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FRI0239 Arthritis complicated with kawasaki disease is not TNF-alpha-dependent
  1. T. Kizawa,
  2. T. Nozawa,
  3. T. Kanetaka,
  4. T. Hara,
  5. M. Kikuchi,
  6. R. Hara,
  7. T. Miyamae,
  8. T. Imagawa,
  9. M. Mori,
  10. S. Yokota
  1. Pediatrics, Yokohama City University, Yokohama, Japan


Background Around 10% of children with Kawasaki disease are still refractory to IVIG, and infliximab, anti-TNF-alpha monoclonal antibody, will be successfully administered as the second line of the treatment for these cases. We investigate whether or not TNF-alpha is responsible for the induction of arthritis in Kawasaki disease.

Objectives To investigate the number of children and the characteristics of arthritis of Kawasaki disease following infliximab treatment.

Methods Among 29 children (2005-2011) with Kawasaki disease who were refractory to IVIG (2 g/kg/day), and treated with infliximab (5 mg/kg), five were complicated with arthritis. The number of arthritis in other intractable children to IVIG was 0 out of 21 children treated with additional IVIG, and 1 out of 10 treated with plasma exchange. The clinical characteristics of arthritis treated with infliximab were investigated retrospectively and the arthritis was examined by musculoskeletal ultrasonography.

Results Arthritis in one child was found early in Day 4 after the disease onset, and arthritis in other 4 children developed later in Day 18–24. Two children affected more than 5 joints including knee and hip joints, and 3 had arthritis on 4 or less joints. The mean titers of MMP-3 levels were high in those with active arthritis (205.5 ng/mL). The affected joints in all the children treated with TNF-alpha were examined by ultrasonography to demonstrate synovial hypertrophy and power Doppler signal indicating active synovial inflammation.

Conclusions Arthritis is sometimes concurrent with Kawasaki disease in the early or convalescent phase of the disease. Our findings indicated that the frequency of concurrent arthritis treated with infliximab, a recommended biologics for juvenile idiopathic arthritis (JIA), was relatively high, and that it was not efficacious against active arthritis in Kawasaki disease suggesting that the synovial inflammation complicated with the disease will be TNF-alpha-independent. We speculated that other proinflammatory cytokines such as IL-6 and IL-1-beta would be responsible for the induction of concurrent arthritis in Kawasaki disease as the same with systemic JIA.

Disclosure of Interest None Declared

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