Androgen Excess as a Major Determinant of Cardiovascular Risk in Women: Evidence from the Polycystic Ovary Syndrome

2011 ◽  
Vol 7 (4) ◽  
pp. 529-534 ◽  
Author(s):  
Carmen Gerogescu Pepene
2008 ◽  
Vol 4 (6) ◽  
pp. 583-594 ◽  
Author(s):  
Charikleia D Christakou ◽  
Evanthia Diamanti-Kandarakis

Polycystic ovary syndrome (PCOS) is associated with a clustering of metabolic and cardiovascular risk factors. Insulin resistance is implicated as the major player in the metabolic abnormalities and contributes to the increased cardiovascular risk associated with the syndrome. However, androgen excess appears to participate as an independent parameter, which further aggravates the cardiovascular and metabolic aberrations in affected women with PCOS. The resultant impact of hyperandrogenemia possibly acquires clinical significance for women's health in the context of PCOS, particularly since recent data support an increased incidence of coronary artery disease and of cardiovascular events directly related to androgen levels in women with the syndrome.


2005 ◽  
Vol 113 (S 1) ◽  
Author(s):  
S Tan ◽  
S Hahn ◽  
K Pleger ◽  
S Sack ◽  
BL Herrmann ◽  
...  

2009 ◽  
pp. 1-7
Author(s):  
Tanzeela Akram ◽  
Shahid Hasan ◽  
Muhammad Imran ◽  
Asima Karim ◽  
Muhammad Arslan

2008 ◽  
Vol 93 (7) ◽  
pp. 2909-2912 ◽  
Author(s):  
Mark O. Goodarzi ◽  
Ning Xu ◽  
Ricardo Azziz

Abstract Context: Adrenal androgen excess is common in polycystic ovary syndrome (PCOS) and appears to be heritable. CYP3A7 metabolizes dehydroepiandrosterone and its sulfate (DHEAS). A promoter variant, CYP3A7*1C, which results in persistent expression in adults, was associated with reduced DHEAS levels in a previous study, which led us to consider CYP3A7*1C as a modulator of adrenal androgen excess in patients with PCOS. Objective: The objective was to replicate the association between CYP3A7*1C and reduced DHEAS levels in PCOS patients and assess its possible role in modulating testosterone levels. Design: Women with and without PCOS were genotyped for CYP3A7*1C, and this variant was tested for association with DHEAS and total and free testosterone. Setting: Subjects were recruited from the reproductive endocrinology clinic at the University of Alabama at Birmingham; controls were recruited from the surrounding community. Genotyping took place at Cedars-Sinai Medical Center (Los Angeles, CA). Participants: A total of 287 white women with PCOS and 187 controls were studied. Main Measurements: CYP3A7*1C genotype, PCOS risk, and androgen levels were measured. Results: PCOS subjects who carried the CYP3A7*1C variant had lower levels of serum DHEAS and total testosterone (P = 0.0006 and 0.046, respectively). The variant was not associated with PCOS risk. Conclusion: This study replicated prior work of the association of CYP3A7*1C and decreased DHEAS in a different population of young PCOS women, providing further genetic evidence that CYP3A7 plays a potential role in modulation of DHEAS levels. Adult expression of CYP3A7 may modify the PCOS phenotype by ameliorating adrenal androgen excess.


2011 ◽  
Vol 18 (2) ◽  
pp. 146-170 ◽  
Author(s):  
H.F. Escobar-Morreale ◽  
E. Carmina ◽  
D. Dewailly ◽  
A. Gambineri ◽  
F. Kelestimur ◽  
...  

2010 ◽  
Vol 34 (6) ◽  
pp. 422-426 ◽  
Author(s):  
M. Rizzo ◽  
R. A. Longo ◽  
E. Guastella ◽  
G. B. Rini ◽  
E. Carmina

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Hassan Kahal ◽  
Stephen L. Atkin ◽  
Thozhukat Sathyapalan

Polycystic ovary syndrome (PCOS) is a common disorder affecting women of reproductive age and it is associated with increased cardiovascular risk. Obesity plays an important role in the pathogenesis of PCOS, and the majority of patients with PCOS are obese. Over the last 20 years, the prevalence of obesity has dramatically increased, with probable associated increase in PCOS. Weight reduction plays an integral part in the management of women with PCOS. In this paper, current available weight reduction therapies in the management of PCOS are discussed.


2007 ◽  
Vol 92 (12) ◽  
pp. 4546-4556 ◽  
Author(s):  
Kelsey E. S. Salley ◽  
Edmond P. Wickham ◽  
Kai I. Cheang ◽  
Paulina A. Essah ◽  
Nicole W. Karjane ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Tommy Kyaw Tun ◽  
Anne McGowan ◽  
Niamh Phelan ◽  
Neuman Correia ◽  
Gerard Boran ◽  
...  

Postprandial dyslipidaemia may be a plausible mechanism by which polycystic ovary syndrome (PCOS) increases cardiovascular risk. We sought to investigate whether the postprandial glucose and insulin and lipid and lipoprotein responses, including that of apolipoprotein B-48 (apoB-48) containing chylomicrons, to a mixed meal are different in obese PCOS women when compared to obese control subjects and whether differences, if any, are related to obesity, insulin resistance (IR), hyperandrogenaemia, or PCOS status. 26 women with PCOS (age30.4±1.2years (mean ± SEM), body mass index (BMI)36.8±1.5 kg/m2) and 26 non-PCOS subjects (age34.1±0.9years, BMI31.5±1.0 kg/m2) were studied before and up to 8 hours following a standard mixed meal. AUC-triglyceride (AUC-TG) was higher and AUC-high-density lipoprotein (AUC-HDL) lower in PCOS women. These differences were not apparent when BMI was accounted for. Insulin sensitivity (SI), AUC-apoB-48, and AUC-apolipoprotein B (AUC-apoB) were found to be independent predictors of AUC-TG, accounting for 55% of the variance. Only AUC-insulin remained significantly elevated following adjustment for BMI. Obesity related IR explains postprandial hypertriglyceridaemia and hyperinsulinaemic responses. Management of obesity in premenopausal women with PCOS is likely to reduce their cardiovascular risk burden.


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