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Titolo:
RELATION OF A COMMON MUTATION IN METHYLENETETRAHYDROFOLATE REDUCTASE TO PLASMA HOMOCYSTEINE AND EARLY-ONSET CORONARY-ARTERY DISEASE
Autore:
DUNN J; TITLE LM; BATA I; JOHNSTONE DE; KIRKLAND SA; ONEILL BJ; ZAYED E; MACDONALD MC; DEMPSEY GI; NASSAR BA;
Indirizzi:
QUEEN ELIZABETH II HLTH SCI CTR,DIV CLIN CHEM,1278 TOWER RD HALIFAX NS B3H 2Y9 CANADA DALHOUSIE UNIV,FAC MED,DEPT PATHOL HALIFAX NS B3H 4H7 CANADA DALHOUSIE UNIV,FAC MED,DEPT MED HALIFAX NS B3H 4H7 CANADA DALHOUSIE UNIV,FAC MED,DEPT EPIDEMIOL & COMMUNITY HLTH HALIFAX NS B3H4H7 CANADA
Titolo Testata:
Clinical biochemistry
fascicolo: 2, volume: 31, anno: 1998,
pagine: 95 - 100
SICI:
0009-9120(1998)31:2<95:ROACMI>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
MYOCARDIAL-INFARCTION; RISK FACTOR; VASCULAR-DISEASE; HUMAN LONGEVITY; RELAXING FACTOR; HEART-DISEASE; HOMOCYST(E)INE; HYPERHOMOCYSTEINEMIA; LIPOPROTEINS; CHOLESTEROL;
Keywords:
MTHFR GENE; HOMOCYSTEINE; FOLATE; CORONARY ARTERY DISEASE; PCR; MUTATION ANALYSIS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
41
Recensione:
Indirizzi per estratti:
Citazione:
J. Dunn et al., "RELATION OF A COMMON MUTATION IN METHYLENETETRAHYDROFOLATE REDUCTASE TO PLASMA HOMOCYSTEINE AND EARLY-ONSET CORONARY-ARTERY DISEASE", Clinical biochemistry, 31(2), 1998, pp. 95-100

Abstract

Objective: In the presence of low serum folate, mutant 5,10-methylenetetrahydrofolate reductase (MTHFR+ [A223V/C677T]) in the homozygous state (+/+), may predispose to higher plasma homocysteine (tHct) levels and coronary artery disease (CAD). To determine the impact of this relationship on predisposition to early-onset GAD, we examined the prevalence of the mutation and plasma tHct in patients with early-onset GAD and compared them to patients manifesting CAD later in life. Methods: Three hundred patients with history of acute myocardial infarction or angina pectoris and angiographically documented CAD were studied. Patients consisted of two groups: group 1 (G1 = 150 patients) presenting with these findings under age 50; while group 2 (G2 = 150) presented for the first time over age 65 years. Prevalence of the MTHFR+ mutation was assessed by molecular analysis, and plasma tHct and folate were measured. An association of the +/+ genotype with early onset CAD could lead to its higher prevalence in the younger age group. Results: Therewas no significant difference in the frequency of the (+/+) genotype between the two groups (G1: 11.3% vs. G2: 11.3%). However, patients with the (+/+) genotype in both groups had higher tHct when plasma folate was below the mean value (G1: p < 0.0001 while G2: p < 0.01). Conclusion: The mutant MTHFR genotype was not found to be a determining factor in early-onset CAD. Higher tHct values were obtained in the older age group, which is expected because other studies have shown that tHctlevels increase with age. A significant relation was shown between MTHFR genotype and low folate status yielding high tHct levels in those with the (+/+) genotype. As this relation was seen in both groups, although to a lesser extent in the older G2, it does not explain the underlying cause of early-onset CAD. Copyright (C) 1998 The Canadian Society of Clinical Chemists.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/11/20 alle ore 18:10:16