Sindrome de Ovario Poliquístico

Revisión de su fisiopatogenia

Autores

  • Carolina Fux Otta
  • Marta Fiol de Cuneo
  • Paula Szafryk de Mereshian

DOI:

https://doi.org/10.31053/1853.0605.v70.n1.20282

Palavras-chave:

síndrome de ovario poliquístico, insulino resistencia, fisiopatogenia

Resumo

El síndrome de ovario poliquístico (SOP), la endocrinopatía ginecológica más frecuente en mujeres en edad fértil, se caracteriza por hiperandrogenismo, anovulación crónica y/u ovarios poliquísticos. A pesar de que su etiología permanece desconocida y que se han propuesto diferentes hipótesis, en la actualidad se jerarquiza a la insulino resistencia como la principal causante del síndrome y su implicancia en las alteraciones metabólicas. La hiperinsulinemia compensatoria contribuye al hiperandrogenismo por diferentes vías: estimulando la síntesis ovárica de andrógenos e inhibiendo la producción hepática de la globulina transportadora de hormonas sexuales. A partir del estudio del ambiente intrauterino, en los últimos años se ha propuesto que el SOP podría tener un origen in útero relacionado con la exposición prenatal a andrógenos. El objetivo del presente trabajo es revisar las principales mecanismos propuestos como causantes del síndrome.

Downloads

Os dados de download ainda não estão disponíveis.

Referências

1- Azziz R, Woods KS, Reyna R, Key TJ, Knochenhauer ES, Vildiz BO. The revalence and features of the polycystic ovary syndrome in unselected population. J Clin Endocrinol Metab 2004, 89: 2745-2749

2- March WA, Moore VM, Willson KJ, Phillips DI, Norman RJ, Davies MJ. The prevalence of polycystic ovary syndrome in a community sample assessed under contrasting diagnostic criteria. Hum Reprod 2010, 25: 544-551

3- Azziz R, Carmina E, Dewailly D, Diamanti-Kandarakis E, Escobar-Morreale HF, Futterweit W, Janssen OE, Legro RS, Norman RJ, Taylor AE, Witchel SF. The Androgen Excess and PCOS Society criteria for the polycystic ovary syndrome: the complete task force report. Fertil Steril 2009, 91: 456-458

4- Fauser BC, Tarlatzis BC, Rebar RW, Legro RS, Balen AH, Lobo R, Carmina E, Chang J, Yildiz BO, Laven JS, Boivin J, Petraglia F, Wijeyeratne CN, Norman RJ, Dunaif A, Franks S, Wild RA, Dumesic D, Barnhart K. 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: 28-38

5- Yen SSC, Vela P, Rankin J. Inappropiate secretion of follicle-stimulating hormone and luteinizing hormone in polycystic ovarian disease. J Clin Endocrinol Metab 1970, 30:435-42

6- Waldstreicher J, Santoro NF, Hall JE, Filicori M, Crowley WF Jr. Hiperfunction of the hypothalamic-pituitary axis in women with polycystic ovarian disease: indirect evidence for partial gonadotroph desensitization. J Clin Endocrinol Metab 1988, 66: 165-172

7- Balen A. The pathophysiology of polycystic ovary syndrome: trying to understand PCOS and its endocrinology. Best Pract Res Clin Obstet Gynaecol 2004, 18: 685-706

8- Arroyo A, Laughlin G, Morales A, Yen SS. Inappropiate gonadotropin secretion in polycystic ovary syndrome: influence of adiposity. J Clin Endocrinol Metab 1997, 82:

3728-3733

9- Ehrmann DA, Barnes RB, Rosenfield RL. Polycysticovary syndrome as a form of functional ovarian hyperandrogenism due to dysregulation of androgen secretion. Endocr Rev 1995, 16: 322-353

10- Gilling-Smith C, Willis DS, Beard RW, Franks S. Hypersecretion of androstenedione by isolated thecal cells from polycystic ovaries. J Clin Endocrinol Metab 1994, 79:1158-1165

11- Wickenheisser JK, Quinn PG, Nelson VL, Legro RS, Strauss JF, McAllister JM. Differential activity of the cytochrome P450c 17 alpha-hydroxylase and steroidogenic acute regulatory protein gene promoters in normal and polycystic ovary syndrome theca cells. J Clin Endocrinol Metab 2000, 85: 2304-2311

12- Nestler JE, Jakubowicz DJ. Decreases in ovarian cytochrome P450c17 alpha activity and serum free testosterone after reduction of insulin secretion in polycystic ovary syndrome. N Engl J Med 1996, 335: 617- 623

13- Hoffman DI, Klive K, Lobo RA. The prevalence and significance of elevated dehydroepiandrosterone sulfate levels in anovulatory women. Fertil Steril 1984, 42: 76-81

14- Hudson RW, Lochnan HA, Danby FW, Margesson LJ, Strang BK, Kimmett SM.11 β-Hydroxiandrostenedione: A marker of adrenal function in hirsutism. Fertil Steril 1990,

54: 1065-1071

15- Yen SC. Endocrinología de la reproducción. Panamericana. Philadelphia. 2001: 465-510, 4ª edición

16- Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA 2001, 285: 2486-2497

17- Diamanti-Kandarakis E, Dunaif A. Insulin resistance and the polycystic ovary syndrome revisited: an update on mechanisms and implications. Endocr Rev 2012, 33:

981-1030

18- Barbieri R, Makris R, Randall R, Daniels G, Kristner R, Ryan K. Insulin stimulates androgen accumulation in incubations of ovarian stroma obtained from women with hyperandrogenism. J Clin Endocrinol Metab 1986, 62: 904-910

19- Nestler JE, Powers LP, Matt DW, Steingold KA, Plymate SR, Rittmaster RS, Clore JN, Blackard WG. A direct effect of hyperinsulinemia on serum sex hormone-binding globulin levels in obese women with the polycystic ovary syndrome. J Clin Endocrinol Metab 1991, 72: 83-89

20- Prelević GM, Wurzburger MI, Balint-Perić L, Nesić JS. Inhibitory effect of sandostatin on secretion of luteinizing hormone and ovarian steroids in polycystic ovary syndrome. Lancet 1990, 336: 900-903

21- Kosova G, Urbanek M. Genetics of the polycystic ovary syndrome. Mol Cell Endocrinol 2012, 0303-7207 [Epub ahead of print]

22- Barker D, Hales C, Fall C, Osmond C, Phipps K, Clark P. Type 2 (non- insulin-dependent) diabetes mellitus, hypertension and hyperlipidaemia (syndrome X): relation to reduced fetal growth. Diabetologia 1993, 36: 62-67

23- Eisner JR, Dumesic DA, Kemnitz JW, Abbott DA. Timing of prenatal androgen excess determines differential impairment in insulin secretion and action in adult female rhesus monkeys. J Clin Endocrinol Metab 2000, 85: 1206-1210

24- Recabarren SE, Sir Petermann T, Lobos A, Codner E, Rojas-García PP, Reyes V. Response to the gonadotropin releasing hormone agonist leuprolide in immature female sheep androgenized in utero. Biol Res 2005, 38: 235-244

25- New MI, Abraham M, Yuen T, Lekarev O. An update on prenatal diagnosis and treatment of congenital adrenal hyperplasia. Semin Reprod Med 2012, 30: 396-399

26- Sir-Petermann T, Maliqueo M, Angel B, Lara HE, Pérez-Bravo F, Recabarren SE. Maternal serum androgens in pregnant women with polycystic ovarian syndrome: possible implications in prenatal androgenization. Hum Reprod 2002, 17: 2573-2579

Publicado

2013-03-13

Edição

Seção

Revisiones de literatura

Como Citar

1.
Fux Otta C, Fiol de Cuneo M, Szafryk de Mereshian P. Sindrome de Ovario Poliquístico: Revisión de su fisiopatogenia. Rev Fac Cien Med Univ Nac Cordoba [Internet]. 13º de março de 2013 [citado 23º de novembro de 2024];70(1):27-30. Disponível em: https://revistas.psi.unc.edu.ar/index.php/med/article/view/20282

Artigos Semelhantes

101-110 de 1954

Você também pode iniciar uma pesquisa avançada por similaridade para este artigo.

Artigos mais lidos pelo mesmo(s) autor(es)

1 2 > >>