madman
Super Moderator
* The emerging indication of gonadotropin therapy for men with androgen-induced infertility is promising. The evidence demonstrates that spermatogenesis can be restored in most affected men with appropriate treatment. Further to this, the literature provides a reassurance to men who require androgens for medical purposes but aspire to preserve their fertility.
Figure 1 The HPG axis in male reproductive physiology. Structurally, FSH and LH are heterodimeric glycoproteins composed of a shared alpha subunit and a hormone-specific beta subunit. The glycoprotein is stabilised by disulfide bonds and varying patterns of glycosylation, with the latter affecting receptor affinity and bioactivity (14). LH acts on the Leydig cells to stimulate testosterone production. This is considered essential for the initiation and maintenance of spermatogenesis in addition to supporting male secondary sexual characteristics and libido. FSH acts on the Sertoli cells to promote the expression of genes require for germ cell support as well as regulating the proliferation and maturation of spermatozoa. The actions of FSH and LH are considered synergistic and thus neither hormone should be considered in isolation in the context of male reproductive endocrinology. This schematic was made using FigureLabs. FSH, follicle-stimulating hormone; GnRH, gonadotropin-releasing hormone; HPG, hypothalamic-pituitary-gonadal; LH, luteinizing hormone.
Conclusions
Gonadotropin therapy occupies an established and important role in the management of male factor infertility. This is particularly the case for men with HH. The evidence supporting its efficacy in this cohort is robust with the majority of men achieving spermatogenesis and substantial proportions achieving pregnancy through natural conception or assisted reproductive technologies. For men with idiopathic infertility, the role of gonadotropins therapy remains less clearly defined. Whilst selected patients may benefit, specifically men with a relative FSH deficiency the evidence does not support the routine use in all men with unexplained oligozoospermia. Further research to identify responsive subgroups and optimise treatment selection is warranted. The emerging indication of gonadotropin therapy for men with androgen-induced infertility is promising. The evidence demonstrates that spermatogenesis can be restored in most affected men with appropriate treatment. Further to this, the literature provides a reassurance to men who require androgens for medical purposes but aspire to preserve their fertility. However, the role of pre-operative gonadotropin therapy for men with NOA prior to a mTESE remains limited. Subsequently, the current EAU guidelines does not endorse their use in this context of male infertility.
The development of pharmacogenomic-guided treatments promises to enhance the efficacy of gonadotropin therapy for male infertility. For clinicians managing male infertility, a thorough understanding of the indications, protocols and expected outcomes of gonadotropin therapy remains essential for providing evidence-based care to affected men and couples.
Figure 1 The HPG axis in male reproductive physiology. Structurally, FSH and LH are heterodimeric glycoproteins composed of a shared alpha subunit and a hormone-specific beta subunit. The glycoprotein is stabilised by disulfide bonds and varying patterns of glycosylation, with the latter affecting receptor affinity and bioactivity (14). LH acts on the Leydig cells to stimulate testosterone production. This is considered essential for the initiation and maintenance of spermatogenesis in addition to supporting male secondary sexual characteristics and libido. FSH acts on the Sertoli cells to promote the expression of genes require for germ cell support as well as regulating the proliferation and maturation of spermatozoa. The actions of FSH and LH are considered synergistic and thus neither hormone should be considered in isolation in the context of male reproductive endocrinology. This schematic was made using FigureLabs. FSH, follicle-stimulating hormone; GnRH, gonadotropin-releasing hormone; HPG, hypothalamic-pituitary-gonadal; LH, luteinizing hormone.
Conclusions
Gonadotropin therapy occupies an established and important role in the management of male factor infertility. This is particularly the case for men with HH. The evidence supporting its efficacy in this cohort is robust with the majority of men achieving spermatogenesis and substantial proportions achieving pregnancy through natural conception or assisted reproductive technologies. For men with idiopathic infertility, the role of gonadotropins therapy remains less clearly defined. Whilst selected patients may benefit, specifically men with a relative FSH deficiency the evidence does not support the routine use in all men with unexplained oligozoospermia. Further research to identify responsive subgroups and optimise treatment selection is warranted. The emerging indication of gonadotropin therapy for men with androgen-induced infertility is promising. The evidence demonstrates that spermatogenesis can be restored in most affected men with appropriate treatment. Further to this, the literature provides a reassurance to men who require androgens for medical purposes but aspire to preserve their fertility. However, the role of pre-operative gonadotropin therapy for men with NOA prior to a mTESE remains limited. Subsequently, the current EAU guidelines does not endorse their use in this context of male infertility.
The development of pharmacogenomic-guided treatments promises to enhance the efficacy of gonadotropin therapy for male infertility. For clinicians managing male infertility, a thorough understanding of the indications, protocols and expected outcomes of gonadotropin therapy remains essential for providing evidence-based care to affected men and couples.
