Blood, Vol. 90 No. 5 (September 1), 1997:
pp. 2116-2117
CORRESPONDENCE
Hepatitis C Virus Infection and Gastric Lymphoproliferation in Patients With Sjögren's Syndrome
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LETTER |
To the Editor:
Current views on B-cell lymphomagenesis suggest that several exogenous factors, acting in a multi-step fashion upon a predisposing condition, may be involved in B-cell clonal expansion, a potentially prelymphomatous stage.1-3 By contrast, clinical/epidemiological and preliminary experimental studies have apparently shown that only H pylori infection is specifically involved in the pathogenesis of gastric B-cell clonality and MALT lymphoma.4 However, our previous data obtained in dyspeptics and patients with Sjögren's syndrome show that in a relevant proportion of cases B-cell clonality is not associated with H pylori infection.5,6 We have proposed that in Sjögren's syndrome H pylori in the stomach could merely act as one of several local triggers of lymphoproliferation.5,6
In this study we tested whether hepatitis C virus (HCV) infection may be involved in the pathogenesis of gastric lymphoproliferation in Sjögren's syndrome. Sjögren's syndrome is a well-known example (such as AIDS) of predisposition to develop B-cell clonal expansion and lymphomas.7 On the other hand, HCV has been implicated in the genesis of non-Hodgkin's lymphoma8,9 and is often present in patients with Sjögren's syndrome and may actually be involved in its pathogenesis.10
We determined B-cell clonality by VDJ-PCR in 27 patients with this disease previously screened for HCV (8 positive, by both anti-HCV and HCV-RNA, and 19 negative). All HCV-positive patients had normal hepatic function. We also studied H pylori infection in gastric biopsy specimens. Of all patients, 15 of 27 (56%) had gastric VDJ clonality. Of all VDJ-positive patients, 7 of 15 (47%) were also HCV-positive as opposed to 1 of 12 (8%) of VDJ-negative patients (Fisher's exact test: P < .05). Of all the HCV-positive patients 7 of 8 (87.5%) were also VDJ-positive. By contrast, H pylori infection was equally distributed among VDJ-positive and VDJ-negative patients (9 of 15 or 60% v 8 of 12 or 67%, respectively, not significant). HCV infection was associated with H pylori in 6 of 8 cases. Cryoglobulinemia was present in one patient per group.
These data show that HCV infection in patients with Sjögren's syndrome is strongly associated with gastric B-cell clonal expansion. In line with the reported possible involvement of HCV in the genesis of gastric11 and other B-cell lymphomas8 our findings indicate that this virus may represent an important (co)factor in early stages of gastric lymphoproliferation in Sjögren's syndrome.
D. Sorrentino
G.F. Ferraccioli
S. DeVita
A. Labombarda
M. Boiocchi
E. Bartoli
Gastrointestinal and Rheumatic Disease Units
Internal Medicine of the Department of Clinical and Experimental Pathology
School of Medicine
University of Udine
First Division of Experimental Oncology
Centro di Riferimento Oncologico-IRCSS
Aviano, Italy
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