Antiphospholipid syndrome (APS) manifests as systemic thrombotic disorders including recurrent deep vein thrombosis, pulmonary thromboembolism, brain stroke and fetal loss in the presence of antiphospholipid antibodies. The syndrome can be secondary to many causes including systemic lupus erythematosus or pulmonary antiphospholipid syndrome. The many etio pathogenic mechanisms involved generally act together so that it is difficult to say which is the main cause, especially in elderly patients.
Systemic lupus erythematosus (SLE) is an auto immune disease of unknown origin affecting virtually all organ systems. Beyond genetic and environmental factors, cytokine imbalances contribute to immune dysfunction, trigger inflammation, and induce organ damage. Patients with the APS who do not have SLE are considered to have the primary antiphospholipid antibody syndrome; patients with SLE who also have both antiphospholipid antibodies and relevant clinical events are considered to have the secondary antiphospholipid antibody syndrome. The evolution depends mainly on the multi-organ involvement and how early immuno suppressive and/or anticoagulant treatment is started. We present a case with SLE who had soft tissue defect requiring reconstruction in this report.