Male Central Hypogonadism in Paediatrics – the Relevance of Follicle-stimulating Hormone and Sertoli Cell Markers

Abstract

The definition of male hypogonadism, used in adult endocrinology, is not fully applicable to paediatrics. A clear understanding of the developmental physiology of the hypothalamic-pituitary-testicular axis is essential for the comprehension of the pathogenesis of hypogonadal states in boys and for the establishment of adequate definitions and classifications in paediatric ages. This is particularly true for central hypogonadism, usually called hypogonadotropic in adults. Because childhood is a period characterised by a physiological state of low gonadotropin and testosterone production, these markers of hypogonadism, typically used in adult endocrinology, are uninformative in the child. This review is focused on the physiological importance of prepubertal Sertoli cell markers – anti-Müllerian hormone (AMH) and inhibin B – and of the intratesticular actions of follicle-stimulating hormone (FSH) and testosterone during early infancy and the first stages of pubertal development. We discuss the role of FSH in regulating the proliferation of Sertoli cells – the main determinant of prepubertal testicular volume – and the secretion of AMH and inhibin B. We also address how intratesticular testosterone concentrations have different effects on the seminiferous tubule function in early infancy and during pubertal development.

Correlation of anti‐Mullerian hormone with humanchorionic gonadotropin test in the evaluation of testicular function of children with 46 XY male hypogonadism: Use of anti‐Mullerian hormone as abiomarker

“…The mean increase in testosterone levels was 302.12 AE 180. 23 Cut-off values calculated for AMH and hCG responses in the groups are provided in Table 3. Patients with GD had lower AMH values than patients with AIS (P < 0.001).…”

“…It is also reported that the serum AMH values are useful in the differential diagnosis of HHG and CDP . While AMH is low in HHG patients due to the lack of FSH stimulation, it is normal in delayed puberty patients.…”

“…It is also reported that the serum AMH values are useful in the differential diagnosis of HHG and CDP. 6,23 While AMH is low in HHG patients due to the lack of FSH stimulation, it is normal in delayed puberty patients. In our study, the mean AMH values were 20.12 AE 9.59 and 100.25 AE 26.13 in HHG and CDP patients, respectively.…”

Biomarkers of male hypogonadism in childhood and adolescence

“…Although basal AMH production is not dependent on gonadotropins [32], FSH stimulates testicular AMH secretion [26,[33][34][35]. In turn, increased testosterone concentrations inhibit AMH secretion [18,36].…”

Anti-Müllerian hormone and letrozole levels in boys with constitutional delay of growth and puberty treated with letrozole or testosterone

“…Another intriguing finding was that the Lz-treated boys had larger testes 6 months after the treatment than those who received low-dose T, although the iB levels did not differ at that time point (Varimo et al, 2019). To better understand the putative effects of Lz and low-dose T on the developing seminiferous epithelium, we now report serum levels of anti-Müllerian hormone (AMH), which is another Sertoli cell product and a suggested surrogate marker for Sertoli cell number and function (Grinspon et al, 2018). It is known that FSH stimulates AMH secretion in prepuberty (Lukas-Croisier et al, 2003;Young et al, 2005), and that the paracrine action of T suppresses AMH levels in early puberty (Rey, 1998).…”