Abstract
This chapter focuses on the various osteoarticular manifestations in the antiphospholipid syndrome (APS). It has recently been reported that patients with APS or isolated anticardiolipin antibodies (aCL) might have an increased risk of developing avascular necrosis (AVN) of bone, independently of steroid therapy, suggesting that a relationship might exist between AVN and aCL. Several reports of AVN occurring in patients with systemic lupus erythematosus (SLE), primary APS, or aCL, in the absence of previous steroid administration, directly suggest that such an association might exist. Isolated aCL have been found in sera of some patients presenting with apparently idiopathic AVN which could be due to a fortuitous association, or a possible presentation of primary APS with a definite arteriopathy and/or local thrombotic disease, or the development of aPL as a consequence of capillary lesions following microfractures in epiphyseal bones, and/or local intravascular coagulation. Femoral heads are the most common site involved by SLE-related or corticosteroid-induced AVN, often bilaterally and other sites include femoral condyles, tibial plateaus, humeral heads, carpal bone, distal tibial bone, and talus. Multiple AVN are commonly found in SLE associated with APS but appear to be less common in primary APS. Although it remains to be proved that AVN represents a definite complication of aPL, there is enough clinical background to support this hypothesis. Thus, aPL should be measured in the patients developing AVN, without past history of steroid therapy or other evidence of usual risk factors, and in SLE patients with or without APS, aPL can be an additional risk factor on the top of steroids for the occurrence of AVN.
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