Polycystic ovarian syndrome and thrombophilia

Tsanadis, G.; Vartholomatos, George; Korkontzelos, Ioannis; Avgoustatos, F.; Kakosimos, George; Sotiriadis, Alexandros; Tatsioni, Athina; Eleftheriou, Athanasios; Lolis, D.

doi:10.1093/humrep/17.2.314

Cited by 54 publications

(35 citation statements)

References 42 publications

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“…Although Tsanadis et al reported that the odds ratio for bearing a mutation on the methylene tetrahydrofolate reductase gene was 1.2-fold higher in women with PCOS than those without it, the mild elevation of the homocysteine levels in our PCOS patients are lower then expected as those of congenital enzymatic deficient patients could be [23].…”

Section: Discussioncontrasting

confidence: 65%

Plasma Homocysteine Levels in Polycystic Ovary Syndrome and Congenital Adrenal Hyperplasia

et al. 2004

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Abstract. The purpose of this study was to determine whether polycystic ovary syndrome (PCOS) and nonclassic 21-hydroxylase deficiency (CAH) are related to hyperhomocysteinemia, and to investigate if there is a correlation between homocysteine levels and insulin sensitivity in women with PCOS and CAH. Fifty patients with PCOS, 50 patients with CAH and 25 control women were included in the study. Blood samplings were performed in the early follicular phase for measuring hormone profile, Vitamin B 12 , folate, homocysteine levels and fasting blood glucose. Ovulatory status was assessed with timed serum progesterone measurements. Homeostasis model assessment-insulin resistance (HOMA-IR) was calculated as a measure of insulin resistance. Mean homocysteine levels were found as (8.9 + 1.9 umol/l and 17.7 + 3.6 umol/l) in the normal group and PCOS respectively (p<0.001), but there was no statistical significance between nonclassic 21-hydroxylase deficiency (9.0 + 2.2 umol/l) and control group. Most of the patients in PCOS group (35 of 50) were significantly insulin resistant. However, there was no insulin resistant patient in CAH or control group. When we compare the two subgroups of PCOS women, the patients with insulin resistance had significantly higher homocysteine levels than the ones who were not insulin resistant. There were positive correlations among serum homocysteine, insulin and androgen levels in PCOS patients. There were no correlations among these parameters in CAH and control groups. Increased homocysteine levels may contribute to increased cardiovascular disease risk in patients with PCOS. The reason for hyperhomocysteinemia seems to be related to insulin resistance but not high androgen levels.

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Section: Discussioncontrasting

confidence: 65%

Plasma Homocysteine Levels in Polycystic Ovary Syndrome and Congenital Adrenal Hyperplasia

et al. 2004

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“…Thus a number of studies have investigated homocysteine and folate metabolism and confirmed the presence of increased serum homocysteine concentration in obese as well as in non-obese PCOS patients (Yilmaz et al, 2005). MTHFR polymorphism does not seem to be more frequent in these patients than in healthy controls (Tsanadis et al, 2002), and the possible determinants of elevated homocysteine concentration are still debated among authors who found significant correlations between homocysteine and insulin resistance or hyperandrogenism (Yarali et al, 2001;Schachter et al, 2003;Vrbikova et al, 2003;Bayraktar et al, 2004;Wijeyaratne et al, 2004) and those who did not (Loverro et al, 2002;Kilic-Okman et al, 2004;Yilmaz et al, 2005). Interestingly, administration of insulin sensitizers, such as metformin, as it is proposed in PCOS patients to improve ovulation induction and other parameters (Stadtmauer and Oehninger, 2005), has led to a further increase of serum homocysteine in these patients, despite the decrease in insulin resistance (Vrbikova et al, 2002;Kilicdag et al, 2005b).…”

Section: Folate Metabolism and Polycystic Ovary Syndromementioning

confidence: 95%

Impact of folate and homocysteine metabolism on human reproductive health

Forges

Monnier‐Barbarino

Alberto

et al. 2007

Human Reproduction Update

248

188

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Folates belong to the vitamin B group and are involved in a large number of biochemical processes, particularly in the metabolism of homocysteine. Dietary or genetically determined folate deficiency leads to mild hyperhomocysteinemia, which has been associated with various pathologies. Molecular mechanisms of homocysteine-induced cellular dysfunction include increased inflammatory cytokine expression, altered nitric oxide bioavailability, induction of oxidative stress, activation of apoptosis and defective methylation. Whereas the involvement of folate metabolism and homocysteine in ageing-related diseases, in several developmental abnormalities and in pregnancy complications has given rise to a large amount of scientific work, the role of these biochemical factors in the earlier stages of mammalian reproduction and the possible preventive effects of folate supplementation on fertility have, until recently, been much less investigated. In the present article, the possible roles of folates and homocysteine in male and female subfertility and related diseases are systematically reviewed, with regard to the epidemiological, pathological, pharmacological and experimental data of the literature from the last 25 years.

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“…Cases of PCOS cluster in families revealed hereditability of both hyperandrogenaemia and hyperinsulinaemia in affected siblings [3,4]. It has been suggested that PCOS may be a thrombophilic state, although the differences were not statistically significant in a comparison study of women with PCOS and positive family history of thrombosis with the control group [5,6].…”

Section: Introductionmentioning

confidence: 97%