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G232 Use of Infliximab in Children with Refractory Kawasaki Disease
  1. S Singh1,
  2. D Suri1,
  3. R Manojkumar2,
  4. N Narula2,
  5. A Gupta1,
  6. A Rawat1
  1. 1Department of Paediatrics, Post Graduate Institute of Medical Education and Research, Chandigarh, India
  2. 2Department of Cardiology, Post Graduate Institute of Medical Education and Research, Chandigarh, India

Abstract

Introduction The aetiology of Kawasaki diasese (KD) is still an enigma. It is known that cytokines have a major role to play in the pathogenesis of this condition. There is evidence of TNF-α activation during the acute phase of KD. Although the drug of choice for treatment of KD is still intravenous immunoglobulin (IVIg), approximately 10–15% patients may not respond to the first dose of IVIg. In such cases, an additional dose of IVIg can be given. Infliximab, a TNF-α inhibitor, is also being increasingly used in such situations. We present our experience with use of infliximab in 9 patients with refractory KD at a tertiary care cente.

Patients and methods We diagnosed 112 children with KD during the period January 2007 – November 2012. The diagnosis of KD was based on the American Heart Association criteria. All children underwent detailed echocardiography examinations by a paediatric cardiologist. Standard treatment protocols (IVIg 2 g/kg along with aspirin) were used in the management of these children. In addition, 9 children with KD received infliximab (REMICADE) during this period. The drug was used in doses of 5–7 mg/kg and given intravenously,. Indicationas for using infliximab were as follows: refractory KD in 6 children; 3 children had come in late (>3 weeks) and had coronary artery abnormalities (CAA) at presentation. 7 patients had developed CAA abnormalities before infliximab therapy: transient mild dilatation-2; aneurysms-3; giant aneurysms-2.

Results Complete response to therapy with cessation of fever occurred in 7/9 patients. Platelet count and C-reactive protein concentrations decreased following infliximab infusion in all, except 2. The latter 2 patients, on follow-up, progressed and developed features consistent with systemic onset juvenile idiopathic arthritis. 4 children with mild CAA (dilatation/small aneurysms) showed complete resolution on follow-up; 2 children with giant aneurysms showed no further progression. No side-effects were noted and there were no significant infusion reactions.

Conclusion Infliximab may have a role in refractory KD, especially when there are CAA. In older children, the use of infliximab is also more economical than IVIg.This has therapeutic implications in resource constrained settings of a developoing country.

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