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.