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ANTICARDIOLIPIN ANTIBODIES IN HIV INFECTED PATIENTS WITH OR WITHOUT IMMUNE THROMBOCYTOPENIC PURPURA

Recently Canoso et a1 (1987) reported a high incidence of anticardiolipin antibodies (ACA) in HIV infected patients. Moreover a strong correlation between ACA and thrombocytopenia has been established in systemic lupus serythematosus or related immune disorders (Harris et aI, 198%) as well as in immunologic thrombocytopenic purpura (ITP) (Harris et a/. 1985b) which frequently complicates the evolution of HIV carriers (Oksenhendler et al, 1987). These data led us to evaluate a possible correlation between the presence of ACA and ITP in HIV positive patients. We examined retrospectively sera from 38 IHIV positive patients with ITP (group I) and 13 HIV positive patients without ITP (group IIa). Neither AIDS nor ARC was observed in these patients. Control groups consisted of 28 HIV negative patients with ITP, associated (group IIIa, n =: 15) or not (group IIIb, n = 1 3 ) with other autoimmune disorders or malignancies and in 3 5 healthy blood donors (group IV). c tests, activated prothrombin time, antinuclear antibodies and clinical features (i.e. infections, thrombosis, neurologic symptoms) were systematically evaluated in these patients. In addition, another group of 26 HIV positive patients without ITP (group IIb), but not evaluated for the serology of syphilis, was also studied for ACA. ACA were assayed according to the ELISA 1:echnique of Canoso et a1 (1987) except for the use of a polyvalent goat peroxidase anti-human immunoglobulin (Institut Pasteur Production). Determinations were performed in triplicate with a simultaneous serum incubation on uncoated plates as control of the non-specific binding to the plastic (blank value). The results were expressd in OD units:< 1000 after subtraction of the ‘blank value’. Seven patients (six in group I, one in group 111). positive in the fluorescent treponemal antibody absorption test, were excluded from the analysis. Results are shown in Fig 1. The mean f 2 SD normal control value (group IV) was 0471f0.096 OD units. ACA were found in 15/71 HIV positive patients, with the same frequency in group I (22%), group IIa (23%) and group IIb (19%). No difference was observed between the frequency of ACA in ITP patients with (22%) or without (37%) HIV infection (x’= 1.64, P=0.20). No clinical manifestations could be attributed to the presence of ACA in HIV positive patients. However, it should be emphasized that five patients in group I presented false dissociated positive syphilis serology associated in two with the lupus anticoagulant. This study shows that ACA frequency was the same in HIV patients with or without ITP and argues against the involvement of these autoantibodies in the pathogenesis of the thrombocytopenia. Our results differ from those of Canoso et a1 (1987) who demonstrated a greater frequency of ACA in HIV carriers. These discrepancies cannot be attributed to technical problems since the results of our control group were similar to those previously described (Harris et al, 1985b). An explanation could be found in the calculation of the results, since we subtracted systematically the ‘blank value’ to avoid 1200.