View : 13 Download: 0
Serum interleukin-6, tumor necrosis factor-α and adiponectin levels in Kawasaki disease
- Serum interleukin-6, tumor necrosis factor-α and adiponectin levels in Kawasaki disease
- Ahn J.; Kim H.G.; Sohn S.; Hong Y.M.
- Ewha Authors
- 홍영미; 손세정
- SCOPUS Author ID
- 홍영미; 손세정
- Issue Date
- Journal Title
- Korean Journal of Pediatrics
- vol. 53, no. 1, pp. 41 - 47
- Purpose: Adiponectin is an endogenous modulator of vascular remodeling that suppresses vascular inflammation. However, the role of adiponectin in Kawasaki disease (KD) has not been elucidated. The purpose of this study is to investigate the correlation between serum adiponectin level and several parameters, such as interleukin (IL)-6, tumor necrosis factor (TNF)-α, lipid profile, and C reactive protein (CRP), and to clarify the association between adiponectin and cardiac function. Methods: Twenty-two KD patients (22 patients in acute phase and 20 patients in subacute phase) were enrolled in the study group. The control group consisted of 31 subjects (13 febrile patients and 18 healthy children). Both groups underwent blood sampling and tissue Doppler imaging (TDI). Results: CRP was significantly increased in the KD group compared with the control group. There were no significant differences in serum TNF-α, IL-6, and adiponectin levels between groups. However, a negative correlation was found between adiponectin level and CRP level or platelet count. Systolic myocardial velocity and A myocardial velocity measured by TDI were decreased significantly in the acute KD group compared with the subacute KD group and control group. Positive correlations were found between adiponectin level and systolic myocardial velocity or A myocardial velocity. Conclusion: In acute KD patients, low adiponectin level was related to severe inflammatory reactions and decreased left ventricular functions.
- Appears in Collections:
- 의학전문대학원 > 의학과 > Journal papers
- Files in This Item:
There are no files associated with this item.
- RIS (EndNote)
- XLS (Excel)
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.