Endocrine Responses to Triptorelin in Healthy Women, Women With Polycystic Ovary Syndrome, and Women With Hypothalamic Amenorrhea.
Abbara. Ali A; Phylactou. Maria M; Eng. Pei Chia PC; Clarke. Sophie A SA; Pham. Toan D TD; Ho. Tuong M TM; Ng. Kah Yan KY; Mills. Edouard G EG; Purugganan. Kate K; Hunjan. Tia T; Salim. Rehan R; Comninos. Alexander N AN; Vuong. Lan N LN; Dhillo. Waljit S WS
Key Findings
- Triporelin causes a similar peak LH increase in healthy, PCOS, and hypothalamic amenorrhea women (ā40ā52āÆIU/L).
- The FSH rise after triptorelin is significantly blunted in women with PCOS or polycystic ovary morphology compared to healthy or HA women.
- Higher serum AMH levels are linked to a reduced FSH response to triptorelin, regardless of ovarian stimulation.
Practical Outcomes
- If youāre using GnRH agonists like triptorelin to manipulate hormone levels, expect a robust LH spike but a modest FSH boost in PCOS or polycystic ovary cases. This means standard doses may not be enough to raise FSH for protocols that need it (e.g., certain fertility or antiāaging regimens), and you might need higher doses or alternative agents. AMH testing can help predict how strong the FSH response will be.
Summary
The study shows that a single dose of the hormoneāblocking peptide triptorelin triggers a strong LH surge in all women, but the rise in FSH is much weaker in women with PCOS or polycystic ovaries. Higher AMH levels (a marker of ovarian reserve) predict an even smaller FSH response, whether the ovaries are stimulated or not.
Abstract
Limited data exist regarding whether the endocrine response to the gonadotropin-releasing hormone receptor agonist (GnRHa) triptorelin differs in women with polycystic ovary syndrome (PCOS) compared with healthy women or those with hypothalamic amenorrhea (HA). We compared the gonadotropin response to triptorelin in healthy women, women with PCOS, or those with HA without ovarian stimulation, and in women with or without polycystic ovaries undergoing oocyte donation cycles after ovarian stimulation. The change in serum gonadotropin levels was determined in (1) a prospective single-blinded placebo-controlled study to determine the endocrine profile of triptorelin (0.2 mg) or saline-placebo in healthy women, women with PCOS, and those with HA, without ovarian stimulation; and (2) a retrospective analysis from a dose-finding randomized controlled trial of triptorelin (0.2-0.4 mg) in oocyte donation cycles after ovarian stimulation. In Study 1, triptorelin induced an increase in serum luteinizing hormone (LH) of similar amplitude in all women (mean peak LH: healthy, 52.3; PCOS, 46.2; HA, 41.3 IU/L). The AUC of change in serum follicle-stimulating hormone (FSH) was attenuated in women with PCOS compared with healthy women and women with HA (median AUC of change in serum FSH: PCOS, 127.2; healthy, 253.8; HA, 326.7 IU.h/L; P = 0.0005). In Study 2, FSH levels 4 hours after triptorelin were reduced in women with at least one polycystic morphology ovary (n = 60) vs normal morphology ovaries (n = 91) (34.0 vs 42.3 IU/L; P = 0.0003). Serum anti-Müllerian hormone (AMH) was negatively associated with the increase in FSH after triptorelin, both with and without ovarian stimulation. FSH response to triptorelin was attenuated in women with polycystic ovaries, both with and without ovarian stimulation, and was negatively related to AMH levels.
Study Information
pubmed
2023
2023-06-16T00:00:00.000Z
10.1210/clinem/dgad026
3