PMID- 32034842 OWN - NLM STAT- MEDLINE DCOM- 20210708 LR - 20210708 IS - 1521-2254 (Electronic) IS - 1099-498X (Linking) VI - 22 IP - 5 DP - 2020 May TI - Associations of MTRR A66G polymorphism and promoter methylation with ischemic stroke in patients with hyperhomocysteinemia. PG - e3170 LID - 10.1002/jgm.3170 [doi] AB - BACKGROUND: Patients with hyperhomocysteinemia (HHcy) have a higher risk of developing ischemic stroke (IS). The association between MTRR A66G polymorphism and promoter methylation with IS in patients with HHcy is also uncertain. The present study aimed to investigate the association between the MTRR polymorphism and methylation with IS in HHcy patients. METHODS: This case-control study included a total of 304 HHcy patients (95 with IS and 209 without IS). Multivariate logistic regression analyses were applied to explore the association between MTRR polymorphism and classical atherothrombotic risk factors with the risk of IS. RESULTS: The log-additive and dominant models were markedly different in participants with IS compared to the control group (p = 0.031 and 0.016, respectively). The log-additive and dominant showed a significant association with IS in the low level plasma homocysteine groups (p = 0.024 and 0.014, respectively). No significant difference of methylation between IS and without IS group (p > 0.05). Patients with high plasma homocysteine had a 4.041-4.941 fold higher risk of IS (p = 0.01, 0.016 and 0.041, respectively) compared to the low plasma homocysteine group. Age, diabetes, hypertension and plasma homocysteine were the risk factors for IS in patients with HHcy (p = 0.033, 0.000, 0.001 and 0.038, respectively). CONCLUSIONS: MTRR A66G polymorphism and an elevated plasma plasma homocysteine level were significantly associated with an increased risk of IS in patients with HHcy. Age, diabetes, hypertension and Hcy were all found to be associated with IS. CI - (c) 2020 John Wiley & Sons, Ltd. FAU - Li, Dankang AU - Li D AD - Department of Epidemiology, School of Public Health, Zhengzhou University, Zhengzhou, Henan, China. FAU - Zhao, Qinglin AU - Zhao Q AUID- ORCID: 0000-0001-7092-2148 AD - Department of Epidemiology, School of Public Health, Zhengzhou University, Zhengzhou, Henan, China. FAU - Zhang, Chengda AU - Zhang C AD - Department of International Medicine, Beaumont Health System, Royal Oak, MI, USA. FAU - Huang, Xiaowen AU - Huang X AD - Department of Epidemiology, School of Public Health, Zhengzhou University, Zhengzhou, Henan, China. FAU - Godfrey, Opolot AU - Godfrey O AD - Department of Epidemiology, School of Public Health, Zhengzhou University, Zhengzhou, Henan, China. FAU - Zhang, Weidong AU - Zhang W AD - Department of Epidemiology, School of Public Health, Zhengzhou University, Zhengzhou, Henan, China. LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20200217 PL - England TA - J Gene Med JT - The journal of gene medicine JID - 9815764 RN - 0LVT1QZ0BA (Homocysteine) RN - EC 1.18.1.- (methionine synthase reductase) RN - EC 1.18.1.2 (Ferredoxin-NADP Reductase) SB - IM MH - Aged MH - Case-Control Studies MH - DNA Methylation MH - Female MH - Ferredoxin-NADP Reductase/*genetics MH - *Genetic Predisposition to Disease MH - Homocysteine/*blood MH - Humans MH - Hyperhomocysteinemia/*blood/complications/*genetics/physiopathology MH - Ischemic Stroke/*blood/complications/*genetics/metabolism MH - Logistic Models MH - Male MH - Middle Aged MH - Polymorphism, Genetic MH - Promoter Regions, Genetic MH - Risk Factors OTO - NOTNLM OT - MTRR OT - hyperhomocysteinemia OT - ischemic stroke OT - methylation OT - polymorphism EDAT- 2020/02/09 06:00 MHDA- 2021/07/09 06:00 CRDT- 2020/02/09 06:00 PHST- 2019/08/31 00:00 [received] PHST- 2020/01/12 00:00 [revised] PHST- 2020/02/04 00:00 [accepted] PHST- 2020/02/09 06:00 [pubmed] PHST- 2021/07/09 06:00 [medline] PHST- 2020/02/09 06:00 [entrez] AID - 10.1002/jgm.3170 [doi] PST - ppublish SO - J Gene Med. 2020 May;22(5):e3170. doi: 10.1002/jgm.3170. Epub 2020 Feb 17.