisition in later life cannot be ruled out, these prospective data
do not support a substantial role of chronic HCV infection in the
etiology of B-cell neoplasia.
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