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      Biomarkers of male hypogonadism in childhood and adolescence

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      Publication date (Electronic, collection):
      Publication date (Electronic, pub):
      Journal: Advances in Laboratory Medicine
      Publisher: De Gruyter
      Keywords: ambiguous genitalia, cryptorchidism, gonadal dysgenesis, hypergonadotropic hypogonadism, hypogonadotropic hypogonadism, micropenis, sexual development disorders, testicle

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          Abstract

          Objectives

          The objective of this review was to characterize the use of biomarkers of male hypogonadism in childhood and adolescence.

          Contents

          The hypothalamic-pituitary-gonadal (HPG) axis is active during fetal life and over the first months of postnatal life. The pituitary gland secretes follicle stimulating hormone (FSH) and luteinizing hormone (LH), whereas the testes induce Leydig cells to produce testosterone and insulin-like factor 3 (INSL), and drive Sertoli cells to secrete anti-Müllerian hormone (AMH) and inhibin B. During childhood, serum levels of gonadotropins, testosterone and insulin-like 3 (INSL3) decline to undetectable levels, whereas levels of AMH and inhibin B remain high. During puberty, the production of gonadotropins, testosterone, and INSL3 is reactivated, inhibin B increases, and AMH decreases as a sign of Sertoli cell maturation.

          Summary and outlook

          Based on our knowledge of the developmental physiology of the HPG axis, these biomarkers can be used in clinical practice to interpret the physiopathology of hypogonadism. Additionally, these markers can have diagnostic value in different forms of hypogonadism that may appear during childhood and adolescence.

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          Most cited references85

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          Variations in the Pattern of Pubertal Changes in Boys

          W. Marshall, J M Tanner (1970)
          Article 0 comments Cited 365 times – based on 0 reviews     Review now
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            Klinefelter's syndrome.

            Fabio Lanfranco, Axel Kamischke, Michael Zitzmann … (2015)
            Klinefelter's syndrome is the most common genetic cause of human male infertility, but many cases remain undiagnosed because of substantial variation in clinical presentation and insufficient professional awareness of the syndrome itself. Early recognition and hormonal treatment of the disorder can substantially improve quality of life and prevent serious consequences. Testosterone replacement corrects symptoms of androgen deficiency but has no positive effect on infertility. However, nowadays patients with Klinefelter's syndrome, including the non-mosaic type, need no longer be considered irrevocably infertile, because intracytoplasmic sperm injection offers an opportunity for procreation even when there are no spermatozoa in the ejaculate. In a substantial number of azoospermic patients, spermatozoa can be extracted from testicular biopsy samples, and pregnancies and livebirths have been achieved. The frequency of sex chromosomal hyperploidy and autosomal aneuploidies is higher in spermatozoa from patients with Klinefelter's syndrome than in those from normal men. Thus, chromosomal errors might in some cases be transmitted to the offspring of men with this syndrome. The genetic implications of the fertilisation procedures, including pretransfer or prenatal genetic assessment, must be explained to patients and their partners.
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              Activation of the Hypothalamic-Pituitary-Gonadal Axis in Infancy: Minipuberty

              Tanja Kuiri-Hänninen, Ulla Sankilampi, Leo Dunkel (2014)
              The hypothalamic-pituitary-gonadal (HPG) axis is active in the midgestational foetus but silenced towards term because of the negative feedback effects mediated by the placental hormones. This restraint is removed at birth, leading to reactivation of the axis and an increase in gonadotrophin levels. Gonadotrophin levels are high during the first 3 months of life but decrease towards the age of 6 months except for FSH levels in girls that remain elevated until 3-4 years of age. After this, the HPG axis remains quiescent until puberty. The postnatal gonadotrophin surge results in gonadal activation in both sexes. In boys, testosterone levels rise to a peak at 1-3 months of age and then decline following LH levels. Postnatal HPG axis activation is associated with penile and testicular growth and therefore considered important for the development of male genitalia. In girls, elevated gonadotrophin levels result in the maturation of ovarian follicles and in an increase in oestradiol levels. Biological significance and possible long-term consequences of this minipuberty remain elusive, as do the mechanisms that silence the HPG axis until puberty. However, the first months of life provide a ‘window of opportunity' for functional studies of the HPG axis prior to pubertal development.
              Article 0 comments Cited 119 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Rodolfo A. Rey
                Journal
                Journal ID (nlm-ta): Adv Lab Med
                Journal ID (iso-abbrev): Adv Lab Med
                Journal ID (publisher-id): almed
                Journal ID (doi): almed
                Title: Advances in Laboratory Medicine
                Publisher: De Gruyter
                ISSN (Electronic): 2628-491X
                Publication date (Electronic, collection): June 2020
                Publication date (Electronic, pub): 21 April 2020
                Volume: 1
                Issue: 2
                Electronic Location Identifier: 20200024
                Affiliations
                deptCentro de Investigaciones Endocrinológicas “Dr. César Bergadá” (CEDIE) , CONICET-FEI- División de Endocrinología , Hospital de Niños Ricardo Gutiérrez , Gallo 1330, C1425EFD, Buenos Aires, Argentina
                deptDepartamento de Histología, Biología Celular, Embriología y Genética, Facultad de Medicina , univUniversidad de Buenos Aires , C1121ABG, Buenos Aires, Argentina
                Author notes
                Corresponding author: Dr. Rodolfo A. Rey, deptCentro de Investigaciones Endocrinológicas “Dr. César Bergadá” (CEDIE) , CONICET-FEI- División de Endocrinología , univHospital de Niños Ricardo Gutiérrez , Gallo 1330, C1425EFD, Buenos Aires, Argentina; and deptDepartamento de Histología, Biología Celular, Embriología y Genética, Facultad de Medicina , univUniversidad de Buenos Aires , C1121ABG, Buenos Aires, Argentina, Phone: +54 11 4963 5931; fax: +54 11 4963 5930, E-mail: rodolforey@ 123456cedie.org.ar
                Article
                Publisher ID: almed-2020-0024
                DOI: 10.1515/almed-2020-0024
                PMC ID: 10159267
                SO-VID: d9ae34c9-9b4e-4048-bf18-704778b8c9f3
                Copyright © © 2020 Rodolfo A. Rey, published by De Gruyter
                License:

                This work is licensed under the Creative Commons Attribution 4.0 International License.

                History
                Date received : 22 December 2019
                Date accepted : 19 January 2020
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                Page count
                Figures: 02, Tables: 02, References: 85, Pages: 13
                Categories
                Subject: Review

                Keywords: ambiguous genitalia,cryptorchidism,gonadal dysgenesis,hypergonadotropic hypogonadism,hypogonadotropic hypogonadism,micropenis,sexual development disorders,testicle
                Data availability:
                Keywords: ambiguous genitalia, cryptorchidism, gonadal dysgenesis, hypergonadotropic hypogonadism, hypogonadotropic hypogonadism, micropenis, sexual development disorders, testicle

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