The antiphospholipid syndrome, first described in 1983,1 is now recognised as an important prothrombotic disorder associated with a specific group of antibodies. Its main clinical feature is thrombosis, both venous and arterial (especially recurrent cerebral ischaemic attacks). Other features include mild thrombocytopenia, chorea, heart valve disease, livedo reticularis, and, most commonly, recurrent pregnancy loss.2 The importance of the syndrome in general medicine, especially in vascular and neurological disease, is now acknowledged. The syndrome has had various names. Hughes originally studied it in patients with systemic lupus erythematosus but recognised that most patients “had atypical lupus, or no lupus at all”–hence the concept of “primary” antiphospholipid syndrome.3 In the early 1990s it was found that a phospholipid binding protein, s2 glycoprotein I, …
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Khamashta et al. (1997) studied this question.
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