Low T3 syndrome in Kawasaki disease: Relation to serum levels of tumor necrosis factor-alpha, interleukin-6 and NT-proBNP.
10.3345/kjp.2009.52.2.234
- Author:
Hye Kyung CHO
1
;
Jin A SOHN
;
Hae Soon KIM
;
Sejung SOHN
Author Information
1. Department of Pediatrics, Ewha Womans University School of Medicine, Seoul, Korea. sohn@ewha.ac.kr
- Publication Type:Original Article
- Keywords:
Mucocutaneous lymph node syndrome;
Euthyroid sick syndrome;
Tumor necrosis factor-alpha;
Interleukin-6;
Pro-brain natriuretic peptide
- MeSH:
Coronary Vessels;
Diagnosis, Differential;
Echocardiography;
Enzyme-Linked Immunosorbent Assay;
Euthyroid Sick Syndromes;
Humans;
Immunoglobulins;
Inflammation;
Interleukin-6;
Interleukins;
Mucocutaneous Lymph Node Syndrome;
Natriuretic Peptide, Brain;
Peptide Fragments;
Thyroid Gland;
Tumor Necrosis Factor-alpha
- From:Korean Journal of Pediatrics
2009;52(2):234-241
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: We investigated the relationship between thyroid hormone and serum tumor necrosis factor (TNF-alpha), 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-alpha, 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-alpha 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-alpha, 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-alpha, 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.
