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Published on: February 8, 2019
Association between FGA gene polymorphisms and coronary artery lesion in Kawasaki disease
Xingzhu Liu1, Yanfei Chen2, Yanfei Yang1
1Department of Special Needs Ward, Kunming Children's Hospital, Kunming, Yunnan, China.
Insights
Genetic variations in the FGA gene may influence coronary artery lesions in children with Kawasaki disease (KD). Specifically, the FGA genotype GA was more prevalent in KD patients with coronary artery lesions compared to those without.
Area of Science:
- Genetics
- Pediatrics
- Cardiology
Background:
- Kawasaki disease (KD) is an acute febrile vasculitis affecting young children.
- Coronary artery lesions (CAL) are a serious complication of KD.
- The role of genetic factors, including FGA gene polymorphisms, in KD pathogenesis and CAL development requires further investigation.
Purpose of the Study:
- To examine the association between FGA gene polymorphisms and the occurrence of coronary artery lesions in children diagnosed with Kawasaki disease.
Main Methods:
- A case-control study involving 234 children with KD, 200 healthy children, and 208 children with non-KD fever.
- Analysis of clinical indicators, serum matrix metalloproteinases (MMPs), TIMP-1, FG-α, fibrinogen levels, and FGA Thr312Ala polymorphism.
- Comparison of FGA genotypes and allele frequencies between KD patients with and without CAL, and control groups.
Main Results:
- KD patients exhibited elevated levels of white blood cell count, platelet count, procalcitonin, C-reactive protein, erythrocyte sedimentation rate, interleukin-6, monocyte chemoattractant protein-1, fibrinogen, MMPs, TIMP-1, and FG-α compared to controls.
- Plasma fibrinogen concentration was significantly higher in KD patients with CAL.
- While overall FGA genotype and allele frequencies did not differ significantly between KD and control groups, the FGA genotype GA was more common in KD children with CAL than in those without.
Conclusions:
- Matrix metalloproteinases (MMPs) and FG-α are significantly upregulated in Kawasaki disease patients.
- FGA gene polymorphisms, particularly the GA genotype, appear to be associated with coronary artery lesions in children with Kawasaki disease.
Objective:
To investigate the correlation between FGA gene polymorphisms and coronary artery lesion in Kawasaki disease.
Methods:
Two hundred and thirty four children with Kawasaki disease (KD group), 200 healthy children (normal group) and 208 children with non-KD fever (fever group) were enrolled. General clinical indicators, the concentration of serum MMPs, TIMP-1, FG-α,fibrinogen level, molecular function (FMPV/ODmax) and FGA Thr312Ala polymorphism were detected individually by testing peripheral venous blood after fasting in the morning.
Results:
There was no significant difference in average age among the three groups, which were 3.03 ± 1.22 years, 3.17 ± 1.30 years, and 3.21 ± 1.31 years, respectively. Compared with those in the fever group, the levels of white blood cell count (WBC), platelet count (PLT), procalcitonin (PCT), C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and fibrinogen (Fg) levels were significantly increased in the KD group. Red blood cell count (RBC) and hemoglobin (Hb) levels were significantly decreased (p < 0.05).The concentration of serum MMPs, TIMP-1, and FG-α in the KD and fever groups were significantly higher than those in the normal group (p < 0.05). The concentration of MMP-2, MMP-3, MMP-9, MMP-13, TIMP-1, and FG-α in the KD group were significantly higher than those in the fever group (p < 0.05).The KD group was divided into two subgroups,55 patients with combined CAL and 179 patients without combined CAL. The plasma fibrinogen concentration in the combined CAL group was significantly higher than that in the non-combined CAL and normal groups (p < 0.01). There was no statistically significant difference in FMPV/ODmax among the three groups (p > 0.05). Compared with normal group, the FGA GG, GA, and AA genotype and G, A allele frequency of the FGA gene polymorphism in the KD group showed no significant difference (p > 0.05). In the KD group, the most common type in children with CAL was GA, while the most common type in children without CAL was GG.
Conclusion:
MMPs and FG-α were significantly upregulated in KD patients. The proportion of FGA genotype GA in children with CAL was significantly higher than that in children without CAL, suggesting that FGA gene polymorphisms affect coronary artery lesion in children with KD.
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