Hepatitis C Virus Infection in Patients with B-Cell Non-Hodgkin Lymphoma

doi:10.1059/0003-4819-127-6-199709150-00002

Hepatitis C Virus Infection in Patients with B-Cell Non-Hodgkin Lymphoma

From University of Southern California School of Medicine, Los Angeles, California; Roche Molecular Systems, Somerville, New Jersey; and Nagoya City University Medical School, Nagoya, Japan. Acknowledgment: The authors thank Gus Miranda for technical assistance. Note: Drs. E. Zuckerman and T. Zuckerman contributed equally to this paper. Grant Support: In part by the Lymphoma Research Foundation of America, Inc. Requests for Reprints: Eli Zuckerman, MD, Department of Internal Medicine A, B'nai Zion Medical Center, 47 Golomb Street, Box 4940, Haifa 31048, Israel. Current Author Addresses: Dr. E. Zuckerman: Department of Internal Medicine A, B'nai Zion Medical Center, 47 Golomb Street, Box 4940, Haifa 31048, Israel.

Abstract

Background: Several studies from Europe have reported a high prevalence (9% to 32%) of chronic hepatitis C virus (HCV) infection in patients with B-cell non-Hodgkin lymphoma. It has been suggested that HCV plays a role in the pathogenesis of B-cell non-Hodgkin lymphoma.

Objective: To determine the prevalence of HCV infection in patients with B-cell lymphoma in the United States.

Design: Controlled, cross-sectional analysis.

Setting: University medical center.

Patients: 120 patients with B-cell lymphoma (78% were Hispanic, 9% were black, 7% were Asian, and 6% were white), 154 patients with other malignant hematologic conditions (control group 1), and 114 patients with nonmalignant conditions (control group 2).

Measurements: Samples were tested for antibodies to HCV by enzyme-linked immunosorbent assay. Hepatitis C virus RNA was detected by reverse-transcription polymerase chain reaction. Genotyping for HCV was done with genotype-specific primers from the HCV core region.

Results: Infection with HCV was detected in 26 patients (22% [95% CI, 15% to 30%]) with B-cell lymphoma compared with 7 of 154 patients (4.5%) in control group 1 and 6 of 114 patients (5%) in control group 2 (P < 0.001). Risk factors for HCV infection were present in 15 patients (60%) with B-cell lymphoma and occurred a median of 15 years before diagnosis of lymphoma. Monocytoid B-cell lymphoma was the most common type of lymphoma found in HCV-positive patients (23% compared with 7% in HCV-negative patients) (P = 0.034).

Conclusions: The prevalence of HCV infection was higher in patients with B-cell non-Hodgkin lymphoma than in controls. The possible role of HCV in the pathogenesis of B-cell lymphoma warrants further investigation.