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Nahid A. Qushmaq 1 and Samar A. Al-Emadi 2
Academic Editor:E. F. Borba and Academic Editor:P. A. Gatenby and Academic Editor:T. Kawakami
1, King Abdullah Medical Complex-Jeddah (KAMCJ), Al-Ameer Nayef Street, North Obhur, P.O. Box 55659, Jeddah 21544, Saudi Arabia
2, Department of Medicine, Rheumatology Section, Hamad Medical Corporation, P.O. Box 3050, Off Al Rayyan Road, Opposite Lulu Center, Doha, Qatar
Received 9 January 2014; Accepted 10 February 2014; 17 April 2014
This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
1. Introduction
A commonly occurring systemic autoimmune disorder, antiphospholipid syndrome (APS or Hughes syndrome), is characterized by arterial and/or venous thrombosis, pregnancy morbidity, or recurrent miscarriage. It is also characterized by thrombocytopenia, increased levels of antiphospholipid antibodies (aPL), such as positive lupus anticoagulant (LAC), which is the most common, and/or anticardiolipin antibodies (aCL) [1] and β 2 -glycoprotein I antibodies [2]. The mechanism of actions proposed for thrombosis includes endothelial injury mediated by free radicals, coagulation malfunction, and compliment activation [3, 4]. Two hit hypotheses have also been proposed for the occurrence of thrombosis. For the first hit, a prothrombotic state is created by the presence of antiphospholipid antibodies. The second hit happens after a prolonged sustenance of antiphospholipid antibodies, following which the thrombosis condition becomes evident [5, 6]. However, not all individuals with high levels of aPL develop thrombosis [3], and hence it cannot be assumed that all antiphospholipid antibodies are thrombogenic [7, 8]. Various clinical studies have shown that aPL-related thrombosis is accompanied by irreversible functional loss of organs and lethality in systemic lupus erythematosus (SLE) [9].
APS was first detected in individuals suffering from SLE and was later recognized in patients with other autoimmune diseases, although at a lower frequency compared to SLE patients. Most of the case studies have shown that patients who have elevated levels of antiphospholipids and were affected by thrombosis also had other common habitual risk factors, such as smoking and a high BMI; allied risk factors included hyperlipidaemia, hypertension, high triglycerides, and type II diabetes [10-13]. While it is still unclear if the presence of antiphospholipid antibodies is...