|
|||||
|
|
||||||
Journal of Clinical Oncology, Vol 24, No 21 (July 20), 2006: pp. 3513-3514 © 2006 American Society of Clinical Oncology. DOI: 10.1200/JCO.2006.06.5912
In ReplyDepartment of Hematology, Necker Hospital, Paris, France
Bicêtre Hospital, Kremlin-Bicêtre, Paris, France
Henri Mondor Hospital, Creteil, France
Bicêtre Hospital, Kremlin-Bicêtre, Paris, France We read with interest the reply of Provencio et al concerning our article on diffuse large B-cell lymphoma (DLBCL) and hepatitis C virus (HCV) infection1, and would like to respond to it. Several explanations may account for the differences observed between our data generated from the Groupe d'Etude des Lymphomes de l'Ádulte population and those reported by Provencio et al. Our population was restricted to patients with DLBCL with HCV infection but without hepatitis (normal value of liver enzymes [WHO grade < 2] and normal hepatic architecture), which may explain the low prevalence (0.5%) of HCV infection in this population of DLBCL. However, in line with other studies from northern Europe2 we have found a prevalence of 2.7% of HCV infection in 219 DLBCL patients who have been treated in the hematology department of Necker Hospital (Paris, France) between 1994 to 1999 (unpublished data). This frequency is not statistically different from the one observed in a population of blood donors in the same geographical area. In contrast, we have found in a subgroup of patients with splenic lymphoma with villous lymphocytes from the same geographical area that the frequency of HCV infection was approximately 15%similar to the rate reported by Provencio et al. Furthermore, we have found that in this population, antiviral therapy induced regression of lymphoma in the majority of cases providing definitive evidences for the role of the virus in lymphomagenesis at least in this histological subtype.3,4 Emphasizing and extending our finding a recent study shows that antiviral therapy may also induce response in patients with other marginal zone lymphoma.5 Interestingly in our study on DLCBL, we have found that 32% of HCV positive patients versus 6% of HCV negative patients exhibited histological features of transformation from a low grade lymphoma more likely of marginal histological subtype. This finding may suggest a role of the virus in lymphomagenesis of large B-cell lymphoma as well. In these cases, however, probably as a result of secondary oncogenic events it is unlikely that antiviral therapy may induce regression of the lymphoma. However, it remains to be determined whether antiviral combination therapy during or after chemotherapy may improve prognosis of this group of patients. Authors' Disclosures of Potential Conflicts of Interest The authors indicated no potential conflicts of interest. REFERENCES
1. Besson C, Canioni D, Lepage E, et al: Characteristicis and outcome of diffuse large B-cell lymphoma in hepatitis C virus-positive patients in LNH 93 and LNH 98 Groupe d'Etude des Lymphomes de l'Ádulte Programs. J Clin Oncol 24:953-960, 2006 2. Gisbert JP, Garcia-Buey L, Pajares JM, et al: Prevalence of hepatitis C virus infection in B-cell non-Hodgkin's lymphoma: Systematic review and meta-analysis. Gastroenterology 125:1723-1732, 2003[CrossRef][Medline] 3. Hermine O, Lefrere F, Bronowicki JP, et al: Regression of splenic lymphoma with villous lymphocytes after treatment of hepatitis C virus infection. N Engl J Med 347:89-94, 2002 4. Saadoun D, Suarez F, Lefrere F, et al: Splenic lymphoma with villous lymphocytes, associated with type II cryoglobulinemia and HCV infection: A new entity? Blood 105:74-76, 2005 5. Vallisa D, Bernuzzi P, Arcaini L, et al: Role of anti-hepatitis C virus (HCV) treatment in HCV-related, low-grade, B-Cell, non-hodgkin's lymphoma: A multicenter Italian experience. J Clin Oncol 22:468-473, 2005
Related Correspondence
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
|||||||||||
|
Copyright © 2006 by the American Society of Clinical Oncology, Online ISSN: 1527-7755. Print ISSN: 0732-183X
|