Antiphospholipid antibodies in Brazilian hepatitis C virus carriers

Abstract

Hepatitis C, a worldwide viral infection, is an important health problem in Brazil. The virus causes chronic infection, provoking B lymphocyte dysfunction, as represented by cryoglobulinemia, non-organ-specific autoantibody production, and non-Hodgkin's lymphoma. The aim of this research was to screen for the presence of antiphospholipid autoantibodies in 109 Brazilian hepatitis C virus carriers without clinical history of antiphospholipid syndrome. Forty healthy individuals were used as the control group. IgA, IgG, and IgM antibodies against cardiolipin and ß2-glycoprotein I were measured with an enzyme-linked immunosorbent assay, using a cut-off point of either 20 UPL or 20 SBU. While 24 (22.0%) hepatitis C carriers had moderate titers of IgM anticardiolipin antibodies (median, 22.5 MPL; 95%CI: 21.5-25.4 MPL), only three carriers (<3%) had IgG anticardiolipin antibodies (median, 23 GPL; 95%CI: 20.5-25.5 GPL). Furthermore, IgA anticardiolipin antibodies were not detected in these individuals. Male gender and IgM anticardiolipin seropositivity were associated in the hepatitis C group (P = 0.0004). IgA anti-ß2-glycoprotein-I antibodies were detected in 29 of 109 (27.0%) hepatitis C carriers (median, 41 SAU; 95%CI: 52.7-103.9 SAU). Twenty patients (18.0%) had IgM anti-ß2-glycoprotein I antibodies (median, 27.6 SMU; 95%CI: 23.3-70.3 SMU), while two patients had IgG antibodies against this protein (titers, 33 and 78 SGU). Antiphospholipid antibodies were detected in only one healthy individual, who was seropositive for IgM anticardiolipin. We concluded that Brazilian individuals chronically infected with hepatitis C virus present a significant production of antiphospholipid antibodies, mainly IgA anti-ß2-glycoprotein I antibodies, which are not associated with clinical manifestations of antiphospholipid syndrome.

Infections and the Antiphospholipid Syndrome

“…Some studies, however, have found an increased incidence of thrombotic disorders in patients with chronic HCV with aPL. Atta et al [35] reported that chronic HCV patients have a significant production of aPL, mainly IgA anti-β2GPI antibodies, which are not associated with clinical manifestations of APS. Other studies have found no relationship between HCV and APS with no clinical manifestation of APS being found in aCL and HCVpositive patients before or during follow-up visits [36][37][38].…”

Viral hepatitis and anti-phospholipid antibodies positivity: A systematic review and meta-analysis

“…Moreover, an association between viral hepatitis and aPL-related thrombotic complications has been also documented [19], suggesting that aPL may not only be an epiphenomenon of the infectious process but they may also play a pathogenic role. However, these data have been challenged in other studies [20,21]. In a previous meta-analysis [22], aCL were found to be significantly more frequent in both HBV-and HCV-infected patients compared to healthy controls (OR 13 and 14, respectively), whereas a trend towards a higher prevalence of anti-␤ 2 GPI -not achieving statistical significance -was found in HCV-infected, but not in HBV-infected subjects.…”

“…Twenty studies (28 data-sets) [15][16][17][18][19][20][21][27][28][29][30][31][32][33][34][35][36][37][38][39], for a total of 2319 cases and 1901 controls, evaluated aCL positivity in hepatitis patients and healthy controls. Hepatitis was found to be significantly associated with aCL positivity as compared to controls (OR: 11.38, 95% CI: 7.92-16.35; P < 0.00001, Fig.…”

“…2), and by the 12 studies [18,20,21,[28][29][30][31][32][33][34]36,37] (1350 patients and 1317 controls) on HCV infection (OR 5.64, 95% CI: 1.69-18.77; P = 0.005, I 2 = 49%; P = 0.05, Fig. 2).…”

“…Eleven studies [16][17][18][19][20][21]27,[32][33][34]36] (13 data-sets) evaluated a total of 257 aCL-positive and 1079 aCL-negative hepatitis patients. The prevalence of thrombotic events resulted significantly higher in aCL-positive than in aCL-negative patients (OR 3.29, 95% CI: 1.79-6.07; P = 0.0001, Fig.…”