Introduction

Testosterone is the principal androgen responsible for male sex differentiation, development of male secondary sexual characteristics, spermatogenesis, libido, and overall male fertility.[1]  Reproductive structures in XX and XY embryos are indistinguishable during the first 6 weeks of embryonic development. Influence begins in fetal life.

Around the 7th week of gestation, the SRY gene on the Y chromosome triggers the differentiation of the bipotential gonad into testes. Sertoli cells organize within the developing testis cords and later form the seminiferous tubules. Sertoli cells secrete Müllerian-inhibiting substance, also called "anti-Müllerian hormone" (AMH), which causes regression of Müllerian structures—the uterus, fallopian tubes, and upper vagina.[2] Fetal Leydig cells migrate into the developing testes and begin testosterone production. Testosterone stabilizes and promotes differentiation of the Wolffian (mesonephric) ducts into the epididymis, vas deferens, and seminal vesicles. In peripheral tissues, testosterone is converted by 5α-reductase into dihydrotestosterone (DHT), which drives the formation of the prostate, scrotum, and penis and contributes to the development of benign prostatic hyperplasia in adult men.[3][4][5]

Testosterone plays a critical role in testicular descent through the inguinal canal, particularly during the final months of gestation.[6] In embryos lacking a Y chromosome and, consequently, the SRY gene, gonads differentiate into ovaries. Fetal ovaries produce minimal amounts of testosterone and AMH. As a result, Wolffian ducts regress, and Müllerian ducts develop normally into the female internal reproductive tract.

Function

Testosterone drives primary male sexual development, including testicular descent, enlargement of the penis and testes, initiation and maintenance of spermatogenesis, growth of facial hair, and deepening of the voice. This hormone also enhances bone density, boosts energy levels, supports cognitive function, and improves mood. Additional effects include increased muscle mass, regulation of body fat distribution, and stimulation of libido in both men and women.[7][8][9][10][11][12][13][14][15][16][17] Testosterone also supports normal erectile function in men.[18][19][20][21][22]

Testicular descent occurs in 2 phases: a transabdominal phase and an androgen-dependent inguinoscrotal phase. The inguinoscrotal phase typically occurs around the 7th month of gestation, when fetal testosterone production increases.[23][24]

Infants with cryptorchidism and otherwise normal testes may experience spontaneous descent within the first few months of life. Current evidence supports referral for surgical orchiopexy if descent has not occurred by 6 months of age, corrected for prematurity.[25] Hormonal therapy, which may involve testosterone or human chorionic gonadotropin, is not routinely recommended because of limited efficacy, inferior outcomes compared with surgery, and potential adverse effects.[26]

Testosterone is a primary regulator of secondary male sexual characteristics—the features associated with phenotypic masculinity.[27] These features include male-pattern body and facial hair growth, deepening of the voice due to laryngeal enlargement, and increased sebum production. Testosterone exerts anabolic effects as well, driving the pubertal growth spurt by stimulating chondrocyte activity at the epiphyseal plates early in puberty and ultimately contributing to epiphyseal closure later in puberty. Testosterone also increases skeletal muscle mass by promoting protein synthesis and can contribute to hair loss in genetically susceptible individuals by increasing DHT, which acts on sensitive scalp follicles to induce miniaturization.[28][29]

Testosterone enhances erythropoiesis, which explains the higher hemoglobin and hematocrit levels observed in men compared with women.[30] Gradual age-related decline in testosterone levels is associated with decreased libido, reduced testicular volume, loss of muscle mass, increased fat deposition, diminished bone density, and reduced red blood cell production, which can contribute to anemia.[31] Testosterone enhances mood, energy, and cognitive ability through activity as a neuroactive hormone, influencing signaling from neurotransmitters such as dopamine and serotonin.[32]

Mechanism

The hypothalamic–pituitary–gonadal axis regulates testosterone levels and gonadal function, with a major rise in activity during puberty. The hypothalamus secretes gonadotropin-releasing hormone (GnRH), which travels through the hypothalamohypophyseal portal system to the anterior pituitary, stimulating secretion of luteinizing hormone and follicle-stimulating hormone (FSH). Luteinizing hormone and FSH are gonadotropic hormones that circulate in the bloodstream and act on receptors in the gonads. Luteinizing hormone acts on Leydig cells to increase testosterone production. Testosterone limits its own secretion via negative feedback. Elevated testosterone levels in the blood provide feedback to the hypothalamus to suppress GnRH secretion and reduce anterior pituitary responsiveness to GnRH.[33]

The hypothalamus releases GnRH in pulses every 1 to 3 hours throughout the reproductive life of male individuals. Despite pulsatile release, average plasma levels of FSH and luteinizing hormone remain relatively constant from the onset of puberty, when levels increase, to the 3rd decade of life, when levels peak and then gradually decline. Testosterone levels remain low before puberty, reflecting low secretion of GnRH and gonadotropins. Changes in neuronal input to the hypothalamus and brain activity during puberty produce a marked increase in GnRH secretion.[34]

Leydig cells in the testes produce testosterone from cholesterol. Luteinizing hormone regulates the initial step in this process.[35] Two important intermediates in this process include dehydroepiandrosterone (DHEA) and androstenedione. Androstenedione is converted to testosterone by 17β-hydroxysteroid dehydrogenase. Most testosterone circulates bound to plasma proteins, such as sex hormone-binding globulin and albumin. The majority of protein-bound testosterone represents an excess reservoir of androgenic hormone for the body. Small amounts of free testosterone in the blood act at the tissue level, primarily in the seminal vesicles, bone, muscle, and prostate gland.

Testosterone is converted to DHT at the cellular level by 5α-reductase. Testosterone and DHT bind to intracellular receptors and regulate protein expression. Both men and women also produce weak-acting androgens in the zona reticularis of the adrenal glands. These weakly active androgens include DHEA and androstenedione. These androgens bind to testosterone receptors with lower affinity but can also be converted to testosterone in peripheral tissues when produced in large amounts.[36]

Related Testing

Hypogonadism

Recognition of testosterone deficiency often begins with careful history-taking and targeted physical examination. Clinical features of male hypogonadism vary depending on whether testosterone deficiency occurs before or after puberty. Prepubertal hypogonadism may present with the following symptoms:

• Delayed bone age
• Delayed or absent secondary sexual characteristics, including limited facial, axillary, and pubic hair
• Eunuchoid body proportions, including arm span greater than height, as well as long limbs
• Gynecomastia
• Infertility or low sperm count after attaining reproductive age
• Micropenis
• Poor muscle development
• Small testes, typically less than 20 mL

Postpubertal hypogonadism features overlap but exclude micropenis and eunuchoid proportions, as pubertal development has already occurred. Findings may include the following:

• Decreased libido
• Decreased muscle mass
• Erectile dysfunction
• Fatigue
• Gynecomastia
• Hot flashes in more severe cases
• Infertility
• Loss of body hair
• Low bone density, including osteoporosis

Diagnostic evaluation of suspected hypogonadism begins with a thorough history and physical examination. When clinical features suggest hypogonadism, measurement of morning serum total testosterone between 8 AM and 10 AM represents the initial laboratory step. When testosterone is low, repeat morning testosterone measurement is required to confirm the finding due to biologic variability.

Subsequent measurement of luteinizing hormone and FSH assists in etiologic classification. Low testosterone with elevated luteinizing hormone and FSH indicates primary hypogonadism consistent with testicular failure. Further evaluation may include karyotyping for chromosomal abnormalities such as Klinefelter syndrome, along with assessment for causes of testicular injury, such as viral orchitis, chemotherapy exposure, testicular torsion, and trauma.

Low testosterone with low or normal luteinizing hormone and FSH indicates secondary hypogonadism involving pituitary or hypothalamic dysfunction. Additional evaluation may include serum prolactin, thyroid-stimulating hormone, free thyroxine, morning cortisol with consideration of adrenocorticotropic hormone axis assessment, and iron studies, as iron overload may suppress the gonadotropic axis. Magnetic resonance imaging of the pituitary is indicated when no reversible cause is identified.

Normal testosterone levels in the presence of symptoms may represent eugonadal low testosterone, often associated with obesity, chronic illness, or medication exposure such as opioids or glucocorticoids, rather than true hypogonadism.[37] Further information is available in the companion StatPearls reference on “Male Hypogonadism.”[38]

Hyperandrogenism

Clinical manifestations of androgen excess depend on age, sex, and the source of excess androgen production. In prepubertal boys, excess androgens may produce virilization characterized by penile enlargement, accelerated linear growth, early pubic hair development, body odor, acne, and voice deepening. In prepubertal girls, excess androgens may result in accelerated growth with advanced bone age, acne, clitoromegaly, hirsutism, and variable degrees of virilization depending on severity.

In men, adrenal androgen excess generally produces minimal clinical effects, as androgen receptors are already near maximal stimulation by endogenous testosterone. In contrast, exogenous testosterone or anabolic steroid exposure may result in muscle hypertrophy, testicular atrophy, infertility, acne, mood changes, and erythrocytosis. In women, androgen excess may present with acne, hirsutism, infertility, male-pattern baldness, and menstrual irregularities, including amenorrhea. Severe cases may progress to virilization, including voice deepening and clitoromegaly.

Testosterone in Pharmacology

Testosterone has established therapeutic applications in selected clinical settings, including certain cases of metastatic breast cancer, delayed puberty in boys (under careful supervision), gender dysphoria (gender-affirming hormone therapy), hypogonadotropic hypogonadism due to pituitary or hypothalamic dysfunction, and primary hypogonadism secondary to testicular failure. Adverse effects associated with testosterone and synthetic androgens include accelerated male-pattern baldness, acne, clitoral enlargement and virilization in female individuals, decreased testicular size, erythrocytosis or polycythemia, gynecomastia due to peripheral aromatization of testosterone to estradiol, hepatic adenomas and cholestatic jaundice particularly with oral 17α- alkylated androgens, infertility due to suppression of luteinizing hormone and FSH, mood and behavioral disturbances like “roid rage,” and prostate enlargement in men. Androgen use is contraindicated during pregnancy due to the risk of virilization of female fetuses.

Androgen antagonism and inhibition are achieved through several pharmacologic classes. Inhibitors of 5α-reductase, including finasteride and dutasteride, are used in benign prostatic hyperplasia and androgenic alopecia. Androgen receptor blockers, including flutamide and bicalutamide, are used in prostate cancer, while spironolactone is used for hirsutism and other androgen-mediated symptoms. GnRH analogs, such as leuprolide, and antagonists like degarelix suppress luteinizing hormone and FSH secretion, producing chemical castration, and are used in prostate cancer, precocious puberty, and endometriosis. Steroid synthesis inhibitors, such as ketoconazole, inhibit testosterone synthesis and are used in Cushing disease.

Clinical Significance

Testosterone-related pathology involves overproduction, underproduction, receptor insensitivity, or impaired metabolism of the hormone. Common testosterone-related pathologies include states of androgen excess or deficiency.

Overproduction of androgens may occur in conditions such as polycystic ovary syndrome, adrenal virilization or adrenal tumors, ovarian or testicular neoplasms, Cushing syndrome, and exogenous steroid use. These conditions are better understood by distinguishing testosterone from DHEA, a relatively weak androgen produced by the adrenal glands, ovaries, and testes. DHEA serves as a precursor for other steroid hormones, including testosterone and estrogen. The sulfated form, DHEA sulfate (DHEAS), is produced predominantly by the adrenal glands and serves as a marker of adrenal androgen production.[39]

In polycystic ovary syndrome, abnormal GnRH secretion increases luteinizing hormone secretion. Luteinizing hormone stimulates androgen production by ovarian theca cells, resulting in hirsutism, male escutcheon, acne, and androgenic alopecia in affected individuals.[40] Adrenal and ovarian tumors typically present with rapidly progressive signs of androgen excess, including hirsutism and virilization. Elevated testosterone with normal DHEAS most commonly suggests an ovarian source of androgen excess. Elevated DHEAS with relatively normal testosterone often indicates an adrenal source of androgen excess.

Decreased testosterone production may occur with aging, certain medications, chemotherapy, hypothalamic or pituitary axis disorders, primary hypogonadism, cryptorchidism, orchitis, and genetic disorders such as Klinefelter and Kallmann syndromes. Klinefelter syndrome is the most common congenital cause of primary hypogonadism. Seminiferous tubule dysgenesis and loss of Sertoli cells result in decreased inhibin levels and increased FSH. FSH upregulates aromatase activity, increasing the conversion of androgens to estrogen. Leydig cell dysfunction further contributes to decreased testosterone levels, with a compensatory increase in luteinizing hormone due to loss of negative feedback.[41] In Kallmann syndrome, failure of GnRH-producing neurons to migrate results in deficient secretion of the hormone. Absence of GnRH leads to decreased luteinizing hormone, FSH, testosterone, and sperm count.[42] Kallmann syndrome is distinguished from other causes of hypogonadotropic hypogonadism by associated olfactory dysfunction, including hyposmia or anosmia.[43][44][45]

The enzyme 5α-reductase converts testosterone to DHT. Patients with 5α-reductase deficiency may present at birth with female, male, or ambiguous external genitalia due to reduced DHT production. Internal male urogenital structures develop normally because AMH is still produced. At puberty, affected individuals, who may have been raised as female due to absent or limited secondary male characteristics, develop male secondary sexual characteristics and may present with primary amenorrhea. Laboratory findings typically demonstrate normal testosterone and luteinizing hormone levels, low DHT levels, and an increased testosterone-to-DHT ratio.[46]

In contrast to 5α-reductase deficiency, androgen insensitivity is characterized by nonfunctional androgen receptors, resulting in undervirilization. Affected individuals, like those with 5α-reductase deficiency, have a 46,XY karyotype. External genitalia are typically female-appearing, and testes are usually undescended.[47] During adolescence, affected individuals present with primary amenorrhea and breast development but lack pubic and axillary hair and do not undergo voice deepening. A blind vaginal pouch is present, and internal female reproductive structures, including the fallopian tubes, uterus, and upper vagina, are absent due to AMH activity. Laboratory findings typically show elevated testosterone and luteinizing hormone levels.[48]

Impaired testosterone metabolism may occur in certain forms of congenital adrenal hyperplasia. In classic congenital adrenal hyperplasia, accounting for approximately 95% of cases and caused by 21-hydroxylase deficiency, newborns commonly present with ambiguous genitalia and may later develop salt wasting, vomiting, hypotension, and metabolic acidosis. Marked accumulation of 17-hydroxyprogesterone is shunted toward adrenal androgen synthesis, resulting in hyperandrogenism. Hyperandrogenism reduces hypothalamic sensitivity to progesterone, leading to increased GnRH synthesis and subsequent elevations in luteinizing hormone and FSH.[49] Elevated luteinizing hormone and FSH increase gonadal steroid production, including 17-hydroxyprogesterone, DHEA, and testosterone. Diagnosis is established with an adrenocorticotropic hormone stimulation test demonstrating an exaggerated 17-hydroxyprogesterone response.[50]

Testosterone supplementation may provide benefit in appropriately diagnosed, symptomatic individuals with hypogonadism, provided that androgen levels are regularly monitored, prostate-specific antigen and hematologic parameters, including hemoglobin and hematocrit, are routinely assessed, and patients are informed of potential adverse effects such as infertility and testicular atrophy. Testosterone therapy is frequently misused, with potentially serious health consequences. Clinicians should remain vigilant for possible hormone misuse.[51]

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References

1.

Gurung P, Yetiskul E, Jialal I. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): May 1, 2023. Physiology, Male Reproductive System. [PubMed: 30860700]

2.

P A A, Arbor TC, Krishan K. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Aug 28, 2023. Embryology, Sexual Development. [PubMed: 32491533]

3.

Kinter KJ, Amraei R, Anekar AA. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jul 30, 2023. Biochemistry, Dihydrotestosterone. [PubMed: 32491566]

4.

Marks LS. 5alpha-reductase: history and clinical importance. Rev Urol. 2004;6 Suppl 9(Suppl 9):S11-21. [PMC free article: PMC1472916] [PubMed: 16985920]

5.

Ng M, Leslie SW, Baradhi KM. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Oct 20, 2024. Benign Prostatic Hyperplasia. [PubMed: 32644346]

6.

Klonisch T, Fowler PA, Hombach-Klonisch S. Molecular and genetic regulation of testis descent and external genitalia development. Dev Biol. 2004 Jun 01;270(1):1-18. [PubMed: 15136137]

7.

Bain J. The many faces of testosterone. Clin Interv Aging. 2007;2(4):567-76. [PMC free article: PMC2686330] [PubMed: 18225457]

8.

Li L, Lin W, Wang Z, Huang R, Xia H, Li Z, Deng J, Ye T, Huang Y, Yang Y. Hormone Regulation in Testicular Development and Function. Int J Mol Sci. 2024 May 26;25(11) [PMC free article: PMC11172568] [PubMed: 38891991]

9.

Rojas-Zambrano JG, Rojas-Zambrano AR, Rojas-Zambrano AF, Barahona-Cueva GE. Benefits of Testosterone Hormone in the Human Body: A Systematic Review. Cureus. 2025 Feb;17(2):e78785. [PMC free article: PMC11807418] [PubMed: 39926620]

10.

Leslie SW, Sooriyamoorthy T. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jan 9, 2024. Erectile Dysfunction. [PubMed: 32965924]

11.

Panchatsharam PK, Durland J, Zito PM. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): May 1, 2023. Physiology, Erection. [PubMed: 30020650]

12.

Fink J, Schoenfeld BJ, Nakazato K. The role of hormones in muscle hypertrophy. Phys Sportsmed. 2018 Feb;46(1):129-134. [PubMed: 29172848]

13.

Tchernof A, Brochu D, Maltais-Payette I, Mansour MF, Marchand GB, Carreau AM, Kapeluto J. Androgens and the Regulation of Adiposity and Body Fat Distribution in Humans. Compr Physiol. 2018 Sep 14;8(4):1253-1290. [PubMed: 30215860]

14.

Sebo ZL, Rodeheffer MS. Testosterone metabolites differentially regulate obesogenesis and fat distribution. Mol Metab. 2021 Feb;44:101141. [PMC free article: PMC7772371] [PubMed: 33307216]

15.

De Oliveira DH, Fighera TM, Bianchet LC, Kulak CA, Kulak J. Androgens and bone. Minerva Endocrinol. 2012 Dec;37(4):305-14. [PubMed: 23235187]

16.

Tenuta M, Hasenmajer V, Gianfrilli D, Isidori AM. Testosterone and Male Bone Health: A Puzzle of Interactions. J Clin Endocrinol Metab. 2025 Jun 17;110(7):e2121-e2135. [PubMed: 40120082]

17.

Glynne S, Kamal A, Kamel AM, Reisel D, Newson L. Effect of transdermal testosterone therapy on mood and cognitive symptoms in peri- and postmenopausal women: a pilot study. Arch Womens Ment Health. 2025 Jun;28(3):541-550. [PMC free article: PMC12092509] [PubMed: 39283522]

18.

Rastrelli G, Corona G, Maggi M. Testosterone and sexual function in men. Maturitas. 2018 Jun;112:46-52. [PubMed: 29704917]

19.

Galansky LB, Levy JA, Burnett AL. Testosterone and Male Sexual Function. Urol Clin North Am. 2022 Nov;49(4):627-635. [PubMed: 36309419]

20.

Rizk PJ, Kohn TP, Pastuszak AW, Khera M. Testosterone therapy improves erectile function and libido in hypogonadal men. Curr Opin Urol. 2017 Nov;27(6):511-515. [PMC free article: PMC5649360] [PubMed: 28816715]

21.

Podlasek CA, Mulhall J, Davies K, Wingard CJ, Hannan JL, Bivalacqua TJ, Musicki B, Khera M, González-Cadavid NF, Burnett AL. Translational Perspective on the Role of Testosterone in Sexual Function and Dysfunction. J Sex Med. 2016 Aug;13(8):1183-98. [PMC free article: PMC5333763] [PubMed: 27436075]

22.

Buvat J, Maggi M, Gooren L, Guay AT, Kaufman J, Morgentaler A, Schulman C, Tan HM, Torres LO, Yassin A, Zitzmann M. Endocrine aspects of male sexual dysfunctions. J Sex Med. 2010 Apr;7(4 Pt 2):1627-56. [PubMed: 20388162]

23.

Ray R, Racine C. Sexual Differentiation. In: Feingold KR, Adler RA, Ahmed SF, Anawalt B, Blackman MR, Chrousos G, Corpas E, de Herder WW, Dhatariya K, Dungan K, Hamilton E, Hofland J, Jan de Beur S, Kalra S, Kaltsas G, Kapoor N, Kim M, Koch C, Kopp P, Korbonits M, Kovacs CS, Kuohung W, Laferrère B, Levy M, McGee EA, McLachlan R, Muzumdar R, Purnell J, Rey R, Sahay R, Shah AS, Sperling MA, Stratakis CA, Trence DL, Wilson DP, editors. Endotext [Internet]. MDText.com, Inc.; South Dartmouth (MA): Jul 24, 2025. [PubMed: 25905232]

24.

Kalfa N, Gaspari L, Ollivier M, Philibert P, Bergougnoux A, Paris F, Sultan C. Molecular genetics of hypospadias and cryptorchidism recent developments. Clin Genet. 2019 Jan;95(1):122-131. [PubMed: 30084162]

25.

Leslie SW, Sajjad H, Villanueva CA. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): May 5, 2024. Cryptorchidism. [PubMed: 29261861]

26.

Elseth A, Leslie SW, Hatley RM. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Apr 20, 2024. Orchiopexy. [PubMed: 32809739]

27.

Handelsman DJ, Hirschberg AL, Bermon S. Circulating Testosterone as the Hormonal Basis of Sex Differences in Athletic Performance. Endocr Rev. 2018 Oct 01;39(5):803-829. [PMC free article: PMC6391653] [PubMed: 30010735]

28.

Salisbury BH, Leslie SW, Tadi P. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jun 8, 2024. 5α-Reductase Inhibitors. [PubMed: 32310390]

29.

Syed HA, Zito PM. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Feb 26, 2024. Alopecia. [PubMed: 30844205]

30.

Bachman E, Travison TG, Basaria S, Davda MN, Guo W, Li M, Connor Westfall J, Bae H, Gordeuk V, Bhasin S. Testosterone induces erythrocytosis via increased erythropoietin and suppressed hepcidin: evidence for a new erythropoietin/hemoglobin set point. J Gerontol A Biol Sci Med Sci. 2014 Jun;69(6):725-35. [PMC free article: PMC4022090] [PubMed: 24158761]

31.

Coviello AD, Kaplan B, Lakshman KM, Chen T, Singh AB, Bhasin S. Effects of graded doses of testosterone on erythropoiesis in healthy young and older men. J Clin Endocrinol Metab. 2008 Mar;93(3):914-9. [PMC free article: PMC2266950] [PubMed: 18160461]

32.

McHenry J, Carrier N, Hull E, Kabbaj M. Sex differences in anxiety and depression: role of testosterone. Front Neuroendocrinol. 2014 Jan;35(1):42-57. [PMC free article: PMC3946856] [PubMed: 24076484]

33.

Plant TM, Marshall GR. The functional significance of FSH in spermatogenesis and the control of its secretion in male primates. Endocr Rev. 2001 Dec;22(6):764-86. [PubMed: 11739331]

34.

Breehl L, Caban O. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Mar 27, 2023. Physiology, Puberty. [PubMed: 30521248]

35.

Nedresky D, Singh G. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Sep 26, 2022. Physiology, Luteinizing Hormone. [PubMed: 30969514]

36.

Clark BJ, Prough RA, Klinge CM. Mechanisms of Action of Dehydroepiandrosterone. Vitam Horm. 2018;108:29-73. [PubMed: 30029731]

37.

Baillargeon J, Kuo YF, Westra JR, Urban RJ, Goodwin JS. Testosterone Prescribing in the United States, 2002-2016. JAMA. 2018 Jul 10;320(2):200-202. [PMC free article: PMC6396809] [PubMed: 29998328]

38.

Sizar O, Leslie SW, Schwartz J. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Feb 25, 2024. Male Hypogonadism. [PubMed: 30422528]

39.

Lin HY, Chen JH, Chen KH. The Sex Hormone Precursors Dehydroepiandrosterone (DHEA) and Its Sulfate Ester Form (DHEAS): Molecular Mechanisms and Actions on Human Body. Int J Mol Sci. 2025 Sep 03;26(17) [PMC free article: PMC12429729] [PubMed: 40943486]

40.

Walters KA, Bertoldo MJ, Handelsman DJ. Evidence from animal models on the pathogenesis of PCOS. Best Pract Res Clin Endocrinol Metab. 2018 Jun;32(3):271-281. [PubMed: 29779581]

41.

Kadam SJ, Leslie SW, Ford GA. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): May 5, 2025. Klinefelter Syndrome. [PubMed: 29493939]

42.

Sonne J, Leslie SW, Lopez-Ojeda W. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Dec 11, 2024. Kallmann Syndrome. [PubMed: 30855798]

43.

Spaziani M, Mileno B, Rossi F, Granato S, Tahani N, Anzuini A, Lenzi A, Radicioni AF. Endocrine and metabolic evaluation of classic Klinefelter syndrome and high-grade aneuploidies of sexual chromosomes with male phenotype: are they different clinical conditions? Eur J Endocrinol. 2018 Apr;178(4):343-352. [PubMed: 29371337]

44.

Bozzola M, Bozzola E, Montalbano C, Stamati FA, Ferrara P, Villani A. Delayed puberty versus hypogonadism: a challenge for the pediatrician. Ann Pediatr Endocrinol Metab. 2018 Jun;23(2):57-61. [PMC free article: PMC6057016] [PubMed: 29969875]

45.

Hauser LJ, Jensen EL, Mirsky DM, Chan KH. Pediatric anosmia: A case series. Int J Pediatr Otorhinolaryngol. 2018 Jul;110:135-139. [PubMed: 29859575]

46.

Mo MB, Sharma L. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jan 10, 2026. 5α-Reductase Deficiency. [PubMed: 30969726]

47.

Singh S, Ilyayeva S. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Feb 28, 2023. Androgen Insensitivity Syndrome. [PubMed: 31194363]

48.

Zhang JR, Zhang PY, Sun LG. [Mild androgen insensitivity syndrome: a case report]. Zhonghua Nei Ke Za Zhi. 2018 Aug 01;57(8):600-602. [PubMed: 30060335]

49.

Sharma L, Singh G. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jan 27, 2025. Congenital Adrenal Hyperplasia. [PubMed: 28846271]

50.

Burdea L, Sharma L, Mendez MD. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jan 17, 2025. 21-Hydroxylase Deficiency. [PubMed: 29630216]

51.

AlShareef S, Gokarakonda SB, Marwaha R. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jun 20, 2023. Anabolic Steroid Use Disorder. [PubMed: 30844201]

Disclosure: George Nassar declares no relevant financial relationships with ineligible companies.

Disclosure: Stephen Leslie declares no relevant financial relationships with ineligible companies.