TNF-α is superior to conventional inflammatory mediators in forecasting IVIG nonresponse and coronary arteritis in Chinese children with Kawasaki disease.

BACKGROUND: Tumor necrosis factor (TNF) -α is of inflammatory cytokines produced chiefly by activated monocyte/macrophages, and has been implicated in the pathogenesis of Kawasaki disease (KD). We elucidated the relationship of plasma TNF-α with conventional inflammatory mediators, clinical classification, intravenous immunoglobulin (IVIG) response and coronary arteritis in the course of KD.

METHODS: Seventy Chinese children with KD were enrolled and divided into 6 subgroups, including complete KD, incomplete KD, IVIG-responsive KD, IVIG-nonresponsive KD, coronary artery (CA) -noninvolvement KD and CA-involvement KD. Blood samples were collected from all subjects at 24h pre- and 48h post-IVIG therapy, respectively. TNF-α, white blood cells counts (WBC), absolute neutrophil counts (ANC), C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and procalcitonin (PCT) were detected.

RESULTS: Plasma TNF-α markedly increased in the acute phase of KD and was positively correlated with CRP and PCT, whereas remained high after IVIG therapy. TNF-α as well as conventional inflammatory mediators could not be used to differentiate the clinical classification of KD, but they may prove beneficial to heighten or reduce the suspicion of incomplete KD. Plasma TNF-α was significantly higher in both IVIG-nonresponsive patients and coronary arteritis patients, but no significant differences were observed in all the other inflammatory mediators. Moreover, plasma TNF-α was positively correlated with the internal diameter of CA.

CONCLUSIONS: TNF-α is superior to conventional inflammatory mediators in forecasting IVIG nonresponse and coronary arteritis in Chinese children with KD.