T(14;18) is not associated with mixed cryoglobulinemia or with clonal B cell expansion in egyptian patients with hepatitis C virus infection.

BACKGROUND/AIM The mechanisms of B-cell lymphoproliferative disorders in chronic hepatitis C virus (HCV) infection are unclear. An increased prevalence of circulating monoclonal B-cells and t(14;18) has been reported. Geographic heterogeneity of prevalence of t(14;18) has been shown to exist. We investigated the prevalence of t(14;18) and B-cell clonality as possible mechanisms of lymphomagenesis in chronic HCV patients, in whom cryoglobulinemia status was previously detected. METHODS A cohort of 111 patients was studied, including 87 patients with chronic HCV disease (18 cryoglobulinemic and 69 non- cryoglobulinemic); 24 HCV-negative, cryoglobulin negative patients with other nonimmune chronic liver diseases were enrolled as controls. The t(14;18) and IgH rearrangement (as a marker of B-cell clonality) were detected by the polymerase chain reaction. RESULTS t(14;18) was detected in 27.6% of HCV patients and in none of the controls. Detection rates were comparable in both cryoglobulin-positive and negative groups (22.2% and 29% , respectively), p=0.769. IgH rearrangement was detected in 39.1% of HCV patients and in none of the controls. The cryoglobulin-positive group showed significantly higher prevalence of IgH rearrangement compared to the cryoglobulin-negative group (61.1% and 33.3% , respectively), p=0.03, OR=3.13 and 95% CI=1.07-9.17. t(14;18) and monoclonal IgH rearrangement detection rates were not associated with each other, p=0.467. CONCLUSIONS t(14;18) is uncommon in HCV-mixed cryogoblulinemia Egyptian patients; it does not seem to play a role in HCV-associated MC and lymphomagenesis in our geographical area. HCV may play a role in mixed cryogoblulinemia and lymphomagenesis, probably by inducing clonal B-cell expansions.