Sertoli cell markers in the diagnosis of paediatric male hypogonadism

2012 ◽  
Vol 25 (1-2) ◽  
Author(s):  
Romina P. Grinspon ◽  
Nazareth Loreti ◽  
Débora Braslavsky ◽  
Patricia Bedecarrás ◽  
Verónica Ambao ◽  
...  
Keyword(s):  
Sertoli Cell ◽  
Male Hypogonadism ◽  
Cell Markers

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

2018 ◽  
Vol 14 (2) ◽  
pp. 67 ◽  
Author(s):  
Romina P Grinspon ◽  
Mariela Urrutia ◽  
Rodolfo A Rey
Keyword(s):  
Sertoli Cell ◽  
Physiological State ◽  
Pubertal Development ◽  
Follicle Stimulating Hormone ◽  
Early Infancy ◽  
Inhibin B ◽  
Clear Understanding ◽  
Male Hypogonadism ◽  
Cell Markers ◽  
Stimulating Hormone

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.

scholarly journals New perspectives in the diagnosis of pediatric male hypogonadism: the importance of AMH as a Sertoli cell marker

2011 ◽  
Vol 55 (8) ◽  
pp. 512-519 ◽  
Author(s):  
Romina P. Grinspon ◽  
Rodolfo A. Rey
Keyword(s):  
Sertoli Cell ◽  
Cell Function ◽  
Cell Activity ◽  
Tanner Stage ◽  
Inhibitory Effect ◽  
Male Hypogonadism ◽  
Fetal Life ◽  
Infancy And Childhood ◽  
Stimulation Tests ◽  
Enzyme Defects

Sertoli cells are the most active cell population in the testis during infancy and childhood. In these periods of life, hypogonadism can only be evidenced without stimulation tests, if Sertoli cell function is assessed. AMH is a useful marker of prepubertal Sertoli cell activity and number. Serum AMH is high from fetal life until mid-puberty. Testicular AMH production increases in response to FSH and is potently inhibited by androgens. Serum AMH is undetectable in anorchidic patients. In primary or central hypogonadism affecting the whole gonad and established in fetal life or childhood, serum AMH is low. Conversely, when hypogonadism affects only Leydig cells (e.g. LHβ mutations, LH/CG receptor or steroidogenic enzyme defects), serum AMH is normal or high. In pubertal males with central hypogonadism, AMH is low for Tanner stage (reflecting lack of FSH stimulus), but high for the age (indicating lack of testosterone inhibitory effect). Treatment with FSH provokes an increase in serum AMH, whereas hCG administration increases testosterone levels, which downregulate AMH. In conclusion, assessment of serum AMH is helpful to evaluate gonadal function, without the need for stimulation tests, and guides etiological diagnosis of pediatric male hypogonadism. Furthermore, serum AMH is an excellent marker of FSH and androgen action on the testis.

Identification of Sertoli cell markers in men with non-obstructive azoospermia

2015 ◽  
Vol 104 (3) ◽  
pp. e289
Author(s):  
A. Agarwal ◽  
R. Sharma ◽  
Z. Cui ◽  
E.S. Sabanegh
Keyword(s):  
Sertoli Cell ◽  
Obstructive Azoospermia ◽  
Cell Markers

scholarly journals Prepubertal gynecomastia in Peutz-Jeghers syndrome: incomplete penetrance in a familial case and management with an aromatase inhibitor

2006 ◽  
Vol 154 (2) ◽  
pp. 221-227 ◽  
Author(s):  
Hervé Lefevre ◽  
Claire Bouvattier ◽  
Najiba Lahlou ◽  
Catherine Adamsbaum ◽  
Pierre Bougnères ◽  
...  
Keyword(s):  
Aromatase Inhibitor ◽  
Sertoli Cell ◽  
Tertiary Care ◽  
Incomplete Penetrance ◽  
Cell Markers ◽  
Estrogen Production ◽  
Aromatase Inhibitor Treatment ◽  
Peutz Jeghers Syndrome ◽  
Estradiol Levels ◽  
Inhibitor Treatment

Background: Peutz-Jeghers syndrome (PJS) is a rare autosomal-dominant disorder characterized by multiple gastrointestinal hamartomatous polyps, mucocutaneous pigmentation and increased predisposition to various neoplasms. Endocrine manifestations in PJS include gynecomastia due to calcified Sertoli cell testicular tumors usually referred to as large-cell calcifying Sertoli cell tumors (LSCT). Objective: To evaluate the value of endocrine markers and aromatase inhibitor treatment in children with PJS and LSCT. Design and setting: Familial cases, followed in a tertiary care center. Patients: Two male siblings aged 7 and 9 years with PJS and LSCT. Intervention: Third generation aromatase inhibitor (anastrozole) in one of the patients. Main outcome measures: Longitudinal measurements of sex-steroids, gonadotropins, Sertoli cell markers and auxological evaluation. Results: The two male siblings with PJS had similar bilateral multifocal testicular calcifications and biochemical evidence of Sertoli cell dysfunction manifested by elevated plasma inhibin-α levels. Only one sibling had gynecomastia. Estradiol levels were normal in both. During treatment with anastrozole, estradiol levels, growth and skeletal maturation, as well as Sertoli cell markers (inhibin B, inhibin-α and anti-Mullerian hormone) decreased. Conclusions: Inhibin-α may be considered as a marker for LSCT in children with PJS, pointing to a specific defect in inhibin regulation in this condition. Moreover, the decrease in Sertoli cell markers during aromatase inhibitor treatment suggests that increased estrogen production is a primary event regulating downstream production of Sertoli cell peptides. Anastrozole is efficient in controlling the clinical features of the disease and should be proposed as an alternative to bilateral orchidectomy, which is often performed in this condition.

Anti-Mullerian Hormone and Inhibin B Levels in Obese Boys; Relations with Cardiovascular Risk Factors

2018 ◽  
Vol 126 (08) ◽  
pp. 528-533 ◽  
Author(s):  
Muammer Buyukinan ◽  
Muge Atar ◽  
Ozgur Pirgon ◽  
Huseyin Kurku ◽  
S. Erdem ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cardiovascular Risk ◽  
Cardiovascular Risk Factors ◽  
Sertoli Cell ◽  
Inhibin B ◽  
Obese Group ◽  
Total Testosterone ◽  
Cell Markers ◽  
Insulin Levels ◽  
Pubertal Boys

Abstract Objective Obesity may reduce sertoli cell functions in men. The aim of the study was to investigate antimullerian hormone (AMH) and inhibin B levels (sertoli cell markers) in obese boys and their relations to cardiovascular risk factors such as insulin sensitivity index, aortic intima media thickness (aIMT) and high sensitive c-reactive protein (hsCRP). Patients, methods 121 obese and 38 healthy lean adolescents were included in the study. Serum AMH, inhibin B, gonadotropins, total testosterone, lipids, hsCRP, glucose and insulin levels were detected and analyzed. Insulin resistance was analyzed using the homeostasis model assessment (HOMA-IR). aIMT was measured by high-resolution B-mode ultrasonography. Results Serum AMH, inhibin B and total testosterone levels were lower in the obese adolescents (p=0.01, p=0.009 and p=0.002, respectively). aIMT measurements (p<0.001, 0.63±0.09 and 0.47±0.06 mm, respectively) and hsCRP levels (p<0.001, 2.5±0.4 and 0.66±0.69 mg/L, respectively) were significantly increased in the obese group. Obese with IR group had decreased AMH levels (p=0.02, 53.0±20.5 and 66.7±19.5 ng/mL, respectively) and increased triglycerides, HOMA-IR, aIMT measurements than non-IR obese group. AMH levels were correlated negatively with body mass index (r:−0.108, p=0.03), HOMA-IR (r:−0.358, p=0.003) and fasting insulin levels (r:−0.389, p=0.001) in obese group with IR. Conclusion We found that concentrations of both sertoli cell markers (AMH and inhibin B) were significantly lower in obese pubertal boys especially in obese with IR. Obesity and IR might be important factors for the sertoli cell impairment in pubertal boys.

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