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HACIA UNA CLASIFICACION RACIONAL DEL SINDROME DE OVARIOS POLIQUISTICOS

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Parece probable establecer una teoría unificada de la fisiopatología del síndrome de ovarios poliquísticos (SOP) según la cual las principales alteraciones son periféricas y predominantemente ováricas. Es sumamente plausible que el aumento de los andrógenos, que parece estar modulado por otros factores, desempeñe un papel central en el trastorno neuroendocrino del SOP.
doi9.jpg Autor:
Suhail a. r Doi
Columnista Experto de SIIC

Institución:
Kuwait University

Artículos publicados por Suhail a. r Doi
Coautor
Kamal A. S Al-Shoumer* 
PhD, FRCP, Kuwait University, Safat, Kuwait*
Recepción del artículo
5 de Agosto, 2007 		Aprobación
14 de Octubre, 2007
Primera edición
17 de Octubre, 2008 		Segunda edición, ampliada y corregida
7 de Junio, 2021

HACIA UNA CLASIFICACION RACIONAL DEL SINDROME DE OVARIOS POLIQUISTICOS

Resumen
Creemos que existen tres fenotipos clínicos del síndrome de ovarios poliquísticos (SOP) que representan distintas formas del mismo trastorno metabólico y que son el resultado de grados variados de disfunción metabólica. Las pacientes con disfunción neuroendocrina y ciclos irregulares (fenotipo A) tienen los grados más leves de hiperinsulinemia, contrariamente a las pacientes con fenotipo B (ciclos irregulares sin disfunción neuroendocrina), que padecen los grados máximos de hiperinsulinemia. Las mujeres con ciclos regulares y que no manifiestan disfunción neuroendocrina (fenotipo C) parecen tener grados intermedios de hiperandrogenemia y disfunción metabólica. Estos datos sugieren que el fenotipo clínico puede ser útil para decidir sobre la terapia y puede surgir, al menos en parte, de diferencias en el grado de disfunción metabólica.

Palabras clave
síndrome de ovarios poliquísticos, clasificación, diagnóstico, oligomenorrea, hirsutismo


Artículo completo
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Extensión:  +/-9.59 páginas impresas en papel A4
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Towards a rational classification of PCOS

Abstract
We believe that there are three clinical phenotypes of PCOS that represent distinct forms of the same metabolic disorder and that are the result of varying degrees of metabolic dysfunction. Patients with neuroendocrine dysfunction and irregular cycles (phenotype A) had the mildest degrees of hyperinsulinemia in contrast to patients with phenotype B (irregular cycles without neuroendocrine dysfunction) who demonstrated the greatest degrees of hyperinsulinemia. Regularly cycling women, who do not manifest neuroendocrine dysfunction (phenotype C), appeared to have intermediate degrees of hyperandrogenemia and metabolic dysfunction. These data suggest that the clinical phenotype can be useful to decide on therapy and may arise, at least in part, from differences in the degree of metabolic dysfunction.

Key words
polycystic ovary syndrome, classification, diagnosis, oligomenorrhea, hirsutism


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Especialidades
Principal: Obstetricia y Ginecología
Relacionadas: Bioquímica, Diagnóstico por Laboratorio, Endocrinología y Metabolismo



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Enviar correspondencia a:
Suhail A. R. Doi, Kuwait University Department of Medicine, 13110, P.O. Box 24923, Safat, Kuwait
Bibliografía del artículo
1. Doi SA, Towers PA, Scott CJ, Al-Shoumer KA. PCOS: an ovarian disorder that leads to dysregulation in the hypothalamic-pituitary-adrenal axis? Eur J Obstet Gynecol Reprod Biol 118:4-16, 2005.
2. ESHRE/ASRM. 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 81:19-25, 2004.
3. Doi SA, Al-Zaid M, Towers PA, Scott CJ, Al-Shoumer KA. Irregular cycles and steroid hormones in polycystic ovary syndrome. Hum Reprod 20:2402-2408, 2005.
4. Doi SA, Al-Zaid M, Towers PA, Scott CJ, Al-Shoumer KA. Ovarian steroids modulate neuroendocrine dysfunction in polycystic ovary syndrome. J Endocrinol Invest 28:882-92, 2005.
5. Doi SA, Al-Zaid M, Towers PA, Scott CJ, Al-Shoumer KA. Steroidogenic alterations and adrenal androgen excess in PCOS. Steroids 71:751-9, 2006.
6. Adams J, Polson DW, Franks S. Prevalence of polycystic ovaries in women with anovulation and idiopathic hirsutism. Br Med J (Clin Res Ed) 293:355-9, 1986.
7. Jahanfar S, Eden JA. Idiopathic hirsutism or polycystic ovary syndrome? Aust N Z J Obstet Gynaecol 33:414-6, 1993.
8. Carmina E, Lobo RA. Do hyperandrogenic women with normal menses have polycystic ovary syndrome? Fertil Steril 71:319-22, 1999.
9. Carmina E, Lobo RA. Polycystic ovaries in Hirsute women with normal menses. Am J Med 111:602-6, 2001.
10. Legro RS, Driscoll D, Strauss JF 3rd, Fox J, Dunaif A. Evidence for a genetic basis for hyperandrogenemia in polycystic ovary syndrome. Proc Natl Acad Sci USA 95:14956-60, 1998.
11. Escobar Morreale HF, Serrano Gotarredona J, Garcia Robles R, Sancho J, Varela C. Mild adrenal and ovarian steroidogenic abnormalities in hirsute women without hyperandrogenemia: does idiopathic hirsutism exist? Metabolism 46:902-7, 1997.
12. Ferriman D, Gallwey JD. Clinical assessment of body hair growth in women. J Clin Endocrinol Metab 21:1440-7, 1961.
13. Derksen J, Moolenaar AJ, Van Seters AP, Kock DF. Semiquantitative assessment of hirsutism in Dutch women. Br J Dermatol 128:259-63, 1993.
14. Arroyo A, Laughlin GA, Morales AJ, Yen SS. Inappropriate gonadotropin secretion in polycystic ovary syndrome: influence of adiposity. J Clin Endocrinol Metab 82:3728-33, 1997.
15. Campbell PJ, Gerich JE. Impact of obesity on insulin action in volunteers with normal glucose tolerance: demonstration of a threshold for the adverse effect of obesity. J Clin Endocrinol Metab 70:1114-8, 1990.
16. Radziuk J. Insulin sensitivity and its measurement: structural commonalities among the methods. J Clin Endocrinol Metab 85:4426-33, 2000.
17. Mather KJ, Hunt AE, Steinberg HO, et al. Repeatability characteristics of simple indices of insulin resistance: implications for research applications. J Clin Endocrinol Metab 86:5457-64, 2001.
18. Levy JC, Matthews DR, Hermans MP. Correct homeostasis model assessment (HOMA) evaluation uses the computer program. Diabetes Care 21:2191-2, 1998.
19. Quon MJ. Limitations of the fasting glucose to insulin ratio as an index of insulin sensitivity. J Clin Endocrinol Metab 86:4615-17, 2001.
20. Mather KJ, Kwan F, Corenblum B. Hyperinsulinemia in polycystic ovary syndrome correlates with increased cardiovascular risk independent of obesity. Fertil Steril 73:150-6, 2000.
21. Van Hooff MH, Van der Meer M, Lambalk CB, Schoemaker J. Variation of luteinizing hormone and androgens in oligomenorrhoea and its implications for the study of polycystic ovary syndrome. Hum Reprod 14:1684-9, 1999.
22. Fleming R, Hopkinson ZE, Wallace AM, Greer IA, Sattar N. Ovarian function and metabolic factors in women with oligomenorrhea treated with metformin in a randomized double blind placebo-controlled trial. J Clin Endocrinol Metab 87:569-74, 2002.
23. Ibanez L, Valls C, Ferrer A, Ong K, Dunger DB, De Zegher F. Additive effects of insulin-sensitizing and anti-androgen treatment in young, nonobese women with hyperinsulinism, hyperandrogenism, dyslipidemia, and anovulation. J Clin Endocrinol Metab 87:2870-4, 2002.
24. Ibanez L, Valls C, Ferrer A, Marcos MV, Rodriguez-Hierro F, De Zegher F. Sensitization to insulin induces ovulation in nonobese adolescents with anovulatory hyperandrogenism. J Clin Endocrinol Metab 86:3595-8, 2001.
25. Pasquali R, Gambineri A, Biscotti D, Vicennati V, Gagliardi L, Colitta D, et al. Effect of long-term treatment with metformin added to hypocaloric diet on body composition, fat distribution, and androgen and insulin levels in abdominally obese women with and without the polycystic ovary syndrome. J Clin Endocrinol Metab 85:2767-74, 2000.
26. Judd S, Terry A, Petrucco M, White G. The source of pulsatile secretion of progesterone during the human follicular phase. J Clin Endocrinol Metab 74:299-305, 1992.
27. De Geyter C, De Geyter M, Huber PR, Nieschlag E, Holzgreve W. Progesterone serum levels during the follicular phase of the menstrual cycle originate from the crosstalk between the ovaries and the adrenal cortex. Hum Reprod 17:933-9, 2002.
28. Maciel GA, Soares Junior JM, Alves da Motta EL, Abi Haidar M, De Lima GR, Baracat EC. Nonobese women with polycystic ovary syndrome respond better than obese women to treatment with metformin. Fertil Steril 81:355-60, 2004.
29. Palomba S, Orio F Jr, Falbo A, Manguso F, Russo T, Cascella T, et al. Prospective parallel randomized, double-blind, double-dummy controlled clinical trial comparing clomiphene citrate and metformin as the first-line treatment for ovulation induction in nonobese anovulatory women with polycystic ovary syndrome. J Clin Endocrinol Metab 90:4068-74, 2005.
30. Amer SA, Li TC, Ledger WL. Ovulation induction using laparoscopic ovarian drilling in women with polycystic ovarian syndrome: predictors of success. Hum Reprod 19:1719-24, 2004.
31. Duleba AJ, Banaszewska B, Spaczynski RZ, Pawelczyk L. Success of laparoscopic ovarian wedge resection is related to obesity, lipid profile, and insulin levels. Fertil Steril 79:1008-14, 2003.
32. Gjonnaess H. Ovarian electrocautery in the treatment of women with polycystic ovary syndrome (PCOS). Factors affecting the results. Acta Obstet Gynecol Scand 73:407-12, 1994.
33. Greenblatt E, Casper RF. Endocrine changes after laparoscopic ovarian cautery in polycystic ovarian syndrome. Am J Obstet Gynecol 156:279-85, 1987.
34. Vicino M, Loverro G, Bettocchi S, Simonetti S, Mei L, Selvaggi L. Predictive value of serum androstenedione basal levels on the choice of gonadotropin or laparoscopic ovarian electrocautery as ovulation induction in clomiphene citrate-resistant patients with polycystic ovary syndrome. Gynecol Endocrinol 14:42-9, 2000.
35. Ficicioglu C, Api M, Ozden S. The number of follicles and ovarian volume in the assessment of response to clomiphene citrate treatment in polycystic ovarian syndrome. Acta Obstet Gynecol Scand 75:917-21, 1996.
36. Lopez-Lopez E, Noguera MC, Fuente T, Parrilla JJ, Abad L. Response to clomiphene citrate in the polycystic ovarian syndrome according to different LH/FSH ratios. Hum Reprod 2:635-8, 1987.
37. Guido M, Romualdi D, Suriano R, Giuliani M, Costantini B, Apa R, et al. Effect of pioglitazone treatment on the adrenal androgen response to corticotrophin in obese patients with polycystic ovary syndrome. Hum Reprod 19:534-9, 2004.
38. Mitwally MF, Casper RF. Use of an aromatase inhibitor for induction of ovulation in patients with an inadequate response to clomiphene citrate. Fertil Steril 75:305-9, 2001.
39. Mitwally MF, Casper RF. Aromatase inhibition for ovarian stimulation: future avenues for infertility management. Curr Opin Obstet Gynecol 14:255-63, 2002.
40. Eagleson CA, Gingrich MB, Pastor CL, Arora TK, Burt CM, Evans WS, et al. Polycystic ovarian syndrome: evidence that flutamide restores sensitivity of the gonadotropin-releasing hormone pulse generator to inhibition by estradiol and progesterone. J Clin Endocrinol Metab 85:4047-52, 2000.
41. Gambineri A, Pelusi C, Genghini S, Morselli-Labate AM, Cacciari M, Pagotto U, et al. Effect of flutamide and metformin administered alone or in combination in dieting obese women with polycystic ovary syndrome. Clin Endocrinol (Oxf) 60:241-9, 2004.
 
 
 
 
 
 
 
 
 
 
 
 
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