Low T3 syndrome in Kawasaki disease: Relation to serum levels of tumor necrosis factor-α, interleukin-6 and NT-proBNP

Abstract

Purpose : We investigated the relationship between thyroid hormone and serum tumor necrosis factor (TNF), interleukin (IL-6) and N-terminal fragment of pro-brain natriuretic peptide (NT-proBNP) in patients with Kawasaki disease (KD). Methods : Serum levels of thyroid hormone, TNF, 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 and IL-6 were determined by sandwich enzyme-linked immunosorbent assay (ELISA). Echocardiography was performed to detect coronary artery lesions (CAL) in KD patients. Results : 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, 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. Conclusion : 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, 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.