2019, Número 2
<< Anterior Siguiente >>
Gac Med Mex 2019; 155 (2)
La esteroidogénesis en el síndrome de ovarios poliquísticos
Ventura-Arizmendi E, Hernández-Valencia M
Idioma: Español
Referencias bibliográficas: 32
Paginas: 184-190
Archivo PDF: 220.24 Kb.
RESUMEN
El síndrome de ovarios poliquísticos es la enfermedad endocrina más frecuente en la edad reproductiva; se caracteriza por
alteraciones menstruales, hiperandrogenismo clínico o bioquímico e identificación ultrasonográfica de quistes ováricos. Las
alteraciones neuroendocrinas y metabólicas que lo acompañan implican desensibilización del eje hipotálamo-hipófisis-ovario,
esteroidogénesis e hiperandrogenismo. Recientemente se ha explorado el papel de la resistencia a la insulina. Se ha establecido
que la principal causa del síndrome de ovarios poliquísticos es el hiperandrogenismo, debido a alteraciones enzimáticas
en la vía esteroidogénica, por lo que existe sobreestimulación por parte de la hormona luteinizante a causa de los pulsos
rápidos generados por la hormona liberadora de gonadotropinas. Diversos factores de crecimiento y citocinas inhiben la
conversión de andrógenos a estrógenos. En la desregulación característica de este síndrome también están involucradas la
activina y las prostaglandinas e, incluso, altos niveles de insulina.
REFERENCIAS (EN ESTE ARTÍCULO)
Sirmans SM, Pate KA. Epidemiology, diagnosis, and management of polycystic ovary syndrome. Clin Epidemiol. 2014;6:1-13.
Terasawa E, Fernandez DL. Neurobiological mechanisms of the onset of puberty in primates. Endocr Rev. 2001;1:111-151.
Besser GM, McNeilly AS, Anderson DC, Marshall JC, Harsoulis P, Hall R, et al. Hormonal responses to synthetic luteinizing hormone and follicle stimulating hormone-releasing hormone in man. Br Med J. 1972; 3:267-271.
Ciccone NA, Kaiser UB. The biology of gonadotroph regulation. Curr Opin Endocrinol Diabetes Obes. 2009;16:321-327
Roe AH, Dokras A. The diagnosis of polycystic ovary syndrome in adolescents. Rev Obstet Gynecol. 2011;4:45-51
Liu C, Peng J, Matzuk MM, Yao HH. Lineage specification of ovarian theca cells requires multicellular interactions via oocyte and granulosa cells. Nat Commun. 2015;6:6934-6955.
Baptiste CG, Battista MC, Trottier A, Baillargeon JP. Insulin and hyperandrogenism in women with polycystic ovary syndrome. J Steroid Biochem Mol Biol. 2010;122:42-52.
Baskind NE, Balen AH. Hypothalamic-pituitary, ovarian and adrenal contributions to polycystic ovary syndrome. Best Pract Res Clin Obstet Gynaecol. 2016;37 80-97.
Gianetti E, Seminara S. Kisspeptin and KISS1R: a critical pathway in the reproductive system. Reproduction. 2008;136 295-301.
Oride A, Kanasaki H, Mijiddorj T, Sukhbaatar U, Ishihara T, Kyo S. Regulation of kisspeptin and gonadotropin releasing hormone expression in rat placenta: study using primary cultures of rat placental cells. Reprod Biol Endocrinol 2015;13:90-98.
Ezzat A, Pereira A, Clarke IJ. Kisspeptin is a component of the pulse generator for GnRH secretion in female sheep but not the pulse generator. Endocrinology. 2015;156:1828-1837.
Hanchate NK, Parkash J, Bellefontaine N, Mazur D, Colledge WH, D’Anglemont- De-Tassigny X, et al. Kisspeptin-GPR54 signaling in mouse NO-synthesizing neurons participates in the hypothalamic control of ovulation. J Neurosci. 2012;32 932-945.
Donoso AO, López FJ, Negro-Vilar A. Cross-talk between excitatory and inhibitory amino acids in the regulation of luteinizing hormone-releasing hormone secretion. Endocrinology. 1992;131:1559-1561.
Gougeon A. Regulation of ovarian follicular development in primates: facts and hypotheses. Endocr Rev. 1996;17:121-155.
Balen AH, Conway GS, Homburg R, Legro RS. Polycystic ovary syndrome. A guide to clinical management. EE. UU.: Taylor & Francis; 2005.
Rosenfield RL, Ehrmann DA. The pathogenesis of polycystic ovary syndrome (PCOS): the hypothesis of PCOS as functional ovarian hyperandrogenism revisited. Endocr Rev. 2016;37:467-520.
Barbieri RL. The endocrinology of the menstrual cycle. En: Rosenwaks Z, Wassarman PM, editores. Human Fertility. Methods and Protocols. EE. UU.: Humana Press; 2014.
Otsuka F, McTavish K, Shimasaki S. Integral role of GDF-9 and BMP-15 in ovarian function. Mol Reprod Dev. 2011;78 9-21.
Rosenfield RL, Barnes RB, Cara JF, Lucky AW. Dysregulation of cytochrome P450c17 alpha as the cause of polycystic ovarian syndrome. Fertil Steril. 1990;53:785-791.
White D, Leigh A, Wilson C, Donaldson A, Franks S. Gonadotrophin and gonadal steroid response to a single dose of a long-acting agonist of gonadotrophin-releasing hormone in ovulatory and anovulatory women with polycystic ovary syndrome. Clin Endocrinol (Oxf). 1995;42:475-481.
Taylor AE, McCourt B, Martin K, Anderson EJ, Adams J, Schoebfeld D, et al. Determinants of abnormal gonadotropin secretion in clinically defined women with polycystic ovary syndrome. J Clin Endocrinol Metab. 1997;82:2248-2256.
Barontini M, García-Rudaz M, Veldhius JD. Mechanisms of hypothalamic- pituitary-gonadal disruption in polycystic ovarian syndrome. Arch Med Res. 2001;32:544-552.
Hirshfeld-Cytron J, Barnes RB, Ehrmann DA, Caruso A, Mortensen MM, Rosenfield RL. Characterization of functionally typical and atypical types of polycystic ovary syndrome. J Clin Endocrinol Metab. 2009;94:1587-1594.
Mason HD, Willis DS, Beard RW, Winston RM, Margara R, Frank S. Estradiol production by granulosa cells of normal and polycystic ovaries: relationship to menstrual cycle history and to concentrations of gonadotrophins and sex steroids in follicular fluid. J Clin Endocrinol Metab. 1994;79:1355-1360.
Rosenfield RL, Mortensen M, Wroblewski K, Littlejohn E, Ehrmann DA. Determination of the source of androgen excess in functionally atypical polycystic ovary syndrome by a short dexamethasone androgensuppression test and a low-dose ACTH test. Hum Reprod. 2011;26: 3138-3146.
Dumesic DA, Oberfield SE, Stener-Victorin E, Marshall JC, Laven JS, Legro RS. Scientific statement on the diagnostic criteria, epidemiology, pathophysiology, and molecular genetics of polycystic ovary syndrome. Endocr Rev. 2015,36:487-525.
Kazer RR, Kessel B, Yen SS. Circulating luteinizing hormone pulse frequency in women with polycystic ovary syndrome. J Clin Endocrinol Metab. 1987;65:233-236.
Qiao J, Feng HL. Extra-and intra-ovarian factors in polycystic ovary syndrome: impact on oocyte maturation and embryo developmental competence. Hum Reprod Update. 2011;17:17-33.
RefSeq: NCBI Reference Sequence Database [Sitio web]. EEUU: National Center for Biothechnology Information/National Library of Medicine; 2008.
Peng HM, Im SC, Pearl NM, Turcu AF, Rege J, Waskell L, et al. Cytochrome b5 activates the 17,20-lyase activity of human cytochrome P450 17A1 by increasing the coupling of NADPH consumption to androgen production. Biochemistry. 2016;55:4356-4365.
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.
Dunaif A. Insulin resistance and the polycystic ovary syndrome: mechanisms and implication for pathogenesis. Endocr Rev. 1997;18:774-800.