Increased incidence of anti-cardiolipin antibodies in patients with hepatitis C is not associated with aetiopathogenetic link to anti-phospholipid syndrome

Objective Chronic infection with hepatitis C virus (HCV) has been found to be associated with various diseases known as extra-hepatic manifestations o f HCV. Recently, HCV has been implicated as a cause of the antiphospholipid syndrome (APLS). We conducted a study in a well-characterized area for epi demiological and prospective studies in the north-western part of Greece in order to address whether an aetiopathogenesis exists between HCV and APLS. Design Seventy-five patients with chronic hepatitis C were investigated for the presence of anti-cardiolipin antibodies (anti-CL) and for a past medic al history supportive to the diagnosis of APLS. In addition, 24 patients wi th well-defined APLS (primary or secondary) and 12 patients with systemic l upus erythematosus (SLE) were tested for the presence of markers of HCV inf ection (anti-HCV and HCV RNA). The SLE patients were anti-Cl-positive but n one of them had developed any of the known clinical features of APLS. In ad dition, 267 healthy subjects were investigated for the presence of anti-CL. Methods IgG and IgM anti-CL were determined by a quantitative isotype-speci fic solid phase enzyme-linked immunosorbent assay set up in our laboratory. Anti-HCV was determined using a third-generation enzyme immunoassay and a confirmatory third-generation recombinant immunoblot assay. Active virus re plication was defined by the detection of HCV RNA using a combination assay based on a reverse transcriptase polymerase chain reaction and a DNA enzym e immunoassay. Results Of the HCV patients, 37.3% had IgG and/or IgM anti-CL (P < 0.00005 compared to healthy controls (2.25%)). However, the mean titres of each spe cific isotype were significantly lower in HCV patients compared with those found in the APLS patients (P < 0.05 for IgM and P < 0.001 for IgG isotypes ). The mean titres of IgG anti-Ct. were also significantly lower in HCV pat ients compared with those found in the SLE patients (P < 0.01). All patient s with APLS or SLE (n = 36) tested negative for HCV infection markers. In a ddition, neither thrombotic events nor thrombocytopenia were associated wit h a positive anti-CL test in HCV patients. Conclusions A significant proportion of HCV patients (37.3%) had detectable anti-CL of low titre. However, this finding was not associated with the de velopment of APLS. On the other hand, none of the APLS patients was positiv e for HCV. Taken together, our data rather failed to reveal an aetiopathoge netic link between HCV and APLS. For this reason, testing for HCV in patien ts with APLS or follow-up for the possibility of the development of APLS in HCV patients cannot be suggested, at least in Greek patients. More prospec tive studies of longer duration are required in order to address whether HC V is involved or not in the aetiopathogenesis of APLS. (C) 2000 Lippincott Williams & Wilkins.