Association of parental hyperhomocysteinemia and C677T Methylene tetrahydrofolate reductase (MTHFR) polymorphism with recurrent pregnancy loss

被引:60
|
作者
Govindaiah, Vinukonda [2 ]
Naushad, Shalk Mohammad [1 ]
Prabhakara, Krishnamurthy [3 ]
Krishna, Prasad Chintakindi [1 ]
Devi, Akella Radha Rama [1 ]
机构
[1] CDFD, Div Diagnost, Hyderabad 500076, Andhra Pradesh, India
[2] New York Med Coll, Dept Pathol, Valhalla, NY 10595 USA
[3] Royal Childrens Hosp, VCGS Pathol, Cytogen Lab, Melbourne, Vic, Australia
关键词
Homocysteine; Recurrent pregnancy loss; Methylene tetrahydrofolate reductase; Polymorphism; DNA damage; METHYLENETETRAHYDROFOLATE REDUCTASE; HUMAN SPERM; SPONTANEOUS-ABORTION; HOMOCYSTEINE LEVELS; THROMBOGENIC AGENT; FOLATE LEVELS; PATERNAL AGE; RISK-FACTOR; WOMEN; PREVALENCE;
D O I
10.1016/j.clinbiochem.2008.12.003
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
Objectives: To investigate the association of parental hyperhomocysteinemia, C677T Methylene tetrahydrofolate reductase (MTHFR) polymorphism and DNA damage with recurrent pregnancy loss (RPL). Design and methods: A case-control study. Reverse phase HPLC, PCR-RFLP and Cytokinesis blocked micronuclei assay were used to assess total plasma homocysteine, C677T MTHFR polymorphism and DNA damage respectively. Student t-test, ANOVA and Fisher exact test were used for statistical analysis. Results: Maternal [mean: 11.6 +/- 5.0 versus 8.6 +/- 4.2 mu mol/L, odds ratio (OR): 4.48] and paternal [mean: 19.6 +/- 9.5 versus 14.2 +/- 7.4 mu mol/L, OR: 6.92] hyperhomocysteinemia, paternal age [OR: 1.16], paternal MTHFR 677T allele [OR: 2.30] and DNA damage were found to increase the risk for RPL. DNA damage showed positive correlation with plasma homocysteine and MTHFR 677T allele. Conclusions: Parental hyperhomocysteinemia, paternal age, paternal C677T MTHFR polymorphism and DNA damage are fisk factors for RPL. DNA damage showed positive correlation with plasma homocysteine and MTHFR 677T allele. (C) 2008 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.
引用
收藏
页码:380 / 386
页数:7
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