PMID- 35721657
OWN - NLM
STAT- MEDLINE
DCOM- 20220621
LR  - 20220716
IS  - 1937-8688 (Electronic)
VI  - 41
DP  - 2022
TI  - The role of methylenetetrahydrofolate reductase C677T gene polymorphism as a risk 
      factor for coronary artery disease: a cross-sectional study in the Sidoarjo 
      Regional General Hospital.
PG  - 212
LID - 10.11604/pamj.2022.41.212.24916 [doi]
LID - 212
AB  - INTRODUCTION: hyperhomocysteinemia (HHcy) may contribute to an increased risk of 
      coronary artery disease (CAD). The underlying mechanisms are not well understood, 
      but other than dietary intake factors, hyperhomocysteinemia may genetically 
      result from a methylenetetrahydrofolate reductase (MTHFR) C677T gene 
      polymorphism. A cross-sectional study was performed to assess whether this 
      mutation was a potential genetic risk factor for CAD. METHODS: this 
      cross-sectional study was performed on 30 CAD patients and 30 normal healthy 
      controls at Sidoarjo Regional General Hospital. The polymorphisms of the MTHFR 
      C677T gene was assessed by polymerase chain reaction (PCR), and plasma 
      homocysteine was measured by chemiluminescence immunoassay (CLIA) and then 
      compared between CAD patients and control subjects by the multivariate logistical 
      regression model. RESULTS: results from an independent sample t-test analysis 
      showed that plasma homocysteine concentrations were significantly higher in CAD 
      patients compared to the control group individuals (13.91 +/- 4.55 mumol/L vs 10.97 
      +/- 3.45 mumol/L; p<0.05). There were no significant correlations between MTHFR 
      C677T gene polymorphism and other risk factors, such as age at diagnosis with 
      acute coronary syndrome, sex, smoking, lipid profile, diabetes, hypertension, 
      C-reactive protein (CRP), creatinine, and homocysteine (p>0.05). In multivariate 
      analysis models, the C677T genotype frequencies were insignificantly different 
      between CAD patients and control subjects (p>0.05). Meanwhile, the results of 
      adjusted odds ratio (aOR), 95% confidence interval (CI), and p-value for 
      homocysteine, age, and smoking were aOR: 1.264, 95% CI : 1.042-1.535, p = 0.018; 
      aOR: 0.916, 95% CI: 0.842-0.997, p = 0.043, and aOR: 5.428, 95% CI 1.532-19.226, 
      p = 0.009, respectively. Homocysteine, age, and smoking were significantly 
      different between CAD patients and control subjects (p<0.05). CONCLUSION: 
      hyperhomocysteinemiais significantly correlated with an increased risk of CAD, 
      but MTHFR C677T gene polymorphism might not contribute to increased CAD risk.
CI  - Copyright: Hairudi Sugijo et al.
FAU - Sugijo, Hairudi
AU  - Sugijo H
AD  - Cardiology and Vascular Medicine Department, Sidoarjo Regional General Hospital, 
      Sidoarjo, Indonesia.
FAU - Sargowo, Djanggan
AU  - Sargowo D
AD  - Internal Medicine Department, Faculty of Medicine, Brawijaya University, Malang, 
      Indonesia.
FAU - Widjajanto, Edi
AU  - Widjajanto E
AD  - Clinical Pathology Department, Faculty of Medicine, Brawijaya University, Malang, 
      Indonesia.
FAU - Romdoni, Rochmad
AU  - Romdoni R
AD  - Cardiology and Vascular Medicine Department, Faculty of Medicine, Airlangga 
      University, Surabaya, Indonesia.
LA  - eng
PT  - Journal Article
DEP - 20220315
PL  - Uganda
TA  - Pan Afr Med J
JT  - The Pan African medical journal
JID - 101517926
RN  - 0LVT1QZ0BA (Homocysteine)
RN  - EC 1.5.1.20 (MTHFR protein, human)
RN  - EC 1.5.1.20 (Methylenetetrahydrofolate Reductase (NADPH2))
SB  - IM
MH  - Case-Control Studies
MH  - *Coronary Artery Disease/genetics
MH  - Cross-Sectional Studies
MH  - Genetic Predisposition to Disease
MH  - Genotype
MH  - Homocysteine/blood/genetics
MH  - Humans
MH  - *Hyperhomocysteinemia
MH  - *Methylenetetrahydrofolate Reductase (NADPH2)/genetics
MH  - Polymorphism, Genetic
PMC - PMC9167480
OTO - NOTNLM
OT  - Coronary artery disease
OT  - gene polymorphism
OT  - homocysteine
OT  - hyperhomocysteinemia
OT  - risk factor
COIS- The authors declare no competing interest.
EDAT- 2022/06/21 06:00
MHDA- 2022/06/22 06:00
PMCR- 2022/03/15
CRDT- 2022/06/20 03:57
PHST- 2020/07/09 00:00 [received]
PHST- 2022/03/03 00:00 [accepted]
PHST- 2022/06/20 03:57 [entrez]
PHST- 2022/06/21 06:00 [pubmed]
PHST- 2022/06/22 06:00 [medline]
PHST- 2022/03/15 00:00 [pmc-release]
AID - PAMJ-41-212 [pii]
AID - 10.11604/pamj.2022.41.212.24916 [doi]
PST - epublish
SO  - Pan Afr Med J. 2022 Mar 15;41:212. doi: 10.11604/pamj.2022.41.212.24916. 
      eCollection 2022.