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MeSH Review

Anovulation

 
 
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Disease relevance of Anovulation

 

Psychiatry related information on Anovulation

  • It is proposed that these closely interlinked phenomena that, particularly in overweight subjects, are associated with anovulation, may confer a biological advantage for women with PCOS at times of food deprivation, when such women may reproduce more successfully than those without PCOS [5].
 

High impact information on Anovulation

  • We administered pulsatile low doses of gonadotropin-releasing hormone (GnRH) (1 to 5 micrograms) to patients whose anovulation was caused by relative and absolute deficiency of endogenous GnRH [6].
  • These data indicate that in these PCO patients the abnormalities of the hypothalamic-pituitary regulation of gonadotropin secretion was not an inherent defect but represented a functional derangement consequent to inappropriate estrogen feedback, which led to a vicious cycle of chronic anovulation and inappropriate gonadotropin secretion [7].
  • It has been shown previously that female mice homozygous for an alpha-fetoprotein (AFP) null allele are sterile as a result of anovulation, probably due to a defect in the hypothalamic-pituitary axis [8].
  • CONTEXT: For the last 40 yr, the first line of treatment for anovulation in infertile women has been clomiphene citrate (CC) [9].
  • CONTEXT: Metformin is successfully used in the treatment of cycle disorders and anovulation in women with polycystic ovary syndrome (PCOS) [10].
 

Chemical compound and disease context of Anovulation

 

Biological context of Anovulation

 

Anatomical context of Anovulation

 

Associations of Anovulation with chemical compounds

  • In a randomized cross-over study of 10 women with PCOD, GnRH (100 micrograms) was injected iv on the fifth day of 2 consecutive cycles, 1 of them following anovulation and progesterone withdrawal bleeding and the other following an induced ovulatory cycle [12].
  • Instead, a central and/or peripheral defect, resulting in overproduction of androgen, may also exist and lead to anovulation in OA women [26].
  • Testosterone, a follicular regulator: key to anovulation [27].
  • To determine whether increased GnRH-LH drive in HAA reflects altered sex steroid exposure caused by chronic anovulation or is an intrinsic hypothalamic attribute, we compared the pulsatile LH response to oral contraceptive (OC)-induced suppression in seven women with HAA, with that of seven eumenorrheic women (EW) [28].
  • Thus, similarly to obese PCOS women, nonobese PCOS subjects with anovulation may also benefit from metformin treatment [29].
 

Gene context of Anovulation

 

Analytical, diagnostic and therapeutic context of Anovulation

References

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  2. Increased androgenic activity and breast cancer risk in premenopausal women. Secreto, G., Toniolo, P., Berrino, F., Recchione, C., Di Pietro, S., Fariselli, G., Decarli, A. Cancer Res. (1984) [Pubmed]
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  4. Naloxone increases the frequency of pulsatile luteinizing hormone secretion in women with hyperprolactinemia. Cook, C.B., Nippoldt, T.B., Kletter, G.B., Kelch, R.P., Marshall, J.C. J. Clin. Endocrinol. Metab. (1991) [Pubmed]
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  18. High frequency of luteal phase deficiency and anovulation in recreational women runners: blunted elevation in follicle-stimulating hormone observed during luteal-follicular transition. De Souza, M.J., Miller, B.E., Loucks, A.B., Luciano, A.A., Pescatello, L.S., Campbell, C.G., Lasley, B.L. J. Clin. Endocrinol. Metab. (1998) [Pubmed]
  19. Low levels of follicle-stimulating hormone receptor-activation inhibitors in serum and follicular fluid from normal controls and anovulatory patients with or without polycystic ovary syndrome. Schipper, I., Rommerts, F.F., Ten Hacken, P.M., Fauser, B.C. J. Clin. Endocrinol. Metab. (1997) [Pubmed]
  20. Preferential induction of c-fos immunoreactivity in vasoactive intestinal polypeptide-innervated gonadotropin-releasing hormone neurons during a steroid-induced luteinizing hormone surge in the female rat. van der Beek, E.M., van Oudheusden, H.J., Buijs, R.M., van der Donk, H.A., van den Hurk, R., Wiegant, V.M. Endocrinology (1994) [Pubmed]
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  23. Ambulatory blood pressure profiles and plasminogen activator inhibitor (PAI-1) activity in lean women with and without the polycystic ovary syndrome. Sampson, M., Kong, C., Patel, A., Unwin, R., Jacobs, H.S. Clin. Endocrinol. (Oxf) (1996) [Pubmed]
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  25. Morphological action of tamoxifen in the endometrium of persistent estrous rats. Patriarca, M.T., Simöes, R.D., Smaniotto, S., De Teves, D.C., Simöes, M.d.e. .D., Evêncio-Neto, J., De Freitas, V., De Lima, G.R. Acta obstetricia et gynecologica Scandinavica. (1996) [Pubmed]
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  27. Testosterone, a follicular regulator: key to anovulation. Haning, R.V., Hackett, R.J., Flood, C.A., Loughlin, J.S., Zhao, Q.Y., Longcope, C. J. Clin. Endocrinol. Metab. (1993) [Pubmed]
  28. Resistance of gonadotropin releasing hormone drive to sex steroid-induced suppression in hyperandrogenic anovulation. Daniels, T.L., Berga, S.L. J. Clin. Endocrinol. Metab. (1997) [Pubmed]
  29. Metformin versus ethinyl estradiol-cyproterone acetate in the treatment of nonobese women with polycystic ovary syndrome: a randomized study. Morin-Papunen, L., Vauhkonen, I., Koivunen, R., Ruokonen, A., Martikainen, H., Tapanainen, J.S. J. Clin. Endocrinol. Metab. (2003) [Pubmed]
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