Changes of Lipid and Lipoprotein Compositions in Kawasaki Disease and its Impact on Cardiac Complications.
- Author:
Sin Weon YUN
1
;
Ho Seok LEE
;
Dong Woon KIM
;
Kang Won RHEE
;
Young Soo JUNG
Author Information
1. Department of Pediatrics, College of Medicine, Chung-Ang University, Seoul, Korea. yswmd@cau.ac.kr
- Publication Type:Original Article
- Keywords:
Kawasaki disease;
HDL cholesterol;
Apolipoprotein A-1;
Lipoprotein (a)
- MeSH:
Child;
Male;
Female;
Humans;
Risk Factors
- From:Korean Journal of Pediatrics
2005;48(12):1370-1377
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Delineation of serum lipid and lipoprotein values in children after Kawasaki disease (KD) is important because of the predilection of this disease for the coronary arteries. METHODS: The KD group was composed of 51 patients who were hospitalized from Jan. 2002 to Dec. 2003. Control was 25 patients with non-KD febrile illness. The levels of total lipid, phospholipid, triglyceride, HDL-cholesterol (HDL-C), LDL-cholesterol, total cholesterol, apolipoprotein A1 (apo A1), apolipoprotein B, and Lipoprotein (a) were measured and compared with Echocardiographic findings. Measurements were obtained in four time periods: acute febrile, subacute, convalescent phase and 1 year after KD. RESULTS: HDL-C (33.64+/-7.49 mg/dL vs 50.43+/-14.41 mg/dL, P< 0.01) and apo A1 (99.75+/-6.39 mg/dL vs 113.34+/-11.35 mg/dL, P< 0.05) were decreased more in the acute febrile period of KD than in the control, but these changes were not correlated with cardiac complications. All lipid profiles were markedly elevated in the subacute stage and normalized in the convalescent stage; there were no changes until 1-year follow up. There were no significant differences in the changes of lipid profiles, including Lp (a) and coronary dilatation, in any time periods. CONCLUSION: KD is associated with important abnormalities in lipid metabolism, but these changes were transient and appear to be due to the disease itself. These data lead us to infer that KD dose not cause such permanent changes in lipid abnormalities as to be considered a risk factor for atherosclerosis, beyond that caused by the disease itself.
