Anti-Müllerian hormone as a seminal marker for spermatogenesis in non-obstructive azoospermia

Abstract

Anti-Müllerian hormone (AMH) also known as Müllerian inhibiting substance or factor, is a Sertoli cell-secreted glycoprotein responsible in male embryos for Müllerian duct regression. However, its role in adults remains unknown. AMH seminal concentrations have been evaluated using an enzyme-linked immunoassay in three groups of young men: group 1, fertile donors (n = 18); group 2, obstructive azoospermia (n = 9) after vasectomy or associated with deferent duct agenesia; and group 3, non-obstructive azoospermia with spermatogenesis deficiency and normal karyotype (n = 23). AMH was present in seminal plasma of most fertile donors at concentrations ranging from undetectable (<3.5 pmol/l) up to 543 pmol/l (geometric mean: 153 pmol/l), higher than the serum level (range <3.5 up to 67 pmol/l, geometric mean: 10.7 pmol/l, n = 13). Seminal AMH concentrations were undetectable in all obstructive azoospermic patients, confirming its testicular origin. In non-obstructive azoospermia (group 3), seminal AMH concentration was lower (range <3. 5-68.5 pmol/l, geometric mean: 17 pmol/l) than in fertile donors (P < 0.003) without correlation with plasma follicle stimulating hormone values. In group 3, comparison of seminal AMH concentration and the results of histological analysis of testicular biopsies revealed that undetectable AMH found in 14 cases was associated in 11 of them with lack of spermatozoa, while detectable concentrations of AMH (10-68.5 pmol/l) found in nine cases were associated in seven of them with persistent spermatogenesis. In the adult, AMH is secreted preferentially towards the seminiferous lumen. Although its relationship with spermatogenesis requires further investigation, our results suggest that seminal AMH may represent a non-invasive marker of persistent hypospermatogenesis in cases of non-obstructive azoospermia which may indicate the likely success of testicular spermatozoa recovery before intracytoplasmic sperm injection.

Serum inhibin B and anti-Müllerian hormone are not superior to follicle-stimulating hormone as predictors of the presence of sperm in testicular fine-needle aspiration in men with azoospermia

“…Seminal plasma AMH has been proposed as a noninvasive marker of persistent hypospermatogenesis in cases of nonobstructive azoospermia (24) or oligoasthenoteratozoospermia (31) because the hormone is secreted predominantly into the seminiferous tubules; nevertheless, its use was not widely adopted, possibly as a result of concerns that the presence of seminal proteases could influence AMH levels in the seminal plasma. In two recent studies, no differences were detected in serum (25) or seminal (26) AMH levels between men with azoospermia with or without spermatozoa during a TESE procedure.…”

“…After manual searching of the results, we located 15 studies for INHB (9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23) and three studies for AMH (24)(25)(26) that directly examined the role of these hormones as predictors of sperm retrieval during a testicular biopsy in men with azoospermia. Nevertheless, in none of these studies was there any report on the combined predictive value of serum INHB and AMH levels.…”

Spermatogenesis and spectral echo‐colour Doppler traces from the main testicular artery

“…Serum inhibin B was claimed to be positively related to sperm retrieval on testicular sperm extraction, and to distinguish UOA from OA [25], but these data were not confirmed [26]. Nitric oxide [2,4], transferrin and its soluble receptors [27], and anti-Müllerian hormone [28] have been proposed as markers of spermatogenesis, but the techniques lack sensitivity and especially specificity.…”

Persistence and intergenerational transmission of differentially expressed genes in the testes of intracytoplasmic sperm injection conceived mice

“…The decrease in AMH and ADCYAP1R1 in newborn males reflects the maturation status of Sertoli cells (Rey et al, 1993;Koh and Won, 2006;Boukari et al, 2009). Another study reported that the loss of AMH was associated with non-obstructive azoospermia (Fenichel et al, 1999). RHOX5 is an androgen-dependent protein, which regulates spermatogenesis (Domanskyi et al, 2007;Hu et al, 2007).…”

“…RHOX5 is an androgen-dependent protein, which regulates spermatogenesis (Domanskyi et al, 2007;Hu et al, 2007). Sertoli cells mediate spermatogenesis by nourishing the development of sperm cells, thus the expression levels of AMH, RHOX5, AD-CYAP1R1, and PDGFRA reflect the functions of Sertoli cells (Fenichel et al, 1999;Jamen et al, 2000;Basciani et al, 2002;Denolet et al, 2006). However, if ICSI affects spermatogenesis, why was the downregulation of Pdgfra followed by the increased expression of Rhox5?…”