ECE2023 Eposter Presentations Pituitary and Neuroendocrinology (234 abstracts)
Induction of secondary sexual characteristics with gonadotropins in an adult male with Kallman syndrome
José Vicente Gil Boix 1 , Guillermo Serra Soler 1 , Javier Bodoque Cubas 2 , Meritxell Viñes Raczkowski 1 , Alicia Sanmartín Sánchez 1 , Andreu Campos Peris 1 , Mercedes Noval Font 1 , Santiago Tofé Povedano 1 & Iñaki Argüelles Jiménez 1
1Hospital Universitari Son Espases, Endocrinology and Nutrition, Palma, Spain; 2Hospital Virgen de la Cinta, Endocrinology and Nutrition, Palma, Spain.
Introduction: Hypogonadotropic hypogonadism is the cause of sexual deficiency, sometimes difficult to differentiate from constitutional growth delay (CGD).
Clinical case: A 19-year-old male consulting endocrinology for delayed puberty. Pointed to, at 13 years of age, as having had CGD. His medical report include a viral meningitis at 8 years of age and anosmia since 3 years of age. He expressed lack of sexual desire and concern about the size of his genitals. On physical examination, his weight was 64 kg, height 175 cm and his Tanner stage was II (A2P2G2). Suspecting Kallman syndrome (KS), due to delayed puberty and anosmia, the following tests were requested: bone age, which was 16 years old; bone mineral densitometry that diagnosed osteoporosis (Z-score −3.6 in the spine and −3.1 total femur); Pituitary MRI showing agenesis of bands and olfactory bulbs. Blood tests showed a normal pituitary hormonal profile, except for hypogonadotropic hypogonadism, low Inhibin-B and elevated Anti-Mullerian Hormone. A genetic study showed a mutation in the FGR1 gene (c.560G>A / p.Arg187His) associated with hypogonadism with or without anosmia, of autosomal dominant inheritance. His mother had the same mutation. With the diagnosis of KS, the different therapeutic options for the induction of secondary sexual characteristics were discussed: testosterone analogues or use of gonadotropins, opting for the second to also achieve gonad development. HCG 1000UI twice a week and rFSH 75UI 3 times a week were started, without side effects. After 8 months of treatment, rFSH was increased to 150UI. The clinical and analytical evolution was adequate, presenting a Tanner IV stage at 13 months and his first seminogram reported hypospermia. (Table 1)
| Basal | 3 months | 7 months | 13 months | |
| FSH (mUI/ml) | 0,7 | 1,1 | 2,8 | 4,6 |
| LH (mUI/ml) | 0,22 | <0,12 | <0,12 | <0,12 |
| Testosterone (ng/ml) | 0,13 | 6,7 | 8,8 | 8,6 |
| 17-beta-estradiol (pg/ml) | <24 | 66 | 58 | 59 |
| Inhibin-B (pg/ml) | 58 | 74 | 71 | 90 |
| Anti-Mullerian (ng/ml) | 67,6 | 21,3 | – | 5,57 |
| Testicles (cc) | 3–4 | 5–6 | 6–7 | 12 |
Conclusions: Importance of early diagnosis and treatment of hypogonadotrophic hypogonadism in KS to perform adequate pubertal induction, achieve sexual and bone maturity, and avoid emotional and social problems. Gonadotropin therapy is an effective alternative to testosterone analogues for achieving induction of secondary sexual characteristics, testicular development and fertility.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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