The putative role of hepatitis C virus (HCV) infection in the pathophysiolo
gy of lymphoproliferative diseases (LPD) is supported by North American and
southern European studies reporting high HCV seroprevalence in patients wi
th B-cell-non-Hodgkin lymphoma (NHL). In order to evaluate the situation in
France, we conducted a retrospective national study about the association
of chronic HCV infection and LPD. 72 Internal Medicine and Infectious Disea
ses departments were contacted. Response rate was 51.4%. We recorded 43 LPD
(19 males, 24 females): 31 B-cell-NHL, 4 Waldenstrom's macroglobulinemia,
3 chronic lymphocytic leukemia, 2 multiple myeloma, 2 lymphomas of the muco
sa-associated lymphoid tissue, and 1 Hodgkin's disease. Mean age at HCV dia
gnosis was 62 years (range 33-84). In 16 cases, LPD occurred in patients kn
own to be HCV-infected. For 11 patients, LPD diagnosis preceded the diagnos
is of HCV infection, whereas diagnosis was done simultaneously in 11 patien
ts. For those with accurate infection date, mean interval between both even
ts was 15.2 years. Fourteen patients had HCV extrahepatic manifestations: 9
mixed cryoglobulinemia, including 7 with NHL, 5 sicca syndrome (5 NHL), an
d both in one patient. Cohort of HCV-infected patients could be accurately
determined for 16 departments, totaling 1,485 patients and 37 cases. Thus,
from our data the frequency of LPD among HCV-infected patients approximates
2.49%. Despite possible bias inherent to this retrospective study, our dat
a support the hypothesis of HCV-associated LPD and particularly B-cell-NHL.
In France, this association is much lower than in Italy. Further studies a
re needed to assess the precise role of HCV in the multistep process leadin
g to monoclonal proliferation. Am. J. Hematol. 64:107-111, 2000. (C) 2000 W
iley-Liss, Inc.