Infliximab reduces the cytokine-mediated inflammation but does not suppress cellular infiltration of the vessel wall in refractory Kawasaki disease.

The aim of our study was to evaluate the efficacy of infliximab for the treatment of patients with refractory Kawasaki disease (KD) and investigate the dynamic changes of cytokines during infliximab treatment. We have performed a study of cytokine and proinflammatory molecule levels in 43 KD patients including 18 responders to IVIG, 14 nonresponders, and 11 patients treated with infliximab. We determined serum levels of soluble TNF receptor I (sTNFR I) and IL-6, as well as VEGF, damage associated molecular pattern (DAMP) molecules; myeloid-related protein (MRP)8/MRP14 and S100A12 sequentially.

Three-dimensional computed tomographic findings of bilateral tracheal bronchus.

A newborn male was admitted with cyanosis and respiratory distress. Echocardiography showed a right heart isomerism associated with a single right ventricle, a double-outlet right ventricle, and pulmonary atresia. Chest X-ray demonstrated severe left upper lobe emphysema and a shift of the mediastinal structures to the right.