Fertility induction in hypogonadotropic hypogonadal men

Abstract

Men with hypogonadotropic hypogonadism (HH) are typically azoospermic, and yet HH is one of the few treatable forms of male infertility. Sperm induction protocols using gonadotrophins aim to replicate the natural endocrine control of spermatogenesis. Previously virilised men with adult-onset HH and normal testicular volume respond well to monotherapy in which human chorionic gonadotrophin (hCG) acts as a long-acting LH-analogue stimulating spermatogenesis. However, this approach is rarely successful for men with congenital HH (CHH) (eg, Kallmann syndrome), for whom combined gonadotrophin therapy (hCG + follicle-stimulating hormone [FSH]) is an absolute requirement to maximise fertility potential. Key baseline predictors of successful spermatogenesis-induction include prior spontaneous testicular development (ie, testicular volume [TV] > 4 mL), serum inhibin B (I ) concentration >60 pg/mL and no history of maldescended testes (cryptorchidism).

Late Effects of Parasellar Lesion Treatment: Hypogonadism and Infertility

“…The addition of FSH to hCG was associated with a better outcome, with similar results achieved for different FSH preparations (urinary derived, highly purified or recombinant) [69]. Other baseline predictors of successful spermatogenesis induction are a testicular volume >4 mL, a serum inhibin B level >60 pg/mL and the absence of previous cryptorchidism [70]. It should also be borne in mind that the outcome of gonadotropin therapy does not seem to be affected by previous testosterone replacement therapy.…”

Comparative Study of the Steroidogenic Effects of Human Chorionic Gonadotropin and Thieno[2,3-D]pyrimidine-Based Allosteric Agonist of Luteinizing Hormone Receptor in Young Adult, Aging and Diabetic Male Rats

“…One of the pharmacological approaches for correcting androgen deficiency and impaired spermatogenesis in male patients with hypogonadotrophic hypogonadism and infertility is the use of gonadotropins, such as luteinizing hormone (LH) and its structural and functional homologue, human chorionic gonadotropin (hCG) [ 1 , 2 , 3 , 4 ]. In Leydig cells of the testes, LH and hCG with high affinity bind to a large extracellular domain (ectodomain) of LH/hCG receptor (LHCGR) belonging to the G protein-coupled receptors (GPCRs) superfamily, thereby causing the activation of heterotrimeric G-proteins (G s , G q/11 ) and β-arrestins [ 5 , 6 , 7 , 8 ].…”

Exogenous Gonadotrophin Stimulation Induces Partial Maturation of Human Sertoli Cells in a Testicular Xenotransplantation Model for Fertility Preservation

“…Moreover, the (i) identification of additional factors that induce complete maturation of Sertoli cells, (ii) the use of regimens that more closely resemble the sequential hormonal profile of the infantile, prepubertal, and pubertal period, and (iii) the investigation of the synergic action of hCG and follicle-stimulating hormone (FSH) may potentially induce somatic and germ cell differentiation. In clinical practice, hCG monotherapy, combined hCG and FSH therapy, and sequential gonadotrophin therapy (FSH pre-treatment followed by hCG and FSH) are considered as effective fertility-inducing treatments for gonadotrophin-deficient men [44][45][46].…”