Modulating effects of mannose binding lectin genotype on arterial stiffness in children after Kawasaki disease
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Published on: December 2, 2014
Yiu-Fai Cheung1, Marco H K Ho, Wai-Kee Ip
1Department of Paediatrics and Adolescent Medicine, University of Hong Kong, Queen Mary Hospital, Pokfulam Rd., Hong Kong, China. xfcheung@hkucc.hku.hk
Insights
Mannose-binding lectin (MBL) genotype influences arterial stiffness in children post-Kawasaki disease (KD). Specific MBL genotypes are linked to increased arterial stiffness, a cardiovascular risk factor, in KD survivors.
Area of Science:
- Cardiovascular Science
- Pediatric Cardiology
- Immunogenetics
Background:
- Systemic arterial stiffness is elevated in children following Kawasaki disease (KD).
- Mannose-binding lectin (MBL) gene mutations have been associated with KD complications and adult atherosclerosis.
- The role of MBL genotype in modulating arterial stiffness post-KD remains unclear.
Purpose of the Study:
- To investigate the hypothesis that MBL genotype influences arterial stiffness in children after KD.
- To assess the relationship between MBL genotype expression levels and arterial stiffness (PWV) in KD patients and controls.
Main Methods:
- Studied 71 KD patients and 41 age-matched controls, measuring blood pressure, brachioradial arterial stiffness (PWV), cholesterol, serum MBL, and MBL genotype.
- Categorized MBL genotypes into high expression (HL) and intermediate/low expression (IL/LL) groups.
- Utilized multiple linear regression to identify determinants of arterial stiffness.
Main Results:
- MBL genotype distributions did not differ between KD patients and controls, or between KD patients with/without coronary aneurysms.
- Patients with IL/LL MBL expression genotypes exhibited significantly faster PWV compared to those with HL genotypes (p=0.027).
- Age, being a KD patient, and the MBL IL/LL genotype were significant determinants of arterial stiffness.
Conclusions:
- MBL genotype significantly modulates arterial stiffness in children following Kawasaki disease.
- The MBL IL/LL genotype is associated with increased arterial stiffness, a key cardiovascular risk factor.
- These findings highlight the potential role of MBL genetics in long-term cardiovascular health after KD.
Abstract:
Systemic arterial stiffness is increased in patients after Kawasaki disease (KD). Recently, associations between mannose-binding lectin (MBL) gene mutation and coronary complications in infants with KD and atherosclerosis in adults have been reported. We tested the hypothesis that MBL genotype modulates arterial stiffness in children after KD. Seventy-one KD patients (42 with and 29 without coronary aneurysms), aged 9.5 +/- 3.7 y, and 41 age-matched controls were studied. We determined and compared their blood pressure, brachioradial arterial stiffness as determined by pulse wave velocity (PWV), fasting total cholesterol, serum MBL level, and MBL genotype. Additionally, the modulating effects of different MBL expression genotypes [high level (HL) versus intermediate or low level (IL/LL)] on arterial stiffness in different groups were assessed. The MBL genotype distributions did not differ between patients and controls (p = 0.41) or between patients with and without coronary aneurysms (p = 0.42). Patients with IL/LL expression genotypes had significantly faster PWV than those with HL expression genotypes (7.93 +/- 1.38 m/s versus 6.67 +/- 2.28 m/s, p = 0.027). This genotype-modulating effect is more pronounced in patients without (HL 8.86 +/- 0.77 m/s versus IL/LL 6.48 +/- 2.32 m/s, p = 0.02) than those with (HL 7.50 +/- 1.41 m/s versus IL/LL 6.80 +/- 2.28 m/s, p = 0.32) coronary aneurysms. Multiple linear regression analysis identified age (beta = 0.26, p = 0.012), being a Kawasaki patient (beta = 0.22, p = 0.015), and MBL IL/LL genotype subgroup (beta = 0.20, p = 0.03) as significant determinants of arterial stiffness in the entire cohort. In conclusion, MBL genotype modulates arterial stiffness, an important cardiovascular risk factor, in children after KD.