Vitamin D and Kawasaki disease

Background Vitamin D deficiency has been widely reported worldwide. Vitamin D is essential for mineral homeostasis and skeletal health, and is also associated with numerous extra-skeletal diseases, including cancer, autoimmune diseases, psychosis, allergies and cardiovascular disease. Recent evidence suggests that vitamin D deficiency might be a risk factor for immunoglobulin resistance in Kawasaki disease (KD), and that levels of 25-hydroxyvitamin D 3 (25(OH)D 3 ) could predict the risk of coronary artery disease in KD patients. These findings have sparked growing interest in exploring the mechanistic and clinical links between vitamin D and KD pathogenesis. However, the relationship between vitamin D levels and KD remains incompletely understood, warranting further comprehensive investigation. Mechanisms and evidence reviewed Previous studies found that proinflammatory cytokines, such as tumor necrosis factor (TNF)-α and interleukin (IL)-6, are elevated during the acute phase of KD and are associated with activation of vascular endothelial cells, which can lead to varying degrees of vascular wall inflammation. Vitamin D, a multifunctional prohormone with well-documented anti-inflammatory properties, may exert protective effects in KD by enhancing endothelial function, reducing coronary artery damage risk, and inhibiting platelet activity to alleviate fibrinolysis, thrombosis, and inflammation. Conclusions This study updates the current understanding of the association between serum vitamin D levels and KD, explores potential regulatory mechanisms underlying this relationship, and identifies critical knowledge gaps to guide future cohort studies and clinical trials in KD research. Early clinical data indicate that adjunctive vitamin D may modulate inflammatory responses in acute KD, but whether supplementation reduces intravenous immunoglobulin (IVIG) resistance or prevents coronary artery lesions remains unproven and requires prospective investigation.