Introduction
Henoch-schöenlein Purpura (HSP), recently more commonly referred to as Ig A vasculitis, is the most common leukocytoclastic vasculitis of small vessels in childhood ([1]. It affects the especially skin and gastrointestinal system, joints, kidneys, rarely other organs. Nonthrombocytopenic purpura, gastrointestinal system bleeding, abdominal pain, arthritis, nephritis, and testicular involvement may occur during the disease [2]. Most cases occur after upper respiratory tract infection. Drugs and vaccines also have been reported to be triggered [3-5].
Although Ig A accumulation has been demonstrated in the affected organs’ small vessels, the etiopathogenesis is still elucidated [6, 7]. It is thought that triggering factors cause endothelial dysfunction by stimulating the vascular endothelium. This situation plays an important role in pathogenesis [8, 9]. Platelets have multiple functions, including hemostasis, inflammation, host defenses, vascular tone. The endothelium has an important role in the regulation of hemostasis. When vascular endothelium is damaged, vasocontraction occurs in vascular smooth muscle, and platelets come together to form the platelets plug [10]. Purpuric rashes, hematuria, hematemesis, and melena in patients with HSP suggest that coagulation disorders may occur [11]. The fact that platelet count, bleeding time, clotting time, prothrombin time, and activated partial thromboplastin time were normal in patients suggest that it is due to vascular cause rather than coagulation disorders [12]. However, in some studies, it has been reported that platelet functions are impaired in patients with HSP [13, 14]. This study aimed to evaluate in vitro platelet aggregation and secretion tests in patients with HSP, an essential vasculitis of childhood.