SFEBES2026 Poster Presentations Reproductive Endocrinology (14 abstracts)
Kisspeptin best distinguishes polycystic ovary syndrome (PCOS) from functional hypothalamic amenorrhoea (FHA) in lean women with oligo/amenorrhoea without hyperandrogenism
Kanyada Koysombat 1,2 , Arthur C Yeung 1 , Bijal Patel 1,2 , Maria Phylactou 1,2 , Jovanna Tsoutsouki 1,2 , Megan Young 1 , Sandhi W Nyunt 1,2 , Aaran H Patel 1,2 , Aureliane Pierret 1,2 , Elisabeth Daniels 1,2 , Ambreen Qayum 1,2 , Pei Chia Eng 1,2 , Edouard G Mills 1,2 , Elizaveta Sheremetyeva 1,3 , Simon Hanassab 1,3 , Channa Jayasena 1,2 , Tricia M-M Tan 1,2 , Sophie A Clarke 1,4 , Alexander N Comninos 1,2 , Ali Abbara 1,2 & Waljit S Dhillo 1,2
1Department of Metabolism, Digestion and Reproduction, London, United Kingdom; 2Department of Endocrinology, Imperial College Healthcare NHS Trust, London, United Kingdom; 3Department of Computing, Imperial College London, London, United Kingdom; 4University College Hospitals NHS Foundation Trust, London, United Kingdom
Background: Polycystic ovary syndrome (PCOS) is the commonest endocrine disorder in women, but accurate diagnosis is challenging. To diagnose PCOS, two of three features are required: 1.Hyperandrogenism, 2.Oligomenorrhoea, 3.Polycystic ovarian morphology on ultrasound (PCOM). The second commonest subtype of PCOS is ‘phenotype-D’ comprising of oligomenorrhoea and PCOM. Its presentation overlaps with that of functional hypothalamic amenorrhoea (FHA), who also have amenorrhoea, 45-50% have PCOM, and rarely have hyperandrogenism. Herein, we compared detailed reproductive profiles of lean women (BMI<25 kg/m2) with PCOS phenotype-D (PCOS-D) vs FHA with PCOM (FHA-PCOM).
Methods: Women with FHA-PCOM (n = 16) or PCOS-D (n = 17), aged 18–35yrs, underwent early-follicular (or random if amenorrhoeic) assessment of LH-pulsatility (10-minutely sampling for 8hrs) and of responses to intravenous boluses of kisspeptin and GnRH. PCOM was defined as ≥20follicles-per-ovary, or anti-Müllerian hormone >23pmol/l where ultrasound was unavailable. Data were presented as mean/median and compared by t-test or Mann–Whitney U test as appropriate.
Results: PCOM was present in all women with PCOS-D and in 41% of FHA. The most discriminatory features between PCOS-D and FHA-PCOM were LH-pulse amplitude (1.18 vs 0.45 IU/l; P < 0.0001), fT3 (4.06 vs 3.26 pmol/l; P < 0.0001), follicular-LH (6.47 vs 2.73 IU/l, P = 0.0003), inhibin B (89.3 vs 43.0 ng/l, P = 0.0085), androstenedione (5.61 vs 3.83 nmol/l, P = 0.0120) and oestradiol (115 vs 87 pmol/l, P = 0.0149). FSH responses to GnRH were higher in FHA-PCOM than PCOS-D (6.79 vs 2.26 IU/l; P = 0.003). Gonadotrophin rises after kisspeptin were higher in FHA-PCOM than PCOS-D: LH (13.63 vs 5.00 IU/l; P = 0.0405), and FSH (10.79 vs 1.74 IU/l; P < 0.0001). Peak FSH rises after kisspeptin differentiated FHA-PCOM from PCOS-D with an auROC of 0.92; p<0.0001.
Conclusion: Kisspeptin challenge test was the most reliable discriminator to distinguish between FHA-PCOM and PCOS-D and can improve the accuracy of diagnosis in challenging cases.
Volume 117
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Endocrine Abstracts
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