Síndrome de ovario poliquístico

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Irina Winnykamien
Albano Dalibón
Pablo Knoblovits

Resumen

El síndrome de ovario poliquísticos (SOP) representa una de las endocrinopatías más frecuentes en la mujer y es la principal causa de hiperandrogenismo (HA). Se trata de un trastorno complejo, multifactorial, poligénico con influencias ambientales. Aunque se han propuestos diferentes criterios para su diagnóstico, se prefiere el uso del más abarcativo (Criterio de Rotterdam) con la presencia de 2 de 3 de los siguientes: 1) HA clínico o bioquímico, 2) oligoanovulación crónica (OA), 3) poliquistosis ovárica por ecografía, excluyendo otras etiologías. Es frecuente su asociación con comorbilidades metabólicas (obesidad, diabetes 2, dislipidemia, apnea del sueño, etc.) y trastornos reproductivos (hiperplasia endometrial e infertilidad), sobre todo en los fenotipos clásicos, con HA y OA. El tratamiento estará orientado a las características clínicas de cada paciente y al deseo reproductivo. La pérdida de peso en aquellas con sobrepeso u obesidad o ambos factores puede restaurar los ciclos menstruales y disminuir el riesgo metabólico y representa la primera línea de tratamiento. Los anticonceptivos orales (ACO) son el tratamiento farmacológico de elección ya que atenúan las manifestaciones de HA y ofrecen protección endometrial. En las pacientes con oligoanovulación que buscan embarazo, el citrato de clomifeno es el tratamiento aconsejado en primera instancia. La metformina podría usarse en aquellas con intolerancia a la glucosa o diabetes 2 y también como segunda línea de tratamiento para restaurar los ciclos e inducir la ovulación

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Winnykamien I, Dalibón A, Knoblovits P. Síndrome de ovario poliquístico . Rev Hosp Ital B.Aires [Internet]. 2017 Mar. 10 [cited 2026 Apr. 26];37(1):10-2. Available from: https://ojs.hospitalitaliano.org.ar/index.php/revistahi/article/view/842

Referencias

McCartney C, Marshall J. Polycystic Ovary Syndrome. N Engl J Med. 2016;375(1):54-64. DOI: https://doi.org/10.1056/NEJMcp1514916

Dumesic D, Oberfield S, Stener-Victorin E, et al. Scientific statement on the diagnostic criteria, epidemiology, pathophysiology, and molecular genetics of polycystic ovary syndrome. Endocr Rev. 2015;36(5):487-525. DOI: https://doi.org/10.1210/er.2015-1018

Zegher F, Ibañez L. Prenatal growth restraint followed by catch-up of weight: a hyperinsulinemic pathway to polycystic ovary syndrome. Fertil Steril. 2006;86(Suppl.1):4-5. DOI: https://doi.org/10.1016/j.fertnstert.2006.03.013

Stracquadanio M, Ciotta L. Low birth-weight is a PCOS risk factor for Southern-Italian women. Gynecol Endocrinol. 2017 Feb 21:1-5. DOI: https://doi.org/10.1080/09513590.2017.1283487

Sir-Petermann T. et al. Maternal serum androgens in pregnant women with polycystic ovarian syndrome: possible implications in prenatal androgenization. Hum Reprod. 2002;17:2573-2579. DOI: https://doi.org/10.1093/humrep/17.10.2573

Crisosto N, Sir-Petermann T, et al. Anti-Müllerian hormone levels in peripubertal daughters of women with polycystic ovary syndrome. J Clin Endocrinol Metab. 2007;92:2739-2743. DOI: https://doi.org/10.1210/jc.2007-0267

Sir-Petermann T, Maliqueo M, Codner E, et al. Early metabolic derangements in daughters of women with polycystic ovary syndrome. J Clin Endocrinol Metab. 2007;92:4637-4642. DOI: https://doi.org/10.1210/jc.2007-1036

Recabarren SE, Smith R, Rios R, et al. 2008. Metabolic profile in sons of women with polycystic ovary syndrome. J Clin Endocrinol Metab. 2008;93:1820-1826. DOI: https://doi.org/10.1210/jc.2007-2256

Sir-Petermann T, et al. Metabolic and reproductive features before and during Puberty in Daughters of Women with polycystic ovary syndrome. J Clin Endocrinol Metab. 2009;94(6):1923-30. DOI: https://doi.org/10.1210/jc.2008-2836

Qin KN and Rosenfield RL. Role of cytochrome P450c17 in polycystic ovary syndrome. Mol Cell Endocrinol. 1998 Oct 25;145(1-2):111-21. DOI: https://doi.org/10.1016/S0303-7207(98)00177-4

Medeiros SF, Barbosa JS, Yamamoto MM. Comparison of steroidogenic pathways among normoandrogenic and hyperandrogenic polycystic ovary syndrome patients and normal cycling women. J Obstet Gynaecol Res. 2015;41(2):254-63. DOI: https://doi.org/10.1111/jog.12524

Yildiz BO and Azziz R. The adrenal and polycystic ovary syndrome. Rev Endocr Metab Disord. 2007;8(4):331-42. DOI: https://doi.org/10.1007/s11154-007-9054-0

Diamanti-Kandarakis E, Dunaif A. Insulin resistance and the polycystic ovary syndrome revisited: an update on mechanisms and implications. Endocr Rev. 2012;33(6):981-1030. DOI: https://doi.org/10.1210/er.2011-1034

Stein IF, Leventhal ML. Amenorrhea associated with bilateral polycystic ovaries. Am J Obs Gynecol. 1935;29:181-91. DOI: https://doi.org/10.1016/S0002-9378(15)30642-6

Zawadzki JK, Dunaif A. Diagnosis criteria for polycystic ovary syndrome; toward a rational approach. Boston: Blackwell Scientific; 1992.

The Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome. Fertil Steril. 2004;81(1):19-25. DOI: https://doi.org/10.1016/j.fertnstert.2003.10.004

Carmina E, Chu M, Lobo R, et al. Phenotypic variation in hyperandrogenic women influences the findings of abnormal metabolic and cardiovascular risk parameters. J Clin Endocrinol Metab. 2005;90(5):2545-9. DOI: https://doi.org/10.1210/jc.2004-2279

Azziz R, Carmina E, Diamanti-Kandarakis E, et al. Positions statement: criteria for defining polycystic ovary syndrome as a predominantly hyperandrogenic syndrome: an Androgen Excess Society guideline. J Clin Endocrinol Metab. 2006;91(11):4237-45. DOI: https://doi.org/10.1210/jc.2006-0178

National Institues of Health, Evidence-based Methodology Workshop on Polycystic Ovary Syndrome December 3-5, 2012. Executive Summary. Available from: https://prevention.nih.gov/docs/programs/pcos/FinalReport.pdf.

Legro R, Arslanian S, Ehrmann D, et al. Diagnosis and treatment of polycystic ovary syndrome: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2013;98(12):4565-92. DOI: https://doi.org/10.1210/jc.2013-2350

Goodman N, Legro R, Carmina E, et al. American Association of Clinical Endocrinologists, American College of Endocrinology, and Androgen Excess and Pcos Society Disease State Clinical Review: Guide To the Best Practices in the Evaluation and Treatment of Polycystic Ovary Syndrome - Part 1. Endocr Pract. 2015;21(11):1291-300. DOI: https://doi.org/10.4158/EP15748.DSC

Conway G, Dewailly Diamanti-Kandarakis E, et al. The polycystic ovary syndrome: a position statement from the European Society of Endocrinology. Eur J Endocrinol. 2014;171(4):P1-29. DOI: https://doi.org/10.1530/EJE-14-0253

Moghetti P, Tosi F, Bonora E, et al. Divergences in insulin resistance between the different phenotypes of the polycystic ovary syndrome. J Clin Endocrinol Metab. 2013;98(4):E628-37 DOI: https://doi.org/10.1210/jc.2012-3908

Bart C, Fauser M, Tarlatzis B et al. Consensus on women’s health aspects of polycystic ovary syndrome (PCOS): the Amsterdam ESHRE/ASRM-Sponsored 3rd PCOS Consensus Workshop Group. Fertil Steril. 2012;97(1):28-38. DOI: https://doi.org/10.1016/j.fertnstert.2011.09.024

Lizneva D, Suturina D, Azziz R et al. Criteria, prevalence, and phenotypes of polycystic ovary syndrome. Fertil Steril. 2016;106(1):6-15. DOI: https://doi.org/10.1016/j.fertnstert.2016.05.003