BACKGROUND: Relationship between Premature Menopause and presence, severity and life-threatening events of coronary artery disease (CAD) has been suggested in recent observations. The present study tried to assess relationship between age of Menopause and severity of CAD in a sample of women with suspected CAD.METHODS: In a cross-sectional study, we included 189 consecutive women with suspected CAD that were candidate for coronary angiography and admitted to the Shafa hospital in Kerman city. Our final population for analysis included women who underwent natural Menopause (n=148) or Premature Menopause (n=41). CAD severity was classified according to the number of coronary artery stenosis ³ 50% in coronary angiography.RESULTS: Among 189 study patients with suspected CAD, 22.0% of those with early Menopause and 23.6% of those with normal Menopause suffered three coronary vessels involvement, while normal angiography features was shown in 39.0% and 40.5%, respectively. Regarding severity of CAD and left main lesions, no significant differences were found between the patients with and without Premature Menopause. According to the multivariable logistic regression model and with the presence of other patients' variables as cofounders, age of Menopause could not predict the presence and severity of CAD in patients with suspected CAD. However, patients' age (OR: 1.11, p<0.001) and family history of CAD (OR: 2.05, p=0.04) were main predictors of the severity of CAD in these patients.CONCLUSIONS: Premature Menopause does not predict occurrence or severity of CAD in women with suspected CAD, but women age and their family history of CAD are main predictors of the severity of CAD.

Background: Premature Menopause is characterized by amenorrhea before age of 40 years, markedly raised serum luteinizing hormone (LH) level, follicle-stimulating hormone (FSH) level and reduced serum level of estradiol. Genome-wide analysis suggested several loci associated with Premature Menopause. Here, we aimed to analyze association of variants at the MCM8, FNDC4, PRRC2A, TLK1, ZNF346 and TMEM150B gene loci with Premature Menopause. Materials and Methods: In this cross-sectional study, a total of 117 women with Premature Menopause were compared to 183 healthy women. Anthropometric indices were measured in all participants: height, weight, body mass index (BMI), waist circumference (WC) and wrist circumference. Eight single-nucleotide polymorphisms (SNPs) of the indicated genes (rs16991615, rs244715, rs451417, rs1046089, rs7246479, rs4806660, rs10183486 and rs2303369) were identified from the literature. Genotyping was performed using tetra-ARMS polymerase chain reaction (PCR) and ASO-PCR methods. Results: T allele of the rs16991615, rs1046089, rs7246479 and rs10183486, C allele of rs244715, rs451417 and rs4806660 as well as TT genotype of rs2303369 were associated with an increased risk of Premature Menopause, likely causing susceptibility to primary ovarian insufficiency (POI) in comparison with C allele. We also found an association between the rs16991615 SNP with Premature Menopause. Frequency of the minor allele in cases was increased for all SNPs in comparison with controls. All minor alleles, except for rs2303369, showed a statistically significant increased odds ratio (OR). However, after Bonferroni correction for multiple testing, none of the P values were remained significant. Conclusion: The selected polymorphisms in MCM8, FNDC4, PRRC2A, TLK1, ZNF346 and TMEM150B genes may potentially affect susceptibility to Premature Menopause, although replication of the results in larger cohort could clarify this.

Premature ovarian failure (POF) is a heterogeneous disorder, defined as Menopause under age 40 years. The prevalence is 1%; POF before age 30 years is much less common. Chromosomal causes have long been recognized - visible deletions of the X chromosome, 45, X/46, XX mosaicism, and autosomal rearrangements (balanced translocations). Toxins or iatrogenic causes (e.g., chemotherapeutic agents) are occasionally implicated; autoimmune causes exist. However, lack of explanations for most cases has led to the deduction that single gene mutations (autosomal or X-linked) must be responsible for most cases of POF. With molecular technology it is now possible to determine if a single cell is perturbed in POF. Many attractive candidate genes exist, usually based on animal models (mice).The most common single gene responsible for POF if perturbed is FMR1 (fragile X), CGG expansion explaining perhaps 5% of sporadic cases. A predictable set of genes whose perturbations cause POF are those encoding gonadotropins (FISH, LH) or their receptors (FSHR, LHR). Mutations in these gonadotropin-related genes are known but rare except for FSHR mutations in Finland. Other genes expressed during oogenesis have been interrogated by ourselves, including DNA binding proteins and transcription factors (NOBOX and LHX8), RNA binding proteins (NANOS, TGFb family members such as GDF9), and G protein receptors (GPR3). Additional genes expressed in oocytes (AT2, KIT, NOGGIN, MIS, MISR, BAX, RFPL4), are attractive candidates. To date causative mutations have still been identified in only a few genes (NOBOX, GDF9, LDX8, BMP 15) each explaining perhaps 1-2% of POF cases. However, population-specific studies are still limited, and a single mutation may prove important in certain populations like FSHR in Finland. Genome wide association studies (GWAS) are in progress and exome-sequencing planned.Clinical significance will arise from identifying POF genes. 1) Better prognosis and ovarian preservation can be offered for younger for younger family members having the same mutation; 2) Therapeutic replacement products can be envisioned to militate against ovarian failure.

Introduction: Osteoporosis is the most common metabolic bone disease that could causes many dangerous fractures. In this condition bone mass reduces, so fractures can easily occur. The aim of this study was assessing the effect of eight weeks of aerobic training on serum parathormone, estrogen and Alkaline phosphatase concentration in Women with Premature Menopause.Methods: Methods: In this study semi-experimental study, in 2014, 21 women with Premature Menopause (age 35-45 year, body mass index (BMI>30 kg/m2), height: 161.19±2.64 and weight 83.97±1.98) were selected by convenience sampling method and they were randomly divided into two groups experimental (n=10) and control (n=11). The subject in experimental group had an aerobic training program for eight week (3 sessions in week, each session 45-60 minutes, the intensity of exercise was 65 to 75 percent of maximum heart rate). Blood samples were taken from the subjects’ 24 hours before the first session and 48 hours after the last training session at end of eight week in order to measure factors such as (parathyroid hormone (PTH), estrogen and some bone metabolism) by using a radioimmunoassay (RIA) and ELISA method in 12 hours of fasting. Then Data for inter and between group comparison, paired and ANCOVA test were used (significance level p<0.05).Results: The result of this study show that, eight weeks aerobic training lead to a significant increase in mean values of serum calcium (p=0.001), phosphor (p=0.001), estrogen (p=0.001), parathormone (p=0.001) in aerobic training group; while, the amount of alkaline phosphatase did not change at the end of period (p=0.92).Conclusion: Eight weeks aerobic training with 65 to 75 percent of maximum heart rate intensity was efficient in increasing of serum calcium, phosphor, estrogen, parathormone in women with Premature Menopause. It is concluded that regular training can help to increase bone density and reduces the risk of fractures in women with Premature Menopause.