We investigated the relationship between thyroid hormone and serum tumor necrosis factor (TNF-α), interleukin (IL-6) and N-terminal fragment of pro-brain natriuretic peptide (NT-proBNP) in patients with Kawasaki disease (KD).

Serum levels of thyroid hormone, TNF-α, IL-6, and NT-proBNP were measured in 52 KD patients in the acute and subacute phase and 10 patients with acute febrile illness (control group). TNF-α and IL-6 were determined by sandwich enzyme-linked immunosorbent assay (ELISA). Echocardiography was performed to detect coronary artery lesions (CAL) in KD patients.

Low T₃ syndrome occurred in 63.5% of KD patients. T₃ in the acute phase of KD was lower than that in the control. In KD patients, T₃ was lowered in the acute phase and elevated in the subacute phase, whereas TNF-α, IL-6 and NT-proBNP were elevated in the acute phase and decreased in the subacute phase. NT-proBNP, and IL-6 were higher in patients with low T₃ than in those with normal T₃. In addition, T₃ inversely correlated with IL-6 and NT-proBNP. Of the 4 patients with CAL, 3 had very low T₃. Compared with intravenous immunoglobulin (IVIG)-responsive patients, IVIG-resistant patients had lower T₃ and higher IL-6 and NT-proBNP.

T₃ decreases in the acute phase of KD and normalizes in the subacute phase without thyroid hormone replacement. Low T₃ may be partially induced by IL-6 rather than TNF-α, and is strongly associated with high NT-proBNP. T₃ in KD may be used for the differential diagnosis, monitoring the activity of the disease, and predicting the severity of inflammation.