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Objective: To evaluate the use of tumor necrosis factor (TNF)-αblockade for treatment of patients with Kawasaki syndrome (KS) who fail to become afebrile or who experience persistent arthritis after treatment with intravenous gamma glob ulin (IVIG) and high-dose aspirin. Study design: Cases were retrospectively col lected from clinicians throughout the United States who had used infliximab, a c himeric murine/human immunoglobulin (Ig)G1monoclonal antibody that binds specifi cally to human TNF-α-1, for patients with KS who had either persistent arthri tis or persistent or recrudescent fever ≥48 hours following infusion of 2 g/kg of IVIG. Results: Response to therapy with cessation of fever occurred in 13 of 16 patients. C-reactive protein (CRP) levelwas elevated in all but one patient before infliximab infusion, and the level was lower following infusion in all 10 patients in whom it was remeasured within 48 hours of treatment. There were no infusion reactions to infliximab and no complications attributed to infliximab a dministration in any of the patients. Conclusion: The success of TNF-αblockade in this small series of patients suggests a central role of TNF-αin KS pathog enesis. Controlled, randomized clinical trials are warranted to determine the ro le of anti-TNF-αtherapy in KS.
Objective: To evaluate the use of tumor necrosis factor (TNF) -α blockade for treatment of patients with Kawasaki syndrome (KS) who fail to become a febrile or who experience persistent arthritis after treatment with intravenous gamma glob ulin (IVIG) and high-dose aspirin Study design: Cases were retrospectively col lected from clinicians throughout the United States who had used infliximab, ac himeric murine / human immunoglobulin (Ig) G1monoclonal antibody that binds specifi cally to human TNF-α-1, for patients with KS who had either Persistent arthri tis or persistent or recrudescent fever ≥48 hours following infusion of 2 g / kg of IVIG. Results: Response to therapy with cessation of intracellular high frequency of 13 of 16 patients. C-reactive protein (CRP) level was elevated in all but one patient before infliximab infusion, and the level was lower following infusion in all 10 patients in whom it was remeasured within 48 hours of treatment. There were no infusion reactions to infliximab and no c omplications attributed to infliximab a dministration in any of the patients. Conclusion: The success of TNF-α blockade in this small series of patients suggests a central role of TNF-αin KS pathog enesis. Controlled, randomized clinical trials are warranted to determine the ro le of anti-TNF-αtherapy in KS.