title: Polymorphisms of methylenetetrahydrofolate reductase are not a risk factor for Kawasaki disease in the Korean population.
abstract: OBJECTIVE
  Hyperhomocysteinemia is known as a risk factor for atherosclerosis. Preclinical arteriosclerosis is noted and premature atherosclerosis is known to be accelerated in Kawasaki disease (KD) patients. Genetic polymorphisms in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene result in elevated plasma homocysteine concentrations and are known to be associated with the development of coronary artery disease. Our hypothesis is that single nucleotide polymorphisms (SNPs) of the MTHFR gene are related to the development of KD and coronary artery lesions (CALs).
  
  
  METHODS
  For this study, we selected 3 candidate single nucleotide polymorphisms (SNPs) (rs2274976, rs1801131, and rs1801133) of MTHFR. These SNPs are located on chromosome 1p36.3. We included 101 KD patients and 306 healthy adults as controls in this study. CALs were seen in 38 patients. Genotypes of the selected SNPs were determined by direct sequencing and analyzed with SNPAlyze.
  
  
  RESULTS
  The genetic distribution and allelic frequency of the 3 MTHFR SNPs (rs2274976, rs1801131, and rs1801133) were not significantly different in patients with KD compared to the control group (P=0.71, 0.17, and 0.96, respectively). There was no difference in the genetic distribution of the MTHFR SNPs between the normal control group and the CAL group (P=0.43, 0.39, 0.52 respectively).
  
  
  CONCLUSIONS
  The genetic distribution of the MTHFR SNPs (rs2274976, rs1801131, and rs1801133) was not different in the KD group compared to the control group. In addition, the genetic distribution of these SNPs was not different in the CAL group compared to the control group in the Korean population.
authors.affiliation: Department of Pediatrics, Kyung Hee University Hospital at Gangdong, Kyung Hee University School of Medicine, Seoul, Korea.
authors.forename: Kyung Lim
authors.initials: KL
authors.lastname: Yoon
authors.forename: Jin Hee
authors.initials: JH
authors.lastname: Ko
authors.forename: Kye Shik
authors.initials: KS
authors.lastname: Shim
authors.forename: Mi Young
authors.initials: MY
authors.lastname: Han
authors.forename: Sung Ho
authors.initials: SH
authors.lastname: Cha
authors.forename: Su Kang
authors.initials: SK
authors.lastname: Kim
authors.forename: Joo Ho
authors.initials: JH
authors.lastname: Jung
references.citation: Circulation. 1997 Apr 15;95(8):2032-6
references.pmid: 9133512
references.citation: Am J Hum Genet. 1996 Jan;58(1):35-41
references.pmid: 8554066
references.citation: JAMA. 2002 Oct 23-30;288(16):2023-31
references.pmid: 12387655
references.citation: Eur J Clin Invest. 2001 Jan;31(1):24-30
references.pmid: 11168435
references.citation: Lancet. 1999 Jul 31;354(9176):407-13
references.pmid: 10437885
references.citation: Circulation. 1997 Jul 15;96(2):412-7
references.pmid: 9244205
references.citation: Coron Artery Dis. 1999 Oct;10(7):443-7
references.pmid: 10562910
references.citation: Arthritis Res Ther. 2010;12(2):R71
references.pmid: 20423475
references.citation: Pediatr Clin North Am. 1999 Apr;46(2):313-29
references.pmid: 10218077
references.citation: Circulation. 1997 Jan 7;95(1):21-3
references.pmid: 8994411
references.citation: J Pediatr. 1998 Aug;133(2):177-9
references.pmid: 9709701
references.citation: Pediatr Cardiol. 2009 Apr;30(3):262-8
references.pmid: 19020792
references.citation: N Engl J Med. 1991 Apr 25;324(17):1149-55
references.pmid: 2011158
references.citation: BMC Cardiovasc Disord. 2006 Sep 26;6:38
references.pmid: 17002799
references.citation: J Clin Invest. 2001 Mar;107(6):675-83
references.pmid: 11254667
references.citation: J Cardiol. 2009 Apr;53(2):226-31
references.pmid: 19304127
references.citation: Nat Genet. 2008 Jul;40(7):827-34
references.pmid: 18583979
references.citation: Pharmacogenet Genomics. 2006 Apr;16(4):265-77
references.pmid: 16538173
references.citation: Pediatr Int. 2000 Jun;42(3):236-40
references.pmid: 10881578