Keywords:
Germany
;
human
;
MODEL
;
EXPOSURE
;
HEPATOCELLULAR-CARCINOMA
;
HISTORY
;
RISK
;
RNA
;
INFECTION
;
FAMILY
;
T cell
;
T-CELL
;
ASSOCIATION
;
POLYMORPHISMS
;
virus
;
LYMPHOMA
;
MALIGNANCIES
;
AGE
;
family history
;
etiology
;
COUNTRIES
;
leukemia
;
PATHOGENESIS
;
REPLICATION
;
case-control studies
;
INDIVIDUALS
;
PREVALENCE
;
INTERVIEW
;
MULTICENTER
;
B-CELL LYMPHOMA
;
immunoassay
;
NON-HODGKINS-LYMPHOMA
;
SERUM
;
MALIGNANCY
;
case-control study
;
RE
;
FAMILIES
;
VIRUS-INFECTION
;
LYMPHOPROLIFERATIVE DISORDERS
;
MIXED CRYOGLOBULINEMIA
;
METAANALYSIS
;
case control studies
;
INTERVAL
;
ENZYME
;
SUBTYPES
;
LYMPHOMAS
;
SIZE
;
FAMILY-HISTORY
;
EUROPEAN COUNTRIES
;
odds ratio
;
B-CELL
;
EXPOSURES
;
MULTICENTER CASE-CONTROL
;
RARE
;
SAMPLE-SIZE
;
HCV INFECTION
Abstract:
Background & Aims: Increasing evidence points toward a role of hepatitis C virus (HCV) infection in the etiology of malignant lymphomas. However, previous epidemiologic studies were limited in size to establish an association between HCV infection and specific lymphoma subtypes. We performed a large, multicenter, case-control study to address this question. Methods: The study comprised 5 European countries and included newly diagnosed cases of any lymphoid malignancy recruited between 1998 and 2004. Controls were matched to cases by 5-year age group, sex, and study center. In-person interviews were conducted to collect data on demographic, medical, and family history as well as environmental exposures. Serum samples of 1807 cases and 1788 controls (excluding human immunodeficiency virus-positive and organ-transplantation subjects) were screened for HCV infection using an enzyme immunoassay. Positive as well as randomly selected negative samples were subjected to HCV RNA detection and HCV genotyping. Results: HCV infection was detected in 53 (2.9%) lymphoma cases and in 41 (2.3%) control subjects (odds ratio [OR], 1.42; 95% confidence interval [CI]: 0.93-2.15). Restricted to individuals who tested positive for HCV-RNA (indicating persistent infection and active viral replication), the OR was 1.82 (95% CI: 1.13-2.91). In subtype-specific analyses, HCV prevalence was associated with diffuse large B-cell lymphoma (OR, 2.19; 95% CI: 1.23-3.91) but not with chronic lymphocytic leukemia or follicular, Hodgkin's, or T-cell lymphoma. The sample size was not sufficient to derive any conclusions for rare lymphoma entities such as splenic marginal zone lymphoma. Conclusions: These results support a model that chronic HCV replication contributes to lymphomagenesis and establish a specific role of HCV infection in the pathogenesis of diffuse large B-cell lymphoma
Type of Publication:
Journal article published
Deep Link:
http://www.dkfz.de/cgi-bin/sel?http://www.dkfz.de/PublicationManager/Show/ShowJournal.aspx%3fpublishedId=3591
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