Yıl: 2005 Cilt: 13 Sayı: 3 Sayfa Aralığı: 229 - 237 Metin Dili: Türkçe İndeks Tarihi: 29-07-2022

Polikistik over sendromu gelişiminde rolü olan etyopatogenetik faktörler

Öz:
Amaç: Polikistik Over Sendromunun farklı kriterlere göre tanımlanması ve bu sendromun gelişiminde rol alan etyopatogenetik faktörlerdeki çeşitliliğin araştırılmasıdır. Method: Polikistik Over Sendromu ilk olarak 1935'de Stein ve Leventhal tarafından tanımlanmıştır. Geçmiş yıllarda klinik tanı amenore, hirsutizm, obesite triadından oluşmaktaydı. Ancak son zamanlarda yapılan çalışmalar ise PKOS'nun geniş, heterojen bir klinik tabloya ve multifaktöriyel bir etyolojiye sahip olduğunu göstermiştir. PKOS'da görülen hiperandrojenizm ve anovulasyon endokrinolojik olarak 4 kompartmanda görülen anormallikler sonucu ortaya çıkar; over, adrenal bez, cilt ve yağ dokusu, hipotalamo-hipofizer aks. PKOS'nda etyopatogenez.de hipotalamo-ptuiter-overyen akstaki değişiklikler, intrinsik over patolojisi, peripubertal ekzajere adrenarş ve fizyolojik insülin rezistansının birlikteliği, obezite, patolojik insülin rezistansı ve pankreasla beta hücre disfonksiyonu ve genetik etyolojiye işaret eden ailesel birikimin rolü kesin olarak gösterilmekle beraber bu konuda halen çalışmalar devam etmektedir. Bu derlemede 'PKOS'nun farklı kriterlere göre tanımlanması ve sendromun gelişiminde rol alan çeşitli etyopatogenetik faktörler anlatılmaktadır. Sonuç: PKOS'da etyopatogenetik faktörlerin tam olarak bilinmesi; hastalığın tanısı, izlemi, tedavisi ve uzun dönem komplikasyonların gelişiminin engellenmesi açısından çok büyük bir önem kazanmaktadır.
Anahtar Kelime: Tanı teknikleri, kadın doğum ve kadın hastalıkları Tanı Etiyoloji Polikistik yumurtalık sendromu Hiperandrojenizm

The etiopathogenetic factors which figure in the development of polycystic ovary syndrome

Öz:
Objective: To define the polycystic ovary syndrome according to different criteria and to investigate the diversity of the etiopathogenetic factors which figure in the development of polycystic ovary syndrome. Method: Polycystic ovary syndrome was first described by Stein and Leventhal in 1935. The clinical diagnosis was based on the triad of amenorrhea, hirsutism and obesity in past years. On the other hand recent studies have shown that PCOS has an extensive, heterogen clinical view and multifactorial etiology. Hyperandrogenism and anovulation seen in PCOS are arised endocrinogically as a consequence of the anomalies of 4 compartments: over, adrenal gland, skin and fat tissue, hypothalamic-pituitary axis. However the alterations of hypothalamic-pituitary-ovarian axis, intrinsic ovary pathology, synergy of peripubertal exagere ad-renarge and physiological insulin resistance, obesity, pathologic insulin resistance and beta cell disfunction of pancreas and the role of familial aggregation indicating the genetic etiology have been definitely revealed in the etiopatho genesis of PCOS, studies are currently carried on this subject. In this review the definition of PCOS according to different criteria and the variable etiopatho genetic factors that figure in the development of this syndrome are explained. Conclusion: Assuming the etiopatho genetic factors entirely become very important for the diagnosis, trial, treatment of the disease and also for the prevention of complications.
Anahtar Kelime: Hyperandrogenism Diagnostic Techniques, Obstetrical and Gynecological Diagnosis Etiology Polycystic Ovary Syndrome

Belge Türü: Makale Makale Türü: Derleme Erişim Türü: Erişime Açık
  • 1. Stein IF, Leventhal MI; Amenorrhea associated with bilateral polycystic ovaries, Am J Obstet Gynecol 29. 181, 1935
  • 2. Berek Jonathan S., Hershlag A., Peterson CM., Endocrine Disorders Novak Gynecology 13th Edition. USA, Lippincott Williams And Wilkins 2002: 871-930.
  • 3. Zawadski JK, Dunaif A. Diagnostic criteria for polycystic ovary syndrome towards a rational approach. In : Dunaif A, Givens JR, Hasekine FP, et al, eds. Polycystic Ovary Syndrome. Blacwell Scientific, 1992: 377-384
  • 4. The Rotterdam ESHRE/ASRM-sponsored PCOS consensus workshop group, Revised 2003 consensus on diagnostic criteria and longterm health risks related to polycystic ovary syndrome (PCOS). Hum Reprod, 2004 19 (1): 41-47.
  • 5. Franks S.; Polycystic ovary syndrome: a changing perspective. Clin Endocrinol (Oxf). 1989 Jul;31(1 ):87-120
  • 6. GoldzieherJW.; Polycystic ovarian disease. Fertil Steril. 1981 Apr;35(4):371-94. Review
  • 7. Dahlgren E.; Polycystic ovary syndrome and risk for myocardial infarction. Evaluated from a risk factor model based on a prospective population study of women. Acta Obstet Gynecol Scand. 1992 Dec;71(8):599-604
  • 8. Balen AH; Polycystic ovary syndrome: the spectrum of the disorder in 1741 patients. Hum Reprod. 1995 Aug;10(8):2107-11
  • 9. Conway G.S.; Heterogeneity of the polycystic ovary syndrome: clinical, endocrine and ultrasound features in 556 patients. Clin Endocrinol {Oxf). 1989 Apr; 30(4):459-70
  • 10. Dunaif A.; Evidence for distinctive and intrinsic defects in insulin ^action in polycystic ovary syndrome. Diabetes. 1992 Oct;41(10):1257-66.
  • 11. Goudas VT.; Polycystic ovary syndrome. Endocrinol Metab Clin North Am. 1997 Dec;26(4):893-912. Review
  • ■12. Goldzieher JW.; Clinical and biochemical features of polycystıc ovarian disease. Fenil Steril. 1963 Nov-Dec; 14:631-53.
  • 13. Aono T; Responses of serum gonadotrophins to LH-releasing hormone and oestrogens in Japanese women with polycystic ovaries. Açta Endocrinol (Copenh). 1977 Aug;85(4):840-9.
  • 14. Serafini P.; 5 alpha-Reductase activity in the genital skin of hirsute women. J Clin Endocrinol Metab. 1985 Feb;60(2):349-55.
  • 15. Knochenhauer E.; Ovarian hormones and adrenal androgens during a woman's life span. J Am Acad Dermatol. 2001 Sep;45(3 Suppl):SJ05-15. Review
  • 16. Carmina E, hobo RA. Do hyperandrogenie women with normal menses have polycystic ovary syndrome? Fertil Steril. 1999 Feb;7J(2):319-22.
  • 17. Creswell JL; Fetal growth, length of gestation, and polycystic ovaries in adult life. Lancet. 1997 Oct 18;350(9085):1131-5.
  • 18. Adams J.; Prevalence of polycystic ovaries in women with anovulation and idiopathic hirsutism. Br Med J (Clin Res Ed). 1986 Aug 9;293(6543):355-9.
  • 19. Koivunen R.; The prevalence of polycystic ovaries in healthy women. Acta Obstet Gynecol Scand. 1999 Feb;78(2): 137-41.
  • 20. Franks S. ve ark. 1997; The genetic basis of polycystic ovary syndrome. Hum Rep rod. 1997 Dec;12(12):2641-8. Review.
  • 21. Carmina E.; Do hyperandrogenic women with normal menses have polycystic ovary syndrome? Fertil Steril. 1999 Feb;71(2):319-22.
  • 22. Wild RA.; Obesity, lipids, cardiovascular risk, and androgen excess. Am J Med. 1995 Jan J6;98(1A):27S-32S. Review.
  • 23. Harris MI; Gestational diabetes may represent discovery of preexisting glucose intolerance. Diabetes Care. 1988 May;ll(5):402-11.
  • 24. Ehrmann DA.; Prevalence of impaired glucose tolerance and diabetes in women with polycystic ovary syndrome. Diabetes Care. 1999 Jan;22(1):141-6
  • 25. Legro RS.; Prevalence and predictors of risk for type 2 diabetes mellitus and impaired glucose tolerance in polycystic ovary . syndrome: a prospective, controlled study in 254 affected women. J Clin Endocrinol Metab. 1999 Jan;84(l): 165-9.
  • 26. Von Eckardstein S.; Elevated low-density lipoprotein-cholesterol in women with polycystic ovary, syndrome. Gynecol Endocrinol. 1996 Oct;10(5):311-8.
  • 27. Christian RC; Prevalence and predictors of coronary artery calcification in women with polycystic ovary syndrome. J Clin Endocrinol Metab. 2003 Jun;88(6):2562-8.
  • 28. Talbott E.; Adverse lipid and coronary heart disease risk profiles in young women with polycystic ovary syndrome: results of a case-control study. J Clin Epidemiol. 1998 May;51(5):415-22.
  • 29. Yaralı H.; Diastolic dysfunction and increased serum homocysteine concentrations may contribute to increased cardiovascular risk in patients with polycystic ovary syndrome. Fertil Steril.2001 Sep;76(3):511-6.
  • 30. Diamenti-Kandarakis E.; Increased endothelin-1 levels in women with polycystic ovary syndrome and the beneficial effect of metformin therapy. J Clin Endocrinol Metab. 2001 Oct;86(10):4666-73.
  • 31. Atiomo WU.; The plasminogen activator system in women with polycystic ovary syndrome. Fertil Steril. 1998 Feb;69(2):236-41.
  • 32. Anderson P.increased Insulin sensitivity and fibrinolytic capacity after dietery intervention in obese women with polycystic ovary syndrome, Metabolism 1995; 44:611-616
  • 33. Guzick DS.; Carotid atherosclerosis in women with polycystic ovary syndrome: initial results from a case-control study. Am J Obstet Gynecol. 1996 Apr; 174(4): 1224-9; discussion 1229-32.
  • 34. Rosenfield RL; Dysregulation of cytochrome P450c 17 alpha as the cause of polycystic ovarian syndrome. Fertil Steril. 1990 May_____;53(5):785-91. Review.
  • 35. Lobo RA.; Elevated bioactive luteinizing hormone in women with the polycystic ovary syndrome. Fertil Steril.1983 May;39(5):674-8.
  • 36. Chang RJ.; Steroid secretion in polycystic ovarian disease after ovarian suppression by a long-acting gonadotropin-releasing hormone agonist. J Clin Endocrinol Metab. 1983 May;56(5):897-903.
  • 37. Rittmaster KS.; Differential suppression of testosterone and estradiol in hirsute women with the superactive gonadotropin-releasing hormone agonist leuprolide. J Clin Endocrinol Metab. 1988 Oct;67(4):651-5
  • 38. Artur J Jakimiuk; 5 a Reductase activity in women with PROS, JCEM 84:2414-2418, 1999
  • 39. Harlow CR.; Lysyl oxidase gene expression and enzyme activity in the rat ovary: regulation by follicle-stimulating hormone, androgen, and transforming growth factor-beta superfamily members in vitro. Endocrinology. 2003 Jan; 144(1):154-62.
  • 40. Hoffman DL; The prevalence and significance of elevated dehydroepiandrosterone sulfate levels in anovulatory women. Fertil Steril. 1984 Jul;42(1):76-81
  • 41. Carmina E. ; Does ethnicity influence the prevalence of adrenal hyperandrogenism and insulin resistance in polycystic ovary syndrome? Am J Obstet Gynecol. 1992 Dec;l67(6):1807-12
  • 42. Ibanez 1993-1996 Ovarian 17-hydroxyprogesterone hyperresponsiveness to gonadotropin-releasing hormone (GnRH) agonist challenge in women with polycystic ovary syndrome is not mediated by luteinizing hormone hypersecretion: evidence from GnRH agonist and human chorionic gonadotropin stimulation testing. J Clin Endocrinol Metab. 1996 Nov;81(ll):4103-7
  • 43. SperoffL, Glass RH., Kase NG. Anovulation and Polycystic Ovary. Clinical Gynecologic Endocrinology and Infertility. 6th Edition. USA, Lippincott Williams And Wilkins, 1999:487-522
  • 44. Edman CD.; Identification of the estrogen product of extraglandular aromatization of plasma androstenedione. Am J Obstet Gynecol. 1978 Feb 15;130(4):439-47.
  • 45. Deslypere JP.; Fat tissue: a steroid reservoir and site of steroid metabolism. J Clin Endocrinol Metab. 1985 Sep;61(3):564-70
  • 46. Hall JE.; Differential regulation of luteinizing hormone, follicle-stimulating hormone, and free alpha-subunit secretion from the gonadotrope by gonadotropin-releasing hormone (GnRH): evidence from the use of two GnRH antagonists. J Clin Endocrinol Metab. ]990 Feb;70(2):328-35
  • 47. Franks S, Gharani N, McCarthy M. Candidate genes in polycystic ovary syndrome. Hum Reprod Update 2001 ;7: 405-10.
  • 48. UrbanekM, Legro RS, Driscoll DA, etal. Thirty-seven candidate genes for polycystic ovary syndrome:strongest evidence for linkage is withfollistatin. Proc NatlAcadSci USA 1999;96: 8573-8.
  • 49. Sarabia V, Lam L, Burdett E. Glucose transport in human scleteal muscle cells in culture. Stimulation by insulin and metformin. J Clin Invest 1992: 90:1386-1395.
  • 50. Palmert MR.; Screening for abnormal glucose tolerance in adolescents with polycystic ovary syndrome. J Clin Endocrinol Metab. 2002 Mar; 87(3): 1017-23.
  • 51: Holte J.; Enhanced early insulin response to glucose in re¬lation to insulin resistance in women with polycystic ovary syndro¬me and normal glucose tolerance. J Clin Endocrinol Metab. 1994 May; 78(5): 1052-8.
  • 52. Nagamani M.; Hyperinsulinemia in hyperthecosis of the ovaries, Am J Obstet gynecol 154: 384, 1986.Dunaif A.; Characterization of groups of hyperandrogenic women with acanthosis nigricans, impaired glucose tolerance, and/or hyperinsulinemia. J Clin Endocrinol Metab. 1987 Sep;65(3):499-507
  • 53. Dunaif A.; Characterization of groups of hyperandrogenic women with acanthosis nigricans, impaired glucose tolerance, and/or hyperinsulinemia. J Clin Endocrinol Metab. 1987 Sep;65(3):499-507
  • 54. Grasinger CC; Vulvar acanthosis nigricans: a marker for insulin resistance in hirsute women. Fertil Steril. 1993 Mar;59(3):583-6
  • 55. Barbieri RL; Hyperandrogenism, insulin resistance, and acanthosis nigricans syndrome: a common endocrinopathy with distinct pathophysiologic features. Am J Obstet Gynecol. 1983 Sep 1; 147(1): 90-101. Review.
  • 56. Dunaif A.; Hyperandrogenic anovulation (PKOS): a unique disorder of insulin action associated with an increased risk of non-insulin-dependent diabetes mellitus. Am J Med. 1995 Jan 16; 98(1A): 33S-39S. Review
  • 57. Kiddy DS.; Improvement in endocrine and ovarian functi¬ on during dietary treatment of obese women with polycystic ovary syndrome. Clin Endocrinol (Oxf). 1992 Jan;36(l): 105-11.
  • 58. Regan L; hypersecretion of lüteinising hormone, infertility, and miscarriage, Lancet 336:1141, 1990
  • 59. Homburg R.; Influence of serum luteinising hormone con¬ centrations on ovulation, conception, and early pregnancy loss in polycystic ovary syndrome. BMJ. 1988 Oct 22;297(6655): 1024-6
  • 60. Tulppala M.; Polycystic ovaries and levels of gonadotrophins and androgens in recurrent miscarriage: prospective study in 50 women. Br J Obstet Gynaecol. 1993 Apr;J00(4):348-52.
  • 61. Pasquali R.; The natural history of the metabolic syndrome in young women withthe polycystic ovary syndrome and the effect of long-term oestrogen-progestagen treatment. Clin Endocrinol (Oxf). 1999Apr;50(4):517-27
  • 62. White MC; The polycystic ovary syndrome. 1. Pathogenesis. BrJHosp Med. 1994 Feb 16-Mar 1;51(4): 167-74. Review.
APA SEVİNÇ F, Bayram M, SOYER C (2005). Polikistik over sendromu gelişiminde rolü olan etyopatogenetik faktörler. , 229 - 237.
Chicago SEVİNÇ F. Ceyhan,Bayram Merih,SOYER Canan Polikistik over sendromu gelişiminde rolü olan etyopatogenetik faktörler. (2005): 229 - 237.
MLA SEVİNÇ F. Ceyhan,Bayram Merih,SOYER Canan Polikistik over sendromu gelişiminde rolü olan etyopatogenetik faktörler. , 2005, ss.229 - 237.
AMA SEVİNÇ F,Bayram M,SOYER C Polikistik over sendromu gelişiminde rolü olan etyopatogenetik faktörler. . 2005; 229 - 237.
Vancouver SEVİNÇ F,Bayram M,SOYER C Polikistik over sendromu gelişiminde rolü olan etyopatogenetik faktörler. . 2005; 229 - 237.
IEEE SEVİNÇ F,Bayram M,SOYER C "Polikistik over sendromu gelişiminde rolü olan etyopatogenetik faktörler." , ss.229 - 237, 2005.
ISNAD SEVİNÇ, F. Ceyhan vd. "Polikistik over sendromu gelişiminde rolü olan etyopatogenetik faktörler". (2005), 229-237.
APA SEVİNÇ F, Bayram M, SOYER C (2005). Polikistik over sendromu gelişiminde rolü olan etyopatogenetik faktörler. Türk Fertilite Dergisi, 13(3), 229 - 237.
Chicago SEVİNÇ F. Ceyhan,Bayram Merih,SOYER Canan Polikistik over sendromu gelişiminde rolü olan etyopatogenetik faktörler. Türk Fertilite Dergisi 13, no.3 (2005): 229 - 237.
MLA SEVİNÇ F. Ceyhan,Bayram Merih,SOYER Canan Polikistik over sendromu gelişiminde rolü olan etyopatogenetik faktörler. Türk Fertilite Dergisi, vol.13, no.3, 2005, ss.229 - 237.
AMA SEVİNÇ F,Bayram M,SOYER C Polikistik over sendromu gelişiminde rolü olan etyopatogenetik faktörler. Türk Fertilite Dergisi. 2005; 13(3): 229 - 237.
Vancouver SEVİNÇ F,Bayram M,SOYER C Polikistik over sendromu gelişiminde rolü olan etyopatogenetik faktörler. Türk Fertilite Dergisi. 2005; 13(3): 229 - 237.
IEEE SEVİNÇ F,Bayram M,SOYER C "Polikistik over sendromu gelişiminde rolü olan etyopatogenetik faktörler." Türk Fertilite Dergisi, 13, ss.229 - 237, 2005.
ISNAD SEVİNÇ, F. Ceyhan vd. "Polikistik over sendromu gelişiminde rolü olan etyopatogenetik faktörler". Türk Fertilite Dergisi 13/3 (2005), 229-237.