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Factors affecting N‐terminal pro‐brain natriuretic peptide elevation in the acute phase of Kawasaki disease
Author(s) -
Yanagisawa Daisuke,
Ayusawa Mamoru,
Kato Masataka,
Watanabe Hirofumi,
Komori Akiko,
Abe Yuriko,
Nakamura Takahiro,
Kamiyama Hiroshi,
Takahashi Shori
Publication year - 2016
Publication title -
pediatrics international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.49
H-Index - 63
eISSN - 1442-200X
pISSN - 1328-8067
DOI - 10.1111/ped.12986
Subject(s) - medicine , tumor necrosis factor alpha , natriuretic peptide , kawasaki disease , brain natriuretic peptide , n terminal pro brain natriuretic peptide , endocrinology , necrosis , cardiology , gastroenterology , heart failure , artery
Background The aim of this study was to investigate the clinical significance and factors that affect N‐terminal pro‐brain natriuretic peptide (NT‐proBNP) elevation in the acute phase of Kawasaki disease (KD) despite the absence of apparent cardiac complications. Methods The laboratory and echocardiography results of 44 KD patients in the acute and subacute phases were reviewed. Results With preserved cardiac function, median NT‐proBNP was significantly elevated in the acute phase compared with the subacute phase (343 pg/mL, IQR, 162–1182 pg/mL vs 98 pg/mL, IQR, 61–205 pg/mL, respectively; P < 0.0001). The respective levels of tumor necrosis factor (TNF)‐α, soluble TNF receptor (sTNFR)1, and sTNFR2 were also significantly elevated in the acute phase compared with the subacute phase: TNF‐α, 3.3 pg/mL (IQR, 2.6–4.8 pg/mL) versus 2.4 pg/mL (IQR 1.9–4.0 pg/mL; P < 0.01), sTNFR1, 2741 pg/mL (IQR, 2080–3183 pg/mL) versus 976 pg/mL (IQR, 814–1247 pg/mL; P < 0.0001), sTNFR2, 5644 pg/mL (IQR, 4693–7520 pg/mL) versus 3169 pg/mL (IQR, 2132–3878 pg/mL; P < 0.0001). Log‐transformed NT‐proBNP was correlated with TNF‐α (r = 0.29, P = 0.056), sTNFR1 (r = 0.60, P < 0.0001), and sTNFR2 (r = 0.65, P < 0.0001). TNF‐α was correlated with sTNFR1 (r = 0.35, P = 0.02) and sTNFR2 (r = 0.51, P < 0.001). Conclusion Tumor necrosis factor‐α may cause NT‐proBNP elevation in the acute phase of KD, and NT‐proBNP level may be an indicator of TNF‐α activity.