Micropenis

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Micropenis
Male micro.jpg
A flaccid micropenis
Specialty Urology
DurationPermanent (lifetime)
Frequencyc. 0.6% of men

A micropenis is an unusually small penis. A common criterion is a dorsal (measured on top) penile length of at least 2.5 standard deviations smaller than the mean human penis size. [1] A micropenis is stretched penile length equal to or less than 1.9 cm (0.75 in) in term infants, and 9.3 cm (3.67 in) in adults. The condition is usually recognized shortly after birth. The term is most often used medically when the rest of the penis, scrotum, and perineum are without ambiguity, such as hypospadias. A microphallus describes a medical term where other sections of genitallia are different, such as hypospadias or cryptorchidism. [2] Micropenis incidence is about 1.5 in 10,000 male newborns in North America. [3]

Contents

Causes

Measuring an erect micropenis Micropenis erect with ruler.jpg
Measuring an erect micropenis

Of the abnormal conditions associated with micropenis, most are conditions of reduced prenatal androgen production or effect, such as abnormal testicular development (testicular dysgenesis), Klinefelter syndrome, Leydig cell hypoplasia, specific defects of testosterone or dihydrotestosterone synthesis (17,20-lyase deficiency, 5α-reductase deficiency), androgen insensitivity syndromes, inadequate pituitary stimulation (gonadotropin deficiency), and other forms of congenital hypogonadism. Micropenis can also occur as part of many genetic malformation syndromes that do not involve the sex chromosomes. It is sometimes a sign of congenital growth-hormone deficiency or congenital hypopituitarism. Several homeobox genes affect penis and digit size without detectable hormone abnormalities.[ citation needed ]

In addition, in utero exposure to some estrogen based fertility drugs like diethylstilbestrol (DES) has been linked to genital abnormalities or a smaller than normal penis. [4]

After evaluation to detect any of the conditions described above, micropenis can often be treated in infancy with injections of various hormones, such as human chorionic gonadotropin and testosterone. [5]

Treatment

Hormone treatment

Growth of the penis both before birth and during childhood and puberty is strongly influenced by testosterone and, to a lesser degree, the growth hormone. However, later endogenous hormones mainly have value in the treatment of micropenis caused by hormone deficiencies, such as hypopituitarism or hypogonadism. [6]

Regardless of the cause of micropenis, if it is recognized in infancy, a brief course of testosterone is often prescribed [7] (usually no more than three months). This usually induces a small amount of growth, confirming the likelihood of further growth at puberty, but rarely achieves normal size. No additional testosterone is given during childhood, to avoid unwanted virilization and bone maturation. (There is also some evidence that premature administration of testosterone can lead to reduced penis size in the adult.) [8]

Testosterone treatment is resumed in adolescence only for boys with hypogonadism. Penile growth is completed at the end of puberty, similar to the completion of height growth, and provision of extra testosterone to post-pubertal adults produces little or no further growth. [5]

Surgery

Because hormone treatment rarely achieves average size, several surgical techniques similar to phalloplasty for penis enlargement have been devised and performed, but they are not generally considered successful enough to be widely adopted and are rarely performed in childhood.[ citation needed ]

In extreme cases of micropenis, there is barely any shaft, and the glans appears to sit almost on the pubic skin. From the 1960s until the late 1970s, it was common for sex reassignment and surgery to be recommended. This was especially likely if evidence suggested that response to additional testosterone and pubertal testosterone would be poor. With parental acceptance, the boy would be reassigned and renamed as a girl, and surgery performed to remove the testes and construct an artificial vagina. This was based on the now-questioned idea that gender identity was shaped entirely from socialization, and that a man with a small penis can find no acceptable place in society.[ citation needed ]

Johns Hopkins Hospital, the center most known for this approach, performed twelve such reassignments from 1960 to 1980,[ citation needed ] most notably[ citation needed ] that of David Reimer (whose penis was destroyed by a circumcision accident), overseen by John Money. By the mid-1990s, reassignment was less often offered, and all three premises had been challenged. Former subjects of such surgery, vocal about their dissatisfaction with the adult outcome, played a large part in discouraging this practice. Sexual reassignment is rarely performed today for severe micropenis (although the question of raising the boy as a girl is sometimes still discussed). [9]

See also

Related Research Articles

<span class="mw-page-title-main">Cryptorchidism</span> Medical condition

Cryptorchidism, also known as undescended testis, is the failure of one or both testes to descend into the scrotum. The word is from Greek κρυπτός 'hidden' and ὄρχις 'testicle'. It is the most common birth defect of the male genital tract. About 3% of full-term and 30% of premature infant boys are born with at least one undescended testis. However, about 80% of cryptorchid testes descend by the first year of life, making the true incidence of cryptorchidism around 1% overall. Cryptorchidism may develop after infancy, sometimes as late as young adulthood, but that is exceptional.

<span class="mw-page-title-main">Growth hormone deficiency</span> Medical condition

Growth hormone deficiency (GHD), or human growth hormone deficiency, is a medical condition resulting from not enough growth hormone (GH). Generally the most noticeable symptom is that an individual attains a short height. Newborns may also present low blood sugar or a small penis size. In adults there may be decreased muscle mass, high cholesterol levels, or poor bone density.

Delayed puberty is when a person lacks or has incomplete development of specific sexual characteristics past the usual age of onset of puberty. The person may have no physical or hormonal signs that puberty has begun. In the United States, girls are considered to have delayed puberty if they lack breast development by age 13 or have not started menstruating by age 15. Boys are considered to have delayed puberty if they lack enlargement of the testicles by age 14. Delayed puberty affects about 2% of adolescents.

<span class="mw-page-title-main">Virilization</span> Biological development of male sex characteristics

Virilization or masculinization is the biological development of adult male characteristics in young males or females. Most of the changes of virilization are produced by androgens.

Congenital adrenal hyperplasia due to 17α-hydroxylase deficiency is an uncommon form of congenital adrenal hyperplasia (CAH) resulting from a mutation in the gene CYP17A1, which produces the enzyme 17α-hydroxylase. It causes decreased synthesis of cortisol and sex hormones, with resulting increase in mineralocorticoid production. Thus, common symptoms include mild cortisol deficiency, ambiguous genitalia in men or amenorrhea at puberty in women, and hypokalemic hypertension. However, partial (incomplete) deficiency often has inconsistent symptoms between patients, and affected women may be asymptomatic except for infertility.

Hypogonadism means diminished functional activity of the gonads—the testicles or the ovaries—that may result in diminished production of sex hormones. Low androgen levels are referred to as hypoandrogenism and low estrogen as hypoestrogenism. These are responsible for the observed signs and symptoms in both males and females.

Pubarche refers to the first appearance of pubic hair at puberty and it also marks the beginning of puberty. It is one of the physical changes of puberty and can occur independently of complete puberty. The early stage of sexual maturation, also known as adrenarche, is marked by characteristics including the development of pubic hair, axillary hair, adult apocrine body odor, acne, and increased oiliness of hair and skin. The Encyclopedia of Child and Adolescent Health corresponds SMR2 with pubarche, defining it as the development of pubic hair that occurs at a mean age of 11.6 years in females and 12.6 years in males. It further describes that pubarche's physical manifestation is vellus hair over the labia or the base of the penis. See Table 1 for the entirety of the sexual maturity rating description.

Kallmann syndrome (KS) is a genetic disorder that prevents a person from starting or fully completing puberty. Kallmann syndrome is a form of a group of conditions termed hypogonadotropic hypogonadism. To distinguish it from other forms of hypogonadotropic hypogonadism, Kallmann syndrome has the additional symptom of a total lack of sense of smell (anosmia) or a reduced sense of smell. If left untreated, people will have poorly defined secondary sexual characteristics, show signs of hypogonadism, almost invariably are infertile and are at increased risk of developing osteoporosis. A range of other physical symptoms affecting the face, hands and skeletal system can also occur.

<span class="mw-page-title-main">Testicular atrophy</span> Reduction in the size and function of the testicles

Testicular atrophy is a medical condition in which one or both testicles diminish in size and may be accompanied by reduced testicular function. Testicular atrophy is not related to the temporary shrinkage of the surrounding scrotum, which might occur in response to cold temperature.

<span class="mw-page-title-main">Partial androgen insensitivity syndrome</span> Medical condition

Partial androgen insensitivity syndrome (PAIS) is a condition that results in the partial inability of the cell to respond to androgens. It is an X linked recessive condition. The partial unresponsiveness of the cell to the presence of androgenic hormones impairs the masculinization of male genitalia in the developing fetus, as well as the development of male secondary sexual characteristics at puberty, but does not significantly impair female genital or sexual development. As such, the insensitivity to androgens is clinically significant only when it occurs in individuals with a Y chromosome. Clinical features include ambiguous genitalia at birth and primary amenhorrhoea with clitoromegaly with inguinal masses. Müllerian structures are not present in the individual.

Clitoral enlargement methods are forms of body modification that have the potential to increase the size of the clitoris and enhance sexual pleasure. Clitoral enlargement can be accomplished through a variety of means, each potentially having certain side effects and risks.

<span class="mw-page-title-main">Disorders of sex development</span> Medical conditions involving the development of the reproductive system

Disorders of sex development (DSDs), also known as variations in sex characteristics (VSC), are congenital conditions affecting the reproductive system, in which development of chromosomal, gonadal, or anatomical sex is atypical.

Puberty is the process of physical changes through which a child's body matures into an adult body capable of sexual reproduction. It is initiated by hormonal signals from the brain to the gonads: the ovaries in a female, the testicles in a male. In response to the signals, the gonads produce hormones that stimulate libido and the growth, function, and transformation of the brain, bones, muscle, blood, skin, hair, breasts, and sex organs. Physical growth—height and weight—accelerates in the first half of puberty and is completed when an adult body has been developed. Before puberty, the external sex organs, known as primary sexual characteristics, are sex characteristics that distinguish males and females. Puberty leads to sexual dimorphism through the development of the secondary sex characteristics, which further distinguish the sexes.

<span class="mw-page-title-main">Aromatase excess syndrome</span> Medical condition

Aromatase excess syndrome is a rarely diagnosed genetic and endocrine syndrome which is characterized by an overexpression of aromatase, the enzyme responsible for the biosynthesis of the estrogen sex hormones from the androgens, in turn resulting in excessive levels of circulating estrogens and, accordingly, symptoms of hyperestrogenism. It affects both sexes, manifesting itself in males as marked or complete phenotypical feminization and in females as hyperfeminization.

Hypergonadotropic hypogonadism (HH), also known as primary or peripheral/gonadal hypogonadism or primary gonadal failure, is a condition which is characterized by hypogonadism which is due to an impaired response of the gonads to the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), and in turn a lack of sex steroid production. As compensation and the lack of negative feedback, gonadotropin levels are elevated. Individuals with HH have an intact and functioning hypothalamus and pituitary glands so they are still able to produce FSH and LH. HH may present as either congenital or acquired, but the majority of cases are of the former nature. HH can be treated with hormone replacement therapy.

<span class="mw-page-title-main">Isolated 17,20-lyase deficiency</span> Medical condition

Isolated 17,20-lyase deficiency (ILD), also called isolated 17,20-desmolase deficiency, is a rare endocrine and autosomal recessive genetic disorder which is characterized by a complete or partial loss of 17,20-lyase activity and, in turn, impaired production of the androgen and estrogen sex steroids. The condition manifests itself as pseudohermaphroditism in males, in whom it is considered to be a form of intersex, and, in both sexes, as a reduced or absent puberty/lack of development of secondary sexual characteristics, resulting in a somewhat childlike appearance in adulthood.

<span class="mw-page-title-main">Leydig cell hypoplasia</span> Medical condition

Leydig cell hypoplasia (LCH), also known as Leydig cell agenesis, is a rare autosomal recessive genetic and endocrine syndrome affecting an estimated 1 in 1,000,000 genetic males. It is characterized by an inability of the body to respond to luteinizing hormone (LH), a gonadotropin which is normally responsible for signaling Leydig cells of the testicles to produce testosterone and other androgen sex hormones. The condition manifests itself as pseudohermaphroditism, hypergonadotropic hypogonadism, reduced or absent puberty, and infertility.

Gonadotropin-releasing hormone (GnRH) insensitivity also known as Isolated gonadotropin-releasing hormone (GnRH)deficiency (IGD) is a rare autosomal recessive genetic and endocrine syndrome which is characterized by inactivating mutations of the gonadotropin-releasing hormone receptor (GnRHR) and thus an insensitivity of the receptor to gonadotropin-releasing hormone (GnRH), resulting in a partial or complete loss of the ability of the gonads to synthesize the sex hormones. The condition manifests itself as isolated hypogonadotropic hypogonadism (IHH), presenting with symptoms such as delayed, reduced, or absent puberty, low or complete lack of libido, and infertility, and is the predominant cause of IHH when it does not present alongside anosmia.

Hypogonadotropic hypogonadism (HH), is due to problems with either the hypothalamus or pituitary gland affecting the hypothalamic-pituitary-gonadal axis. Hypothalamic disorders result from a deficiency in the release of gonadotropic releasing hormone (GnRH), while pituitary gland disorders are due to a deficiency in the release of gonadotropins from the anterior pituitary. GnRH is the central regulator in reproductive function and sexual development via the HPG axis. GnRH is released by GnRH neurons, which are hypothalamic neuroendocrine cells, into the hypophyseal portal system acting on gonadotrophs in the anterior pituitary. The release of gonadotropins, LH and FSH, act on the gonads for the development and maintenance of proper adult reproductive physiology. LH acts on Leydig cells in the male testes and theca cells in the female. FSH acts on Sertoli cells in the male and follicular cells in the female. Combined this causes the secretion of gonadal sex steroids and the initiation of folliculogenesis and spermatogenesis. The production of sex steroids forms a negative feedback loop acting on both the anterior pituitary and hypothalamus causing a pulsatile secretion of GnRH. GnRH neurons lack sex steroid receptors and mediators such as kisspeptin stimulate GnRH neurons for pulsatile secretion of GnRH.

<span class="mw-page-title-main">Gynecomastia</span> Endocrine system disorder of human male breast

Gynecomastia is the abnormal non-cancerous enlargement of one or both breasts in males due to the growth of breast tissue as a result of a hormone imbalance between estrogens and androgens. Gynecomastia can cause significant psychological distress or unease.

References

  1. ↑ Lee PA, Mazur T, Danish R, et al. (1980). "Micropenis. I. Criteria, etiologies and classification". The Johns Hopkins Medical Journal. 146 (4): 156–63. PMID   7366061.
  2. ↑ "Microphallus: Practice Essentials, Pathophysiology, Epidemiology". 29 December 2022 – via eMedicine.{{cite journal}}: Cite journal requires |journal= (help)
  3. ↑ ScienceDaily.com (2004). "Surgeons Pinch More Than An Inch From The Arm To Rebuild A Micropenis," 6 Dec. 2004, retrieved 2 April 2012.
  4. ↑ Center for Disease Control. "DES Update: Consumers".
  5. 1 2 Hatipoglu N, Kurtoglu S (December 2013). "Micropenis: Etiology, Diagnosis and Treatment Approaches". Journal of Clinical Research Pediatric Endocrinology. 5 (4): 217–223. doi:10.4274/Jcrpe.1135. PMC   3890219 . PMID   24379029.
  6. ↑ "Hypogonadism". The Lecturio Medical Concept Library. Retrieved 26 July 2021.
  7. ↑ Ishii T, Sasaki G, Hasegawa T, Sato S, Matsuo N, Ogata T (2004). "Testosterone enanthate therapy is effective and independent of SRD5A2 and AR gene polymorphisms in boys with micropenis". J. Urol. 172 (1): 319–24. doi:10.1097/01.ju.0000129005.84831.1e. PMID   15201804.
  8. ↑ McMahon DR, Kramer SA, Husmann DA (1995). "Micropenis: does early treatment with testosterone do more harm than good?". J. Urol. 154 (2 Pt 2): 825–9. doi:10.1016/S0022-5347(01)67175-1. PMID   7609189.
  9. ↑ Calikoglu AS; Calikoglu, A (1999). "Should boys with micropenis be reared as girls?". J. Pediatr. 134 (5): 537–8. doi: 10.1016/S0022-3476(99)70236-2 . PMID   10228285.
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