Androgens During Infancy, Childhood, and Adolescence: Physiology and Use in Clinical Practice

Mason, Kelly; Schoelwer, Melissa J.; Rogol, Alan D.

doi:10.1210/endrev/bnaa003

Cited by 53 publications

(50 citation statements)

References 317 publications

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“…The sources of androgen are the adrenal glands, the gonads (ovaries, testes), the brain, and the placenta in pregnant women. Androgens exert their action through intracellular receptors [ 3 ]. The adrenal glands are the source of DHEA and DHEA-S, which are relatively weak androgens.…”

Section: Endocrine Regulations Of the Hair Folliclementioning

confidence: 99%

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Hormonal Effects on Hair Follicles

Grymowicz

Rudnicka

Podfigurna

et al. 2020

IJMS

111

109

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The hair cycle and hair follicle structure are highly affected by various hormones. Androgens—such as testosterone (T); dihydrotestosterone (DHT); and their prohormones, dehydroepiandrosterone sulfate (DHEAS) and androstendione (A)—are the key factors in terminal hair growth. They act on sex-specific areas of the body, converting small, straight, fair vellus hairs into larger darker terminal hairs. They bind to intracellular androgen receptors in the dermal papilla cells of the hair follicle. The majority of hair follicles also require the intracellular enzyme 5-alpha reductase to convert testosterone into DHT. Apart from androgens, the role of other hormones is also currently being researched—e.g., estradiol can significantly alter the hair follicle growth and cycle by binding to estrogen receptors and influencing aromatase activity, which is responsible for converting androgen into estrogen (E2). Progesterone, at the level of the hair follicle, decreases the conversion of testosterone into DHT. The influence of prolactin (PRL) on hair growth has also been intensively investigated, and PRL and PRL receptors were detected in human scalp skin. Our review includes results from many analyses and provides a comprehensive up-to-date understanding of the subject of the effects of hormonal changes on the hair follicle.

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Section: Endocrine Regulations Of the Hair Folliclementioning

confidence: 99%

“…This review provides a comprehensive up-to-date understanding of the subject of the hormonal effects on the hair follicle. This review also highlights the significant progress in research that has been made in recent years on the effects of hormonal changes on hair at different stages of the life of women [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

Hormonal Effects on Hair Follicles

Grymowicz

Rudnicka

Podfigurna

et al. 2020

IJMS

111

109

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“…Regarding the reproductive phenotype, male KS patients with ANOS1 variants display a complete penetrance of CHH and their pre- and postnatal gonadotropin deficit is severe with a high frequency of micropenis, cryptorchidism and complete absence of gonadal development ( 15 , 16 ).…”

Section: Review Of the Literaturementioning

confidence: 99%

“…Current research regarding the pathophysiology of CHH provides evidence that genetic abnormalities play a key role in the development of the disease and is estimated that a genetic cause is apparent in almost 50% of CHH cases ( 1 , 6 ). Up-to-date there have been reported more than 60 putative loci for CHH, 17 of which have been linked with KS ( 1 , 6 , 13 – 16 ).…”

Section: Introductionmentioning

confidence: 99%

GnRH Deficient Patients With Congenital Hypogonadotropic Hypogonadism: Novel Genetic Findings in ANOS1, RNF216, WDR11, FGFR1, CHD7, and POLR3A Genes in a Case Series and Review of the Literature

et al. 2020

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Background: Congenital hypogonadotropic hypogonadism (CHH) is a rare genetic disease caused by Gonadotropin-Releasing Hormone (GnRH) deficiency. So far a limited number of variants in several genes have been associated with the pathogenesis of the disease. In this original research and review manuscript the retrospective analysis of known variants in ANOS1 ( KAL1), RNF216, WDR11, FGFR1, CHD7 , and POLR3A genes is described, along with novel variants identified in patients with CHH by the present study. Methods: Seven GnRH deficient unrelated Cypriot patients underwent whole exome sequencing (WES) by Next Generation Sequencing (NGS). The identified novel variants were initially examined by in silico computational algorithms and structural analysis of their predicted pathogenicity at the protein level was confirmed. Results: In four non-related GnRH males, a novel X-linked pathogenic variant in ANOS1 gene, two novel autosomal dominant (AD) probably pathogenic variants in WDR11 and FGFR1 genes and one rare AD probably pathogenic variant in CHD7 gene were identified. A rare autosomal recessive (AR) variant in the SRA1 gene was identified in homozygosity in a female patient, whilst two other male patients were also, respectively, found to carry novel or previously reported rare pathogenic variants in more than one genes; FGFR1 / POLR3A and SRA1/RNF216 . Conclusion: This report embraces the description of novel and previously reported rare pathogenic variants in a series of genes known to be implicated in the biological development of CHH. Notably, patients with CHH can harbor pathogenic rare variants in more than one gene which raises the hypothesis of locus-locus interactions providing evidence for digenic inheritance. The identification of such aberrations by NGS can be very informative for the management and future planning of these patients.

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“…Testosterone and estradiol play critical, wide-ranging roles during development, before and beyond the traditional notion of a reproductive lifespan. In fetal life, testosterone is crucial for sexual differentiation and the proper development of male external genitalia ( 1 ). During late pregnancy and the first 6 months of neonatal life (i.e., minipuberty), testosterone and follicle-stimulating hormone play a major role in priming the male reproductive axis for fertility potential in later life ( 2 ).…”

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confidence: 99%