History

The antiphospholipid syndrome (APS), first described in 1983 by Dr. Graham Hughes and his team at the Hammersmith Hospital, included recurrent arterial and venous thromboses, fetal losses, and thrombocytopenia in the presence of autoan-tibodies, the so-called antiphospholipid antibodies (aPL). Although a wide variety of clinical manifestations have been added over the last 5 years, these major features have stood the test of time. Many patients with APS have clinical and laboratory features common to other autoimmune diseases, particularly systemic lupus erythematosus (SLE). Such patients are defined as having secondary APS to distinguish them from patients with features of APS alone (primary APS-PAPS). There appears to be very few differences, if any, between the clinical complications associated with the primary and the secondary form of the syndrome, and the rates of arterial or venous thrombosis or fetal loss do not appear to be different. Distinguishing between PAPS and APS due to SLE can sometimes be difficult since many features, such as thrombocytopenia, anemia, renal, and central nervous system involvement, can be seen in both the conditions.

Historical description of aPL is summarized in Table 1.1.

Table 1.1. Historical description of antiphospholipid antibodies (aPL).

1906

Wasserman reaction (reagin)

1941

Reagin binds cardiolipin

1952

False-positive test for syphilis

1952

Lupus anticoagulant (LA)

1960s

LA: association with thrombosis

1970s

LA: association with fetal loss

1983

Anticardiolipin antibody (aCL)

1980s

Detailed description of anti phospholipid syndrome (APS)

1990

Phospholipid binding proteins (P2GPI)

1990s

Animal models for APS

1999

Classification criteria for definite APS

2006

Classification criteria updated

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