Table 1.
Alternate therapies for IVIG resistance in Kawasaki disease
| Medicine | Dosage | Mechanistic action | Reference |
|---|---|---|---|
| Methylprednisolone | 20−30 mg/kg, maximum 1 g/day (oral administration) | Blocked inflammatory cytokines which resulted in the immunosuppressive effect | [42•] |
| Prednisone/prednisolone | 1−2 mg/kg/day (intravenous injection, oral administration after symptom relief) | Inhibited the transcription of different inflammatory cytokines and promoted the transcription of anti-inflammatory cytokines and proteins | [4,55] |
| Infliximab | 5 mg/kg (intravenous injection) | Binded and inhibited TNF-α, prevented the release of proinflammatory cytokine and interleukin | [4] |
| Anakinra | 2−6 mg/kg/day (oral administration) | Downregulated various IL-1ß-mediated inflammatory responses, and as a receptor antagonist competitively inhibit the binding between IL-1 and the receptor | [4] |
| Canakinumab | 4 mg/kg (body weight <40 kg) (oral administration) | Suppressed the inflammation through the neutralization of IL-1β | [63] |
| Plasmapheresis (PE) | – | Replaced the plasma harboring the inflammatory cytokines by another colloid including plasma or albumin from donor | [66] |
| Cyclosporine | 4−8 mg/kg/day (intravenous injection or oral administration) | Inhibited the calcineurin-NFAT signaling pathway and increased the activity of T cells | [70] |
| Methotrexate | 10 mg/m2/week (oral administration) | Inhibited lymphocyte proliferation and as a folic acid antagonist | [70] |