2011, Number 3
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Rev Mex Med Repro 2011; 3.4 (3)
Endocrine and metabolic analysis of polycystic ovary syndrome phenotypes
Toro CRJ, Estrada SML, Cárdenas NMG
Language: Spanish
References: 13
Page: 118-122
PDF size: 72.05 Kb.
ABSTRACT
Background: First standardization for diagnosis of polycystic ovaries syndrome was that of National Institute of Child Health and Human Development in 1990, which included hyperandrogenism and anovulation. In 2003, European Society of Human Reproduction and Embriology and American Society of Reproductive Medicine added concept of polycystic ovaries. There is a few information about metabolic complications in women with phenotypes defined according to Rotterdam criteria, especially in the case of phenotypes without hyperandrogenism.
Objective: To elucidate metabolic-endocrine difference among polycystic ovaries syndrome phenotypes.
Patients and method: We designed a prospective, observative and comparative study at Reproductive Medicine Clinic from General Hospital Tacuba (ISSSTE) that included 70 patients between 15 and 45 years old with polycystic ovary syndrome diagnosed according to Rotterdam definition, from January 1, 2009 to May 31, 2010. They were classified in four different phenotypes in order to analyze their endocrine-metabolic issues.
Results: Complete phenotype and phenotype C (hyperandrogenism + polycystic) had remarkable metabolic and endocrine characteristics. Patients with phenotype B (oligoovulation + hyperandrogenism) had lower waist-hip ratio and prolactin concentrations. Phenotype D (oligovulation + polycystic) represent a form of PCOS intermediate or milder metabolic risk profile.
Conclusions: Phenotypes with hyperandrogenism are of higher risk, whereas phenotype without hyperandrogenism has a less risky metabolic profile.
REFERENCES
Stein IF, Leventhal ML. Amenorrhea associated with bilateral polycystic ovaries. Am J Obstet Gynecol 1935;29:181-191.
Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome. Rotterdam ESHRE/ASRM sponsored PCOS Consensus Workshop Group. Fertil Steril 2004;81:19-25.
Azziz R, Carmina E, Dewailly D, Diamanti-Kandarakis E, et al. Positions statement: criteria for refining polycystic ovary syndrome as a predominantly hyperandrogenic syndrome: an Androgen Excess Society guideline. J Clin Endocrinol Metab 2006;91:4237-4245.
Ehrmann D, Barnes R, Rosenfield R, Cavaghan M, Imperial J. Prevalence and predictor of impaired glucose tolerance and diabetes in women with polycystic ovary syndrome. Diabetes Care 1999;22:141-146.
Dokras A, Bochner M, Hollinrake E, Markham S, et al. Screening women with polycystic ovary syndrome for metabolic syndrome. Obstet Gynecol 2005;106:131-137.
Maruyama C, Imamura K, Teramoto T. Assessment of LDL, particle size by triglyceride/HDL-cholesterol ratio in nondiabetic, healthy subjects without prominenty hyperlipidemias. J Atheroscler Thromb 2003;10:186-191.
Norman RJ, Hague WM, Masters SC, Wang XJ. Subjects with polycystic ovaries without hyperandrogenaemia exhibit similar disturbances in insulina and lipid profiles as those with polycystic ovary syndrome. Hum Reprod 1995;10:2258-2261.
Shroff R, Syrop C, Davis W, van Voorhis B, Dokras A. Risk of metabolic complications in the new PCOS phenotypes base on the Rotterdam criteria. Fertil Steril 2007;88:1389-1395.
Morán C. Síndrome de ovario poliquístico: hiperandrogenismo por disfunción gonadotrópica y resistencia a la insulina. Rev Mex Reprod 2008;1(2):79-85.
Legro RS, Chiu P, Kunselman AR, Bentley CM, et al. Polycystic ovaries are common in women with hyperandrogenic chronic anovulation but do not predict metabolic or reproductive phenotype. J Clin Endocrinol Metab 2005;90:2571-2579.
Jovanovic VP, Carmina E, Lobo RA. Not all women diagnosed with PCOS share the same cardiovascular risk profiles. Fertil Steril 2010;94:826-832.
Xoita N, Lazaros L, Georgiou I, Tsatsoulis A. CYP19 gene: a genetic modifier of polycystic ovary syndrome phenotyope. Fertil Steril 2010;94:250-254.
Xu N, Taylor KD, Azziz R, Goodarzi MO. Variants in the HMG-CoA reductase (HMGCR) gene influence component phenotypes in polycystic ovary syndrome. Fertil Steril 2010;94:255-260.