Key result
Convalescent Kawasaki disease patients had significantly increased PPARγ mRNA abundance and lower high-molecular-weight adiponectin levels compared to controls.
Why the study?
Does Kawasaki disease alter PPARγ expression and adiponectin profiles in a way that predisposes to atherosclerosis?
Observational (n=50)
Does Kawasaki disease alter PPARγ expression and adiponectin profiles in a way that predisposes to atherosclerosis?
Kawasaki disease is associated with increased PPARγ transcript abundance and decreased high-molecular-weight adiponectin, suggesting a potential mechanism for premature atherosclerosis development.
May signal metabolic predisposition to atherosclerosis in Kawasaki disease survivors; leaves open causal confirmation in prospective studies.
BACKGROUND: It remains controversial whether Kawasaki disease (KD) is a risk factor for the onset of atherosclerosis. An imbalance of peroxisome proliferator-activated receptor γ (PPARγ) and adiponectin appears to play a role in the onset of atherosclerosis in adults, and we therefore examined PPARγ mRNA expression and adiponectin profiles in the peripheral white blood cells obtained from KD patients. METHODS: A total of 50 subjects were studied: nine patients with acute KD, 20 patients with convalescent KD, and 21 age-matched controls. The gene expression of PPARγ, monocyte chemoattractant protein-1, and CC chemokine receptor 2 present in the blood were quantified. The relative gene expression, adiponectin levels, and the three adiponectin isoforms were compared among the subjects. RESULTS: The abundance of PPARγ and CC chemokine receptor 2 mRNA was significantly increased in convalescent KD patients. The monocyte chemoattractant protein-1 level was also increased in convalescent KD patients. The level of high-molecular-weight adiponectin was significantly lower in convalescent patients compared to controls. The PPARγ transcription levels negatively correlated with apolipoprotein A-I levels in acute KD patients. CONCLUSIONS: The transcript abundance of PPARγ and low levels of high-molecular-weight adiponectin in KD patients may have important clinical implications on the development of premature atherosclerosis. Because the potential risk for developing atherosclerosis has not yet been verified, long-term observation is important, even in convalescent KD patients without coronary artery lesions.
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Fukunaga et al. (2010) conducted an observational in Kawasaki disease (n=50). Kawasaki disease vs. Age-matched controls was evaluated on Gene expression of PPARγ, monocyte chemoattractant protein-1, CC chemokine receptor 2, and adiponectin levels. Convalescent Kawasaki disease patients had significantly increased PPARγ mRNA abundance and lower high-molecular-weight adiponectin levels compared to controls.
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