[Platelets, from laboratory parameter to key player in Kawasaki disease: a scoping review]

Kawasaki disease (KD) is an acute systemic vasculitis of unknown etiology that primarily affects children under 5 years of age. Despite the availability of established diagnostic criteria, diagnosis remains challenging due to the lack of specific biomarkers. Platelets may serve as biomarkers due to their role in vascular inflammation and immune activation. This review aims to compile evidence on platelet activation in KD. The PRISMA-ScR statement was followed. A literature search was conducted across five databases. Original studies on KD were included, without language or publication date restrictions. Reviews, case reports, animal studies, and duplicates were excluded. Of 936 records, 27 studies were included for full-text analysis. Ten studies involving 24,373 patients provided evidence of platelet hyperreactivity during the acute phase. Platelet count showed a sensitivity of 60% and a specificity of 77.6% for differentiating KD from other febrile illnesses. Elevated platelet levels were associated with a higher risk of coronary complications, including dilation and aneurysms. Biomarkers such as CD40L and microRNAs (miR-223, miR-15a-5p, miR-27a-3p) were associated with vascular lesions. A low platelet count correlated with increased resistance to intravenous immunoglobulin (IVIG). In KD, platelets exhibit baseline hyperreactivity and promote thrombosis and leukocyte recruitment, with sustained platelet activation favoring aneurysm formation. Antiplatelet therapy improves platelet function and reduces thromboxane B2; its efficacy depends on immature platelets and platelet heterogeneity. The V279F polymorphism in PAF-AH was associated with lower enzymatic activity and resistance to IVIG.