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Endocrine Abstracts (2019) 63 P308 | DOI: 10.1530/endoabs.63.P308

ECE2019 Poster Presentations Reproductive Endocrinology 1 (40 abstracts)

Reproductive phenotype in 265 men with congenital hypogonadotropic hypogonadism and 531 men with acquired hypogonadotropic hypogonadism: a monocentric comparative study

Luigi Maione 1 , Julie Sarfati 1 , Valérie Bernard 1 , Céline Gonfroy 1 , Christel Jublanc 2 , Sylvie Salenave 1 , Séverine Trabado 3 , Philippe Chanson 1 & Jacques Young 1


1Department of Reproductive Endocrinology, Bicêtre Hospital, University Paris Saclay, Le Kremlin-Bicêtre, France; 2Department of Endocrinology, Pitié-Salpêtrière Hospital, Paris, France; 3Depatment of Hormonology, Bicêtre Hospital, University Paris Saclay, Le Kremlin-Bicêtre, France.


Context: Hypogonadotropic hypogonadism (HH), defined by LH and FSH deficiencies, lead to impairment in testicular growth, testicular hormonal secretions and spermatogenesis. HH can have a prenatal (congenital HH, CHH) or post-natal (acquired HH, HHA) onset. Direct comparison of reproductive phenotypes (RP) between CHH and AHH has not been systematically performed in large series representative of these two populations.

Patients and methods: 60 normal men, 265 men with CHH (Kallmann syndrome 44%; normosmic CHH 56%) and 531 men with AHH from a single center were included. Causes for AHH included pituitary tumors (74.6%), other intracranial tumors (12.7%, (craniopharyngioma 8.3%)), infiltrative diseases (3.5%) and other causes (9.2%). Testicular volumes (TV), serum gonadotropins, sex steroids (testosterone (T) and estradiol (E2)) and testicular peptides (inhibin B (IB), AMH and INSL3) were measured before therapy.

Results: TV was larger in AHH (16.7±6.0 ml) than in CHH (3.1±1.9 ml; P<0.0001). LH, FSH, T and E2 were higher in AHH than in CHH (P<0.0001 for all parameters). IB and INSL3 were also higher in AHH than in CHH men, respectively (126±87 vs 59±55 pg/ml, and 566±372 vs 60±40 pg/ml, P<0.001). Conversely, serum AMH and SHBG levels were lower in AHH than in CHH (246±234 vs 46±38 pmol/l, and 35±22 vs 26±21 nmol/l, respectively, P<0.0001). In the subgroup of AHH patients caused by craniopharyngioma (n=44), TVs and T, E2, IB and INSL3 levels were significantly lower than in patients with AHH caused by pituitary adenomas (P<0.001).

Conclusions: Our data clearly demonstrate that RP is more impaired in CHH than in AHH. Preservation of the gonadotrope/testicular axis (GTA) activation during the fetal, neonatal and pubertal periods in AHH probably could account for these differences. Severity of GTA impairment in patients with craniopharyngioma could be related to the severity of hypothalamic/pituitary lesions caused by these tumors and/or aggressiveness of therapeutic procedures.

Volume 63

21st European Congress of Endocrinology

Lyon, France
18 May 2019 - 21 May 2019

European Society of Endocrinology 

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