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It has been reported that the level of anticardiolipin antibodies (aCL) is probably genetically determined, as HLA-DR7 (or HLA-DR4) has been shown to be associated with persistently high levels of aCL.1 No reported data are available about genetic factors implicated in ischaemic or thrombotic events in patients with systemic lupus erythematosus (SLE) without antiphospholipid antibodies (aPL).
In this study we examined the frequency of the platelet GPIIb/IIIa-P1A2 polymorphism in a series of patients with SLE. We assessed the relationship between the A2 allele prevalence2 and the clinical and immunological manifestations, as possible predisposing biological factors to major ischaemic manifestations such as central nervous system (CNS) lupus or Raynaud’s phenomenon as defined according to the American College of Rheumatology (ACR) Committee.3
We studied a cohort of 109 patients with SLE attending the rheumatology referral centres of the universities of Udine, Pisa, and Milan, classified according to the ACR criteria. For comparison, 161 patients with rheumatoid arthritis (systemic inflammatory disease), 54 with systemic sclerosis (chronic ischaemic-thrombotic vasculopathy), and 128 healthy blood donors (HBD) recruited from the blood transfusion service were studied. The clinical and laboratory manifestations were carefully examined to detect a possible association between genotypes and symptoms, signs, and immunological characteristics. In particular, we focused on nephritis, vasculitis, …