**1. Introduction**

Kawasaki disease (KD) is an inflammatory acute febrile vasculitis that can also lead to coronary artery weakening, aneurysm formation, and myocardial infarction. The incidence of this disease varies considerably between ethnic groups: in Asians are up to 20 times higher than Caucasians. KD is most prominently recognized in Japan, Korea, and Taiwan, reflecting increased genetic susceptibility among Asian populations. The highest incidence is reported in Japan: about 90 per 100,000 [1, 2]. Although nearly 50 years have passed from the first description, the etiology of KD remains a mystery. Since the incidence of the disease is high among Japanese people, it can be speculated that this people may have some sort of genetic characteristic that leaves them susceptible to KD. In addition, both clinical and epidemiological findings strongly suggest that some infectious agent or bacterial super-antigenic toxin can play a pathogenetic role in genetically susceptible individuals [3]. Despite KD patients in the acute phase receive high-dose intravenous

immunoglobulin (IVIG) and aspirin therapy, up to 5% of those affected will develop coronary aneurysms, predisposing them to thrombotic complications that could result in atherosclerosis, myocardial infarction, and/or death [4]. In fact, risk factors for the development of atherosclerosis such as C-reactive protein (CRP), oxidative stress (OS), and inflammatory cytokines, are increased in the acute phase of KD [5]. Moreover, in the acute phase of the disease, often patients undergo thrombocytosis that can exert a pathogenic role in the cardiovascular complications that characterize KD. However, in KD progression, the major risk is endothelial injury and coronary artery weakening, favoring the formation of aneurysms in 1:5 untreated children with KD as well as myocardial infarction, ischemic heart, and sudden death [6]. OS linked to inflammation that characterizes KD disease, has recently been included among the potentially useful diagnostic biomarkers in the vasculature of KD [7]. Several lines of evidence suggest that in KD patients, systemic OS may promote: (i) endothelial dysfunction through increased production of oxygen- and nitrogen-derived species (ROS/RNS); (ii) alter red blood cell (RBC) homeostasis, resulting in a sort of premature aging in these circulating cells that could lead to anemia and formation of blood clots; and (iii) stimulate platelet functions and defective platelet apoptosis program, resulting in thrombocytosis that can exert a pathogenetic role in the cardiovascular complications occurring in KD [8].
