Paediatric Rheumatology
Macrophage migration inhibitory factor -173 polymorphism and risk of coronary alterations in children with Kawasaki disease
G. Simonini, E. Corinaldesi, C. Massai, F. Falcini, F. Fanti, M. De Martino, R. Cimaz
CER3681
2009 Vol.27, N°6
PI 1026, PF 1030
Paediatric Rheumatology
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PMID: 20149326 [PubMed]
Abstract
OBJECTIVES:
To investigate the possible relationship between MIF –173 polymorphism and susceptibility to, and severity of, Kawasaki disease (KD) in a cohort of Italian patients.
METHODS:
Sixty-nine patients (43 F, 26 M, median age 29 months, range 3-135 months) with KD and 60 sex-matched healthy caucasian children were genotyped for MIF-173. Typing of the MIF gene -173 G/C was performed by PCR and restriction fragment length polymorphism.
RESULTS:
Eight out of 69 (12%) KD children were non-responders: 7 required an additional IVIG infusion, while 1 received 2 IVIG infusions and then steroid administration. 9/69 (13%) KD children developed coronary artery abnormalities (CAA) during the second to fourth week of disease, and 4 of them required an additional IVIG infusion. MIF genotyping did not show significant differences between patients and controls. KD patients carrying a MIF -173*C allele developed CAA more frequently than those without MIF- (7/9 77.8% vs. 16/60 26.7%, OR 9.6, 95% CI 1.80–21.2, p<0.005). Non-responders to a single IVIG infusion carried the MIF -173*C allele more frequently than responders (6/8 = 75% vs. 17/61 = 28%, OR 5.1, 95% CI 1.42–22.31 p<0.014). In multiple regression analysis, KD patients carrying a MIF -173*C allele were found to have an increased risk of coronary involvement (OR 7.7, 95% CI 1.36–16.1, p=0.021).
CONCLUSIONS:
We showed that children carrying the MIF polymorphism -173*C had a higher percentage of CAA. A potential relationship between a MIF polymorphism and risk of CAA in KD might be considered.