Arora Kanika, Guleria Sandesh, Jindal Ankur Kumar, Rawat Amit, Singh Surjit
Allergy Immunology Unit, Department of Pediatrics, Advanced Pediatrics Centre, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Genes Dis. 2019 Sep 12;7(1):62-66. doi: 10.1016/j.gendis.2019.09.003. eCollection 2020 Mar.
Kawasaki disease (KD) is a medium vessel vasculitis with predilection to cause coronary artery abnormalities. KD is now the most common cause of acquired heart disease in developed countries. Thrombocytosis is consistently found in patients with KD, usually in 2nd to 3rd week of illness. Thrombocytopenia has occasionally been reported in the acute phase of KD. An increase or decrease in platelet number in patients with KD was initially considered to be a benign phenomenon. However, recent literature on platelet biology in KD has suggested that platelets are not only increasing but are rather activated. This phenomenon has been found to increase the risk of thrombosis in these patients. Similarly a fall in platelet counts during acute stage of KD has also been found to be associated with increased severity of disease. In this review, we update on the current best understanding about pathogenic role of platelets in patients with KD.
川崎病(KD)是一种易导致冠状动脉异常的中血管血管炎。KD目前是发达国家后天性心脏病的最常见病因。血小板增多在KD患者中始终存在,通常在病程的第2至3周。KD急性期偶尔有血小板减少的报道。KD患者血小板数量的增加或减少最初被认为是一种良性现象。然而,最近关于KD血小板生物学的文献表明,血小板不仅数量增加,而且被激活。已发现这种现象会增加这些患者发生血栓形成的风险。同样,KD急性期血小板计数下降也被发现与疾病严重程度增加有关。在本综述中,我们更新了目前对KD患者血小板致病作用的最佳认识。