Antigonadotropin

An antigonadotropin is a drug which suppresses the activity and/or downstream effects of one or both of the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH). This results in an inhibition of the hypothalamic-pituitary-gonadal (HPG) axis, and thus a decrease in the levels of the androgen, estrogen, and progestogen sex steroids in the body. Antigonadotropins also inhibit ovulation in women and spermatogenesis in men. They are used for a variety of purposes, including for the hormonal birth control, treatment of hormonally-sensitive cancers, to delay precocious puberty and puberty in transgender youth, as a form of chemical castration to reduce the sex drives of individuals with hypersexuality or pedophilia, and to treat estrogen-associated conditions in women such as menorrhagia and endometriosis, among others. High-dose antigonadotropin therapy has been referred to as medical castration.

Antigonadotropin
Drug class
Class identifiers
UseFor the treatment of androgen and estrogen-related medical conditions.
ATC codeG03XA
Biological targetGnRH receptor, gonadotropin receptors (FSHR, LHR), sex steroid receptors (AR, ER, PR)
In Wikidata

The best-known and widely used antigonadotropins are the gonadotropin-releasing hormone (GnRH) analogues (both agonists and antagonists).[1] However, many other drugs have antigonadotropic properties as well, including compounds acting on sex steroid hormone receptors such as progestogens, androgens, and estrogens (due to negative feedback on the HPG axis),[2][3] as well as steroid synthesis inhibitors such as danazol and gestrinone.[4][5] Since progestins have relatively little effect on sexual differentiation compared to the other sex steroids, potent ones such as cyproterone acetate, medroxyprogesterone acetate, and chlormadinone acetate are often used at high doses specifically for their antigonadotropic effects.[2][6][7]

Danazol, gestrinone, and paroxypropione have all been classified specifically as antigonadotropins.[8]

Prolactin has antigonadotropic effects and hyperprolactinemia can cause hypogonadism.[9][10]

Opioids have antigonadotropic effects and can reduce luteinizing hormone and testosterone levels in men.[11][12][13] A 2015 systematic review and meta-analysis found that opioid therapy decreased testosterone levels in men by about 165 ng/dL (5.7 nmol/L) on average, which was a reduction in testosterone level of almost 50%.[11] In contrast to opioids, opioid antagonists, like naltrexone, have progonadotropic effects, and can increase luteinizing hormone and testosterone levels.[14]

See also

References
  1. Jonathan S. Berek; Emil Novak (2007). Berek and Novak's Gynecology. Lippincott Williams & Wilkins. p. 212. ISBN 978-0-7817-6805-4. Retrieved 29 May 2012.
  2. de Lignières B, Silberstein S (April 2000). "Pharmacodynamics of oestrogens and progestogens". Cephalalgia: An International Journal of Headache. 20 (3): 200–7. doi:10.1046/j.1468-2982.2000.00042.x. PMID 10997774. S2CID 40392817.
  3. Gooren L (October 1989). "Androgens and estrogens in their negative feedback action in the hypothalamo-pituitary-testis axis: site of action and evidence of their interaction". Journal of Steroid Biochemistry. 33 (4B): 757–61. doi:10.1016/0022-4731(89)90488-3. PMID 2689784.
  4. Jonathan S. Berek; Emil Novak (2007). Berek and Novak's Gynecology. Lippincott Williams & Wilkins. p. 1167. ISBN 978-0-7817-6805-4. Retrieved 29 May 2012.
  5. Singh H, Jindal DP, Yadav MR, Kumar M (1991). "Heterosteroids and drug research". Progress in Medicinal Chemistry. 28: 233–300. doi:10.1016/s0079-6468(08)70366-7. ISBN 9780444812759. PMID 1843548.
  6. Bercovici JP (September 1987). "[Progestational contraception]". La Revue du Praticien (in French). 37 (38): 2277–8, 2281–4. PMID 3659794.
  7. Chassard D, Schatz B (2005). "[The antigonadrotropic activity of chlormadinone acetate in reproductive women]". Gynécologie, Obstétrique & Fertilité (in French). 33 (1–2): 29–34. doi:10.1016/j.gyobfe.2004.12.002. PMID 15752663.
  8. George W.A. Milne (8 May 2018). Drugs: Synonyms and Properties: Synonyms and Properties. Taylor & Francis. pp. 674–. ISBN 978-1-351-78989-9.
  9. Bernard V, Young J, Binart N (June 2019). "Prolactin - a pleiotropic factor in health and disease". Nat Rev Endocrinol. 15 (6): 356–365. doi:10.1038/s41574-019-0194-6. PMID 30899100.
  10. Saleem M, Martin H, Coates P (February 2018). "Prolactin Biology and Laboratory Measurement: An Update on Physiology and Current Analytical Issues". Clin Biochem Rev. 39 (1): 3–16. PMC 6069739. PMID 30072818.
  11. Bawor M, Bami H, Dennis BB, Plater C, Worster A, Varenbut M, Daiter J, Marsh DC, Steiner M, Anglin R, Coote M, Pare G, Thabane L, Samaan Z (April 2015). "Testosterone suppression in opioid users: a systematic review and meta-analysis". Drug Alcohol Depend. 149: 1–9. doi:10.1016/j.drugalcdep.2015.01.038. PMID 25702934.
  12. Coluzzi F, Billeci D, Maggi M, Corona G (December 2018). "Testosterone deficiency in non-cancer opioid-treated patients". J Endocrinol Invest. 41 (12): 1377–1388. doi:10.1007/s40618-018-0964-3. PMC 6244554. PMID 30343356.
  13. Smith HS, Elliott JA (July 2012). "Opioid-induced androgen deficiency (OPIAD)". Pain Physician. 15 (3 Suppl): ES145–56. PMID 22786453.
  14. Tenhola H, Sinclair D, Alho H, Lahti T (February 2012). "Effect of opioid antagonists on sex hormone secretion". J Endocrinol Invest. 35 (2): 227–30. doi:10.3275/8181. PMID 22183092.
This article is issued from Wikipedia. The text is licensed under Creative Commons - Attribution - Sharealike. Additional terms may apply for the media files.