PMID- 24278430
OWN - NLM
STAT- MEDLINE
DCOM- 20150102
LR  - 20221207
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 8
IP  - 11
DP  - 2013
TI  - Association between GRIN3A gene polymorphism in Kawasaki disease and coronary 
      artery aneurysms in Taiwanese children.
PG  - e81384
LID - 10.1371/journal.pone.0081384 [doi]
LID - e81384
AB  - Kawasaki disease (KD) is pediatric systemic vasculitis with the classic 
      complication of coronary artery aneurysm (CAA). It is the leading cause of 
      acquired cardiovascular diseases in children. Some severe cases present with 
      multi-organ involvement or neurological dysfunction. To identify the role of the 
      glutamate receptor, ionotropic, N-methyl-d-aspartate 3A (GRIN3A) in KD, we 
      investigated genetic variations in GRIN3A in a Taiwanese cohort of 262 KD 
      patients (76 with and 186 without CAA complications). We used univariate and 
      multivariate regression analyses to identify the associations between clinical 
      characteristics and GRIN3A genetic variations in KD. According to univariate 
      regression analysis, CAA formation in KD was significantly associated with fever 
      duration (p < 0.0001), first Intravenous immunoglobulin (IVIG) used (days after 
      day one of fever) (p < 0.0001), and the GRIN3A (rs7849782) genetic variant (p < 
      0.001). KD patients with GG+GC genotype showed a lower rate of developing CAA 
      (GG+GC genotype: odds ratio = 0.26; 95% CI = 0.14-0.46). Significant associations 
      were identified between KD with CAA complication and the GRIN3A (rs7849782) 
      genetic variant by using multivariate regression analysis. Specifically, 
      significant correlations were observed between KD with CAA complications and the 
      presence of GG+GC genotypes for the GRIN3A rs7849782 single-nucleotide 
      polymorphism (full model: odds ratio = 0.25; 95% CI = 0.14-0.46). Our results 
      suggest that a polymorphism of the GRIN3A gene may play a role in KD 
      pathogenesis.
FAU - Lin, Ying-Ju
AU  - Lin YJ
AD  - Department of Medical Research, China Medical University Hospital, Taichung, 
      Taiwan ; School of Chinese Medicine, China Medical University, Taichung, Taiwan.
FAU - Chang, Jeng-Sheng
AU  - Chang JS
FAU - Liu, Xiang
AU  - Liu X
FAU - Hung, Chien-Hui
AU  - Hung CH
FAU - Lin, Ting-Hsu
AU  - Lin TH
FAU - Huang, Shao-Mei
AU  - Huang SM
FAU - Jeang, Kuan-Teh
AU  - Jeang KT
FAU - Chen, Chia-Yen
AU  - Chen CY
FAU - Liao, Chiu-Chu
AU  - Liao CC
FAU - Lin, Cheng-Wen
AU  - Lin CW
FAU - Lai, Chih-Ho
AU  - Lai CH
FAU - Tien, Ni
AU  - Tien N
FAU - Lan, Yu-Ching
AU  - Lan YC
FAU - Ho, Mao-Wang
AU  - Ho MW
FAU - Chien, Wen-Kuei
AU  - Chien WK
FAU - Chen, Jin-Hua
AU  - Chen JH
FAU - Huang, Yu-Chuen
AU  - Huang YC
FAU - Tsang, Hsinyi
AU  - Tsang H
FAU - Wu, Jer-Yuarn
AU  - Wu JY
FAU - Chen, Chien-Hsiun
AU  - Chen CH
FAU - Chang, Li-Ching
AU  - Chang LC
FAU - Tsai, Fuu-Jen
AU  - Tsai FJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20131122
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (GRIN3A protein, human)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
SB  - IM
MH  - Asian People/genetics
MH  - Child, Preschool
MH  - Coronary Aneurysm/*genetics
MH  - Female
MH  - Genetic Association Studies
MH  - *Genetic Predisposition to Disease
MH  - Genotype
MH  - Humans
MH  - Infant
MH  - Linkage Disequilibrium
MH  - Male
MH  - Mucocutaneous Lymph Node Syndrome/*genetics
MH  - Odds Ratio
MH  - *Polymorphism, Single Nucleotide
MH  - Receptors, N-Methyl-D-Aspartate/*genetics
MH  - Taiwan
PMC - PMC3838481
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2013/11/28 06:00
MHDA- 2015/01/03 06:00
PMCR- 2013/11/22
CRDT- 2013/11/27 06:00
PHST- 2013/05/07 00:00 [received]
PHST- 2013/10/14 00:00 [accepted]
PHST- 2013/11/27 06:00 [entrez]
PHST- 2013/11/28 06:00 [pubmed]
PHST- 2015/01/03 06:00 [medline]
PHST- 2013/11/22 00:00 [pmc-release]
AID - PONE-D-13-18778 [pii]
AID - 10.1371/journal.pone.0081384 [doi]
PST - epublish
SO  - PLoS One. 2013 Nov 22;8(11):e81384. doi: 10.1371/journal.pone.0081384. 
      eCollection 2013.