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      Call for Papers: Epidemiology and Health Impacts of Neuroendocrine Tumors

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      About Neuroendocrinology: 3.2 Impact Factor I 8.3 CiteScore I 1.009 Scimago Journal & Country Rank (SJR)

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      Hypogonadotropic Hypogonadism in Infants with Congenital Hypopituitarism: A Challenge to Diagnose at an Early Stage.

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          Abstract

          Combined pituitary hormone deficiency (CPHD) presents a wide spectrum of pituitary gland disorders. The postnatal gonadotropic surge provides a useful period to explore the gonadotropic axis for assessing the presence of congenital hypogonadotropic hypogonadism (CHH).

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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.
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            Changes in anti-Müllerian hormone (AMH) throughout the life span: a population-based study of 1027 healthy males from birth (cord blood) to the age of 69 years.

            L Aksglaede, K. Sørensen, M. Boas … (2010)
            Anti-Müllerian hormone (AMH), which is secreted by immature Sertoli cells, triggers the involution of the fetal Müllerian ducts. AMH is a testis-specific marker used for diagnosis in infants with ambiguous genitalia or bilateral cryptorchidism. The aim of the study was to describe the ontogeny of AMH secretion through life in healthy males. This was a population-based study of healthy volunteers. PARTICIPANTS included 1027 healthy males from birth (cord blood) to 69 yr. A subgroup was followed up longitudinally through the infantile minipuberty [(in cord blood, and at 3 and 12 months), n=55] and another group through puberty [(biannual measurements), n=83]. Serum AMH was determined by a sensitive immunoassay. Serum testosterone, LH, and FSH were measured, and pubertal staging was performed in boys aged 6 to 20 yr (n=616). Serum AMH was above the detection limit in all samples with a marked variation according to age and pubertal status. The median AMH level in cord blood was 148 pmol/liter and increased significantly to the highest observed levels at 3 months (P<0.0001). AMH declined at 12 months (P<0.0001) and remained at a relatively stable level throughout childhood until puberty, when AMH declined progressively with adults exhibiting 3-4% of infant levels. Based on this extensive data set, we found detectable AMH serum levels at all ages, with the highest measured levels during infancy. At the time of puberty, AMH concentrations declined and remained relatively stable throughout adulthood. The potential physiological role of AMH and clinical applicability of AMH measurements remain to be determined.
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              A window of opportunity: the diagnosis of gonadotropin deficiency in the male infant.

              Melvin M. Grumbach (2005)
              A common cause of micropenis is congenital hypogonadotropic hypogonadism, whether isolated or associated with multiple pituitary hormone deficiencies. The postnatal surge in FSH, LH, and testosterone in the male infant as a consequence of the continued function of the fetal GnRH pulse generator provides a 6-month window of opportunity to establish the diagnosis of hypogonadotropic hypogonadism and alert the clinician to the possibility of its association with multiple pituitary hormone deficiencies. When ACTH or GH deficiency or both deficiencies are present, hypoglycemia and cortisol deficiency can lead to neonatal and infantile death or increased morbidity. Establishing the diagnosis of hypogonadotropic hypogonadism in infancy preempts the uncertainties and delays in distinguishing constitutional delay in puberty from hypogonadotropic hypogonadism. Accordingly, hormone replacement therapy can be initiated at the normal age of pubertal onset. The ontogenesis of infantile testicular function, including the possible significance of the infantile surge in gonadotropins and testosterone, is reviewed. The molecular basis for certain developmental disorders associated with hypogonadotropic hypogonadism and micropenis is considered and the management and treatment of congenital hypopituitarism discussed.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): Horm Res Paediatr
                Title: Hormone research in paediatrics
                Publisher: S. Karger AG
                ISSN (Electronic): 1663-2826
                ISSN (Print): 1663-2818
                Publication date (Electronic): 2015
                Volume: 84
                Issue: 5
                Affiliations
                [1 ] Centro de Investigaciones Endocrinolx00F3;gicas x2018;Dr. Cx00E9;sar Bergadx00E1;' (CEDIE), Divisix00F3;n de Endocrinologx00ED;a, Hospital de Nix00F1;os Ricardo Gutix00E9;rrez, Buenos Aires, Argentina.
                Article
                Publisher Item ID: 000439051
                DOI: 10.1159/000439051
                PubMed ID: 26355950
                SO-VID: df659f32-ac63-45cf-ac8d-3dc57d76f0ec
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