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AB0184 Thrombospondin 1, an Antiangiogenic and Proapoptotic Factor, is Elevated in the Plasma of Patients with Antiphospholipid Syndrome
  1. M.D. Patsouras
  2. on behalf of MP Sikara, AG Tzioufas and PG Vlachoyiannopoulos
  1. Pathophysiology, Medical School University of Athens, Athens, Greece


Background Antiphospholipid syndrome (APS) is an acquired thombophillia characterized by recurrent thromboembolism and pregnancy morbidity. Thrombospondin (TSP-1) is a matricellular glycoprotein secreted by platelets upon activation with antiangiogenic and proapoptotic properties. Thrombospondin exerts its actions on endothelian cells through its receptors CD47 and CD36. The latter has already been shown to be involved in the activation of monocytes by antiphospholipid antibodies

Objectives To investigate the involvement of thrombospondin 1 in the Antiphospholipid syndrome

Methods The study involved patients fulfilling the diagnostic criteria of APS, a healthy control (n=46) and a disease control goup (SLE n=26). Plasma, serum and platelets were isolated from the above groups.

Plasma and platelet intracellular TSP-1 levels were determined using an ELISA.

Results APS patients had higher plasma levels of TSP-1 than the healthy control group and the SLE patients (APS: mean 390.0 ng/ml intarquartile range 95.90-437.7 ng/ml versus HC: 185.3 [46.3-236.6 ng/ml], p<0.0001 and versus SLE: 153.0 [8.2-267.2 ng/ml], p=0.029). Moreover the plasma to intacellular levels ratio between APS and HC is not different suggesting not only platelet degranulation but overexpression as well.

Regarding the clinical aspects of APS there was no statistically significant difference between patients with thromboembosism and pregnancy morbidity or between venous and arterial events. However, there was significant difference between the patients who had experienced miscarriages only (403.2 ng/ml) and those had both misacarriages and thrombosis (130.1 ng/ml).

Conclusions Preliminary results suggest that APS patients have higher levels of TSP-1 in plasma and platelets overexpress TSP-1 suggesting a possible involment in thrombus formation and inhibition of angiogenesis that needs to be clarified.

Disclosure of Interest None declared

DOI 10.1136/annrheumdis-2014-eular.5473

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