Sir, Anti‐phospholipid antibodies (aPLa) are a heterogeneous family of immunoglobulins directed to negatively charged phospholipids binding particular plasma proteins that behave as co‐factors, e.g. β 2 glycoprotein I (β 2‐GPI), prothrombin, protein C, protein S and annexin V. aPLa characterize the anti‐phospholipid syndrome with thrombosis, thrombocytopenia and recurrent spontaneous abortions, but they can also be detected in connective tissue diseases, in particular systemic lupus erythematosus, and, more rarely, in lymphoproliferative disorders and infectious diseases such as syphilis, malaria, hepatitis A and mononucleosis. In infectious diseases, aPLa bind antigens in the absence of β 2‐GPI, which is required as a cofactor in autoimmune diseases [1]. In addition, thrombosis and thrombocytopenia can be associated with antibodies to β 2‐GPI alone. The complete aPLa system has never been investigated in systemic sclerosis (SSc) [2–4]. Anticardiolipin antibodies (aCLa), usually studied in routine tests, have been found not to be associated with more severe ischaemia or other manifestations of the disease.
No takes yet. Share an insight, caveat, or question.
Aurora Parodi (2001) studied this question.
Synapse has enriched 5 related papers. Consider them for comparative context:
More from British journal of rheumatology