Micropenis

Mahdi Alsaleem; Stephen Leslie

Micropenis

Author: Mahdi Alsaleem Editor: Stephen W. Leslie Updated: 6/25/2025 12:37:00 AM

Introduction

Micropenis is an objective diagnosis characterized by a stretched penile length that is more than 2.5 SD below the mean compared to age-matched normal values. The penis appears otherwise normal in appearance, function, and structure.[1][2] The diagnostic criteria vary depending on age, geographic region, and ethnicity.[2][3][4][5][6]

In cases of micropenis, the scrotum, testicles, median raphe, foreskin, and the position of the urethral meatus are typically normal.[7] The condition is usually diagnosed at birth or during early childhood.[1]

As a general guide, the stretched penile lengths that generally suggest a micropenis are listed below.

Newborns or babies: Less than 1.9 cm.[2][4]
Prepubertal boys: 3.8 cm or less.[2][8]
Adults: Less than 7.5 cm.[9][10][11][12]

More detailed information on age-specific stretched penile lengths can be found in the History and Physical section below.

Given the significant psychological distress and anxiety associated with the condition, timely and accurate diagnosis of micropenis is essential. Once the diagnosis is confirmed, treatment should be initiated promptly and coordinated by a multidisciplinary healthcare team.

Etiology

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Etiology

The human penis originates from the genital tubercle. By 5 to 6 weeks of gestation, this structure appears as a bulge or elevation of the perineum, known as the genital swellings, located on either side of the cloacal membrane.[4][13][14] These swellings comprise the following 3 germ layers:

Ectoderm, which forms the penile skin and prepuce
Mesoderm, which develops into the corpora cavernosa
Endoderm, which gives rise to the penile urethra [4][14]

In humans, chromosomal sex is determined at fertilization as either female (XX) or male (XY). Early in fetal development, the embryo possesses both mesonephric (Wolffian) ducts, which can develop into male reproductive structures, and paramesonephric (Müllerian) ducts, which can develop into female reproductive structures. The presence or absence of the SRY gene, located on the Y chromosome, determines the regression or development of these embryonic structures during organogenesis. The SRY gene stimulates gonadal differentiation into testicular tissue in males. Please see StatPearls' companion resources, "Embryology, Mullerian-Inhibiting Factor" and "Embryology, Wolffian Ducts," for more information.

At this early stage of development, the testes secrete 3 essential hormones that are crucial for the sexual differentiation process in males, as listed below.

Anti-Müllerian hormone (AMH): AMH is secreted by the Sertoli cells in the testes and prevents the development of female reproductive organs by promoting the regression of the Müllerian (paramesonephric) ducts in males. Please see StatPearls' companion resources, "Embryology, Mullerian-Inhibiting Factor" and "Embryology, Mullerian Ducts (Paramesonephric Ducts)," for more information.
Dihydrotestosterone (DHT): DHT is responsible for the development of male sexual characteristics, including scrotal maturation, penile growth, and testicular enlargement. Please see StatPearls' companion resource, "Biochemistry, Dihydrotestosterone," for more information.
Testosterone: This hormone stimulates the development of the mesonephric ducts into the internal male reproductive structures, including the seminal vesicles, vas deferens, and epididymis. Please see StatPearls' companion resource, "Physiology, Testosterone," for more information.

Under the influence of these three hormones, the male reproductive and genitourinary systems begin to develop during the late first trimester, between 8 and 12 weeks of gestation. Please see StatPearls' companion resources, "Embryology, Mullerian-Inhibiting Factor," "Embryology, Wolffian Ducts," and "Embryology, Urethral Folds," for more information.

Maternal human chorionic gonadotropin (hCG) stimulates Leydig cells to produce testosterone, which is then metabolized in utero into the more potent DHT. High levels of fetal androgens during the second trimester further accelerate penile growth and anatomical development.[15] Micropenis typically results from reduced testosterone production in utero during the third trimester (usually beginning around 12 weeks), assuming normal development up to that time.[8] Please see StatPearls' companion resources, "Biochemistry, Dihydrotestosterone" and "Embryology, Sexual Development," for more information.

In the postnatal period, further development of male sexual characteristics is regulated by hormones controlled by the hypothalamic-pituitary axis, including gonadotropin-releasing hormone (GnRH), follicle-stimulating hormone (FSH), and luteinizing hormone (LH).[8] The highest levels of postnatal androgens occur during the so-called "mini-puberty" period, which begins after the first month of life and typically lasts until around 6 months of age.[16][17][18][19] Disruptions at any point in this hormonal cascade may lead to undervirilization, genital abnormalities, or micropenis.

Androgen deficiency before 12 weeks of gestation typically causes genital ambiguity, whereas deficiency occurring after 12 weeks results in isolated micropenis.[8] Micropenis usually arises from insufficient fetal testosterone production after the 12th week of gestation and/or during the postnatal “mini-puberty” period within the first 3 months of life.[2][8] The most common cause of reduced fetal and neonatal testosterone is hypothalamic or pituitary dysfunction leading to hypogonadotropic hypogonadism, followed by primary testicular failure, which presents as hypergonadotropic hypogonadism.[2][8][4][20]

Micropenis may occur with any of the following conditions:

5-Alpha (5α)-reductase deficiency. (Please see StatPearls' companion resource, "5-Alpha-Reductase Deficiency," for more information.)
17-Beta hydroxysteroid dehydrogenase (17β-HSD) deficiency.[16]
Addison disease. (Please see StatPearls' companion resource, "Addison Disease," for more information.)
Androgen insensitivity due to receptor defects and/or resistance. (Please see StatPearls' companion resource, "Androgen Insensitivity Syndrome," for more information.)
Anorchia (absence of testes).
Congenital hypogonadotropic hypogonadism. (Please see StatPearls' companion resource, "Hypopituitarism," for more information.)
Down syndrome (Please see StatPearls' companion resource, "Down Syndrome," for more information.)
Fetal exposure to pesticides and other toxic chemicals.[21]
Gonadal dysgenesis. (Please see Statpearls' companion resource, "Ambiguous Genitalia and Disorders of Sexual Differentiation," for more information.)
Growth hormone deficiency.[22]
Hypopituitarism, which is characterized by hypoglycemia, hypogonadotropic hypogonadism, and growth disturbances. (Please see StatPearls' companion resource, "Hypopituitarism," for more information.)
Kallmann syndrome, which is characterized by hypogonadotropic hypogonadism, osteoporosis, hearing impairment, and anosmia. (Please see StatPearls' companion resource, "Kallmann Syndrome," for more information.)
Kleefstra syndrome.[23]
Klinefelter syndrome (47,XXY). This is associated with small testicles, infertility, gynecomastia, poor coordination, and reading difficulties.[24] (Please see StatPearls' companion resource, "Klinefelter Syndrome," for more information.)
Lawrence-Moon-Biedl syndrome.[25][26]
H-receptor defects.[16]
Noonan syndrome, which is characterized by hypertelorism, short neck, low-set ears, skeletal malformation, bleeding disorders, and pulmonary valve stenosis. (Please see StatPearls' companion resource, "Noonan Syndrome," for more information.)
Primary testicular failure.
Prader-Willi syndrome, which is characterized by hypotonia, obesity, intellectual disabilities, undescended testes, micropenis, small hands and feet (Please see StatPearls' companion resource, "Prader-Willi Syndrome," for more information.)
Rare forms of congenital adrenal hyperplasia (deficiency in steroidogenic acute regulatory protein [STAR], 3-beta hydroxysteroid dehydrogenase [3β-HSD], and 17α-hydroxylase). (Please see StatPearls' companion resources, "17-Hydroxylase Deficiency" and "Congenital Adrenal Hyperplasia," for more information.)
Robinow syndrome, which is a rare inherited disorder primarily affecting the skeleton, is characterized by short arms, legs, and fingers, genital anomalies, and facial distortion.[27]
Silver-Russell syndrome (also known as Russell-Silver syndrome), which is a rare genetic disorder characterized by dwarfism resulting from intrauterine growth restriction. This is characterized by poor postnatal growth, a relatively large head, triangular facial features, a prominent forehead, and body asymmetry. Intelligence is typically unaffected.[28][29][30]
Trisomies of chromosomes 8, 13, 18, and 21. (Please see StatPearls' companion resources, "Trisomy 13" and "Edwards Syndrome," for more information.)
Vanishing testes syndrome.[2][8][31][32]

In some cases, the etiology remains unclear even after performing an extensive evaluation.

Epidemiology

The incidence of micropenis in North America is approximately 1.5 per 10,000 male newborns.[33] Globally, the average incidence is estimated at 0.6% of all males, or about 1 in every 300 male births.[34] However, reported rates vary widely due to differences in diagnostic criteria across countries and study populations.[6][34]

Research indicates statistically significant differences in mean penile length among newborns of different ethnic backgrounds—Black newborns (3.2–3.5 cm), Caucasians (2.6 cm), East Indians (2.5 cm), and Chinese (2.3 cm).[3][6][35][36] Other studies have proposed population-specific penile length standards for Brazilian, Indian, Japanese, and Turkish infants and children.[5][8][37][38][39][40]

A 2024 systematic review and meta-analysis confirmed that mean stretched penile length and flaccid circumference vary significantly across geographical regions. The longest mean stretched penile lengths were observed in individuals from North and South America (9.86 cm), followed by those from Europe (9.71 cm), the Eastern Mediterranean (9.3 cm), Africa (9.22 cm), Southeast Asia (8.21 cm), and the Western Pacific region (8 cm).[5] These findings indicate that the stretched penile length threshold for diagnosing micropenis varies substantially by geographical region.[5]

A recent systematic review and meta-analysis found that the average global penile length has gradually increased over time, with a 24% rise observed over the past 29 years.[41]

History and Physical

The clinical diagnosis of micropenis is typically made following a thorough history and physical examination. Once diagnosed, additional testing is warranted to identify any associated abnormalities and determine the underlying etiology. A detailed maternal history is the first step in evaluating micropenis. Factors such as consanguinity and a family history of ambiguous genitalia increase the likelihood of inherited conditions. In addition, it is also important to inquire about maternal medication use, as exposure to anti-androgens (eg, flutamide, testolactone, enzalutamide, and spironolactone) during pregnancy can disrupt in-utero virilization.

Physical examination is the most critical component in evaluating micropenis. Signs of undervirilization associated with low blood pressure and tachycardia may suggest adrenal insufficiency related to rare forms of congenital adrenal hyperplasia (CAH). Accurate measurement of stretched penile length is essential during the physical examination. The penile shaft should be fully stretched, and the length measured dorsally from the pubic symphysis—after compressing the suprapubic fat pad—to the tip of the glans, with the foreskin retracted as much as possible. Taking the average of multiple measurements helps improve accuracy.

Stretched Penile Length

Various techniques have been described for measuring stretched penile length in neonates and infants.[42] These include the use of rigid rulers, flexible measuring tapes, vernier calipers, cotton swabs, wooden spatulas, tongue depressors, modified syringes with suction, and ultrasonography.[42] Proper retraction of the foreskin is essential to accurately identify the distal landmark—the tip of the glans.[42] If adequate foreskin retraction is not possible, the measurement will be less accurate. For instance, in infants with phimosis or redundant foreskin that limits glans exposure, the final measurement may only serve as an approximate estimate.[42]

Variations in the degree of stretching applied can create inaccuracies in the measurements.[42]
When using a ruler or a flexible tape, parallax errors may occur.[42]
Most rulers and measuring tapes have the zero mark a few millimeters from the actual edge, which must be considered during measurement.[42]

Having an assistant greatly aids in obtaining an accurate measurement of stretched penile length using tools such as a flexible tape measure, ruler, spatula, tongue depressor, cotton swab, or the syringe and suction technique.[42][43][44][45][46][47]

A rigid ruler is the most commonly used and simplest method for measuring a stretched penile length.[42] The ruler allows for depression of the prepubic fat pad and alignment along the stretched penis. An assistant can use a second ruler placed perpendicularly to gently press against the glans, helping to accurately identify the distal extension.[42] If the penis has curvature, such as from chordee, a flexible tape measure may be preferred, although it typically requires assistance for accurate measurement.[42][48][49] Vernier calipers are not specifically designed for this anatomical application and must be used with caution to avoid injury.[42][50]

The penis should be stretched until increased resistance is felt to ensure consistency in measurement.[42][43][44][51] Accurately measuring stretched penile length in a crying or squirming newborn can be difficult, and the assistance of a second person is often essential when using any of the standard techniques.[42][43][44][45][46][47] The commonly used methods for measuring stretched penile length in neonates are discussed below.

Rigid Marker Technique

While holding and stretching an infant's penis with one hand, the examiner places a tongue depressor at the base of the pubic symphysis.[42]
The examiner then grasps the tongue depressor with the same hand along with the stretched penis.
A marker is used to indicate the distal tip of the penis on the tongue depressor.
The marked distance on the tongue depressor is subsequently measured.
Having an assistant perform the marking can simplify the process.
Alternatively, a cotton swab or wooden spatula may be used in place of the tongue depressor.

Syringe and Suction Technique

A 10 mL disposable syringe is used by first removing the piston and cutting off the entire luer lock end, leaving only the cylinder.
The piston is then reinserted into the cut end of the cylinder, and the flanged, uncut end is placed over the penis.
The modified syringe is firmly pressed onto the pubic area.
By gently withdrawing the piston, a mild suction is created, which draws the penis into the syringe barrel while excluding scrotal tissue and prepubic fat.
The clinician or an assistant can then mark the length of the penis on the syringe cylinder with a marker for later measurement.
The syringe and suction method has been suggested to be technically simple, more reproducible, and less operator-dependent than other techniques for measuring stretched penile length.[42][52]

Ultrasonography

Ultrasonography can be used to accurately and reliably measure stretched penile length.[42][53]
Ultrasound is generally considered more accurate than manual measurement methods.[42]
This technique offers reproducibility, eliminates variability from manual traction, and is not affected by factors such as obesity, phimosis, body habitus, redundant foreskin, or excessive prepubic fat.[12][42][53][54]
Ultrasound may be the optimal measurement modality for patients with a buried penis, extreme obesity, excessive foreskin, severe phimosis, or a webbed scrotum.[42]
Prenatal measurement of fetal penile length is also possible using ultrasonography.[55]

A stretched penile length measuring less than 2.5 SD below the mean for the corresponding age and geographic region confirms the diagnosis of micropenis.[2] After age 5, penile growth is typically minimal until testosterone levels increase at puberty. Please see StatPearls' companion resource, "Physiology, Puberty," for more information.

Suggested lower normal limits of stretched penile lengths (in centimeters) according to age are listed below (see Image 1. Age-Specific Lower Limits [<2.5 SD Below the Mean] of Stretched Penile Lengths [in centimeters]).[2][9][10][11][12][39][56][57]

Preterm infants born at 30 weeks of gestation: 1.5 cm
Preterm infants born at 34 weeks of gestation: <2 cm
Term infants: 2.5 cm
Individuals aged 1: 2.6 cm
Individuals aged 5: 3.5 cm
Individuals aged 10: 3.8 cm
Adults: 7.5 cm

As average penile size varies significantly across geographic regions, an international consensus recommends using a stretched penile length of less than 2 cm at birth and less than 4 cm after age 5 as a reasonable global standard for defining micropenis.[8]

Careful and comprehensive palpation of the gonads is a crucial step in evaluating micropenis. Key aspects to assess and document include the appearance and maturity of the scrotal sac, the size and location of both testes, the presence and position of the urethral meatus, any curvature of the penile shaft, and any associated dysmorphic features. Additional areas to examine include facial anomalies, skin hyperpigmentation, hypertension, unusual height, gynecomastia, and abnormalities in hearing or smell.[8]

The majority of prepubertal boys brought in by their parents for evaluation of possible micropenis are obese, with significant suprapubic fat pads and a buried but normally sized penis.

A diagnosis of micropenis can be reasonably made based on stretched penile length relative to age, as follows:

In full-term neonates, a stretched penile length of less than 1.9 cm indicates congenital micropenis.[2][4]
At the age of 5, a stretched penile length of less than 4 cm is considered a micropenis.[2][8]
In adults, a stretched penile length of less than 7.5 cm (2.95 inches) confirms the diagnosis.[9][10][11][12]

Evaluation

Once a physical examination confirms the presence of micropenis, further evaluation is essential to identify the underlying etiology and guide the treatment plan. A standardized diagnostic approach typically includes the components mentioned below.[2][8]

Baseline hormonal panel: The levels of DHT, growth hormone, LH, FSH, testosterone, and androstenedione (a precursor sex hormone) should be assessed.[2][7][8]

Evaluation of congenital adrenal dysfunctions: The levels of progesterone, 17-OH progesterone, androstenedione, and 17-hydroxypregnenolone should be assessed to rule out rare types of congenital adrenal hyperplasia associated with male undervirilization.[2][8]

Serum glucose assessment: Hypoglycemia may indicate hypopituitarism. If detected, serum glucose, electrolytes, insulin, thyroid-stimulating hormone (TSH), thyroxine (T4), and cortisol levels should be evaluated for potential cortisol deficiency. Please see StatPearls' companion resource, "Addison Disease," for more information.[58][59]

Counterregulatory hormone assessment: Cortisol and human growth hormone have essential roles in maintaining serum glucose levels. Deficiency in one or both may contribute to hypoglycemia. Please see StatPearls' companion resources, "Neonatal Hypoglycemia" and "Hypoglycemia," for more information.

hCG stimulation test: This is used to evaluate gonadal function by measuring serum testosterone levels before and after hCG administration.[2][8][16][60][61]
- hCG is typically administered intramuscularly (IM) at a dosage of 1000 IU daily for 3 days or 1500 IU every other day for 2 weeks.
- A post-stimulation testosterone level below 300 ng/dL suggests gonadal dysgenesis.
- If LH and FSH levels are concurrently elevated and testosterone levels remain low, this may indicate testicular absence or primary testicular failure.
- Defects in testosterone synthesis can be assessed by measuring testosterone precursors, such as 17-hydroxyprogesterone (17-OH progesterone), dehydroepiandrosterone, and androstenedione, before and after administration of hCG.

Inhibin B and AMH levels may be useful in selected cases to determine the presence of functional testicular tissue.[62] Low levels of AMH combined with normal inhibin B suggest persistent Müllerian duct syndrome.[62]

Karyotype analysis is recommended to confirm a 46,XY genotype.[8]

Pelvic ultrasound is used to evaluate the gonads and internal genital structures. The presence of female internal genitalia may indicate a virilized phenotypic female (46,XX genotype), which is often associated with 21-hydroxylase deficiency. Please see Statpearls' companion resources, "Ambiguous Genitalia and Disorders of Sexual Differentiation," "21-Hydroxylase Deficiency," and "Congenital Adrenal Hyperplasia," for more information.

Pituitary gland hypofunction (hypopituitarism) should be suspected if there is evidence of hormonal dysfunction or hypoglycemia (Please see StatPearls' companion resource, "Hypopituitarism," for more information.)[63][64]

If both LH and testosterone levels are elevated, the diagnosis can be confirmed by examining DHT levels and the testosterone-to-DHT ratio.[34]

A low DHT level with an elevated testosterone-to-DHT ratio suggests 5α-reductase deficiency, as the enzyme is responsible for converting testosterone into DHT.[34][65] Please see StatPearls' companion resource, "5-Alpha-Reductase Deficiency," for more information.
A high DHT level with a low testosterone-to-DHT ratio points to partial androgen insensitivity syndrome. Please see StatPearls' companion resource, "Androgen Insensitivity Syndrome," for more information.[34][66]

Normal serum levels of inhibin B and AMH (both produced by active Sertoli cells) indicate the presence of functional testicular tissue.[16][62] Low AMH levels combined with normal inhibin B levels suggest persistent Müllerian duct syndrome.[16][67]

Findings of associated hypospadias, cryptorchidism, or incomplete scrotal fusion suggest a disorder of sexual development. Please see Statpearls' companion resource, "Ambiguous Genitalia and Disorders of Sexual Differentiation," for more information.

Congenital Hypopituitarism

Congenital hypopituitarism is rare, with an estimated incidence of 1 in 4000 to 1 in 10,000 births.[68] The condition usually presents with nonspecific findings, which makes early diagnosis challenging.[58][59] Hypoglycemia is often the first sign of hypopituitarism in newborns with micropenis.[58][59] Other common signs include prolonged neonatal jaundice, poor weight gain, abnormal electrolytes (notably, hyponatremia without hyperkalemia), hemodynamic instability, body temperature dysregulation, nystagmus, strabismus, short stature, optic nerve atrophy, cleft lip or palate, and septo-optic dysplasia.[63][64][68][69][70] Additional findings may include recurrent urinary tract infections, apnea, lethargy, seizures, polyuria, increased body fat, and midline central nervous system malformations.[59] Please see StatPearls' companion resource, "Hypopituitarism," for more information.

A diagnostic workup for neonatal hypopituitarism should include assessments of adrenocorticotropic hormone (ACTH), TSH, T4, LH, FSH, prolactin, cortisol, and growth hormone.[64] A magnetic resonance imaging (MRI) of the brain should be performed to evaluate the pituitary gland if hypopituitarism is suspected.[59][63]

In cases of hypoglycemia, cortisol deficiency should be promptly investigated and quickly treated if diagnosed.[58][59]
Birth weight is generally normal, as fetal growth is not usually affected.[58][59]
Congenital hypopituitarism may result from developmental disorders of the pituitary gland, birth trauma, asphyxia, or genetic mutations, although the precise etiology of the disorder is not well understood.[58][64]
Acquired forms of hypopituitarism are quite rare in neonates.
Congenital hypopituitarism may involve isolated or multiple hormonal deficiencies.[71]
Neonates exhibiting nystagmus should undergo an evaluation of pituitary function.[59][72]
Genetic testing should also be considered to help determine the underlying cause.[58]

Congenital Growth Hormone Deficiency

Congenital growth hormone deficiency is the most common isolated pituitary disorder in childhood, with an estimated incidence of 1 in 3500 births in the United States.[58][59][73] Growth hormone stimulation testing is contraindicated in infants aged 1 or younger.[58]

Key clinical features of congenital growth hormone deficiency include hypoglycemia and micropenis.[58][59] Interestingly, fetal growth and birth weight are typically normal despite the deficiency.

Treatment / Management

Most children with micropenis achieve normal penile size and length by adulthood without treatment.[1][74] Monitoring the overall growth rate may be more significant than measuring and following the stretched penile length.[1] Body mass index (BMI) is the most significant predictor of eventual penile growth by adulthood, whereas baseline stretched penile length is surprisingly a less reliable indicator.[1][75]

Clinical trials evaluating medical and surgical interventions for micropenis have yielded variable results.[1] Treatment approach typically depends on the primary etiology, age at presentation, degree of penile atrophy, and desired outcome. A reasonable plan involves initiating medical therapy first, followed by surgical intervention if medical treatment fails to achieve the desired results. As many patients experience normalization of penis size after puberty, careful shared decision-making and thorough discussion of options are essential.[1][74]

The goals of micropenis management include:

Ability to achieve normal sexual function.
Preserve sperm count and fertility.
Minimize social embarrassment related to micropenis.
Ensure normal urinary function in the standing position.

Medical Treatment

The standard medical treatment of congenital micropenis would generally include:

Testosterone is available as an IM injection or a topical gel for children with micropenis. Testosterone is administered either as an IM injection or a topical gel in children with micropenis. A commonly used, effective, traditional dosing regimen involves administering testosterone IM at a dosage of 25 mg every 3 weeks for a total duration of 3 months.[76][77]
- This regimen serves both therapeutic and diagnostic purposes. Failure to achieve a significant increase in penile size may indicate androgen insensitivity.[4][8][76][77][76][78][79][80][81]

(B2)

The use of 5% testosterone topical cream in children and infants aged 8 or younger has shown promising outcomes.[82]
- In a study, 45 out of 50 patients (90%) demonstrated a statistically significant increase in both penile length and serum testosterone levels after 30 days of treatment with the topical hormone cream.[82]

Children aged 12 and older may be treated with IM hCG at a dose of 1500 to 2000 IU administered weekly for 6 weeks. Please refer to the "Mini-puberty" section below for further information.[78]

DHT 2.5% gel, a potent metabolite of testosterone, has demonstrated efficacy primarily in case reports and small series, particularly in infants with 5α-reductase deficiency.[79][83][84]
- One protocol involved the topical application of DHT to the periscrotal region 3 times a day for 5 weeks.[2]
- In selected newborns, DHT therapy has been associated with an increase in stretched penile length of at least 120%.[84]
- Topical DHT may be considered in cases where standard testosterone therapy fails.[2][84]
- Caregivers, particularly mothers, should exercise caution when administering topical therapy by wearing gloves to prevent inadvertent skin absorption.

(B2)

Boys with isolated growth hormone deficiency may benefit from hormonal supplements, which can promote penile growth along with other physiological effects.[20][85]
- Testosterone supplements are usually unnecessary for patients with isolated growth hormone deficiency.[20][85]

Human recombinant FSH and LH therapy may be considered in children with hypogonadotropic hypogonadism, where it has been shown to promote significant penile growth.[2][8][80][86][87](B3)

A favorable response would be at least a 3.5 cm increase or a doubling of the stretched penile length after the initial course of testosterone therapy.[2][60][77][88] A course of testosterone therapy can be repeated if the initial response is inadequate.[2][16][77] If there is still no response, topical DHT therapy should be considered.[2][84] Please see StatPearls' companion resource, "Kallmann Syndrome," for more information.

Patients with hypogonadotropic hypogonadism will experience a progressive decrease in penile androgen responsiveness, which naturally becomes more pronounced during early adulthood.[2][89] As the concentration of penile androgen receptors increases with early testosterone treatment, androgen therapy should optimally be initiated before the early adulthood period.[2][89]

Supplemental testosterone therapy is relatively ineffective for treating micropenis in adults or children after puberty.[81] However, initiating testosterone therapy at the onset of puberty may provide some benefit.[77] As most testosterone formulations are designed for adult male hypogonadism, clinicians should carefully monitor androgen levels in boys undergoing therapy to avoid supratherapeutic dosing.[90]

Many boys with micropenis caused by gonadotropin deficiency will not undergo normal puberty. In these cases, testosterone should be administered to induce puberty, with gradual dose increases to reach full adult replacement levels and closely mimic natural pubertal progression.[91] To preserve fertility, treatment with hCG and recombinant FSH is recommended to stimulate endogenous testosterone production and support spermatogenesis.[92][93][94][95] Ideally, this therapy should be managed under the supervision of a specialist in male fertility and reproductive medicine.(A1)

Mini-puberty

Mini-puberty is a normal, temporary phase of increased gonadotropin production that briefly reaches adult levels, beginning within the first few months of life.[17][18] During a "mini-puberty" phase, gonadotropin levels typically peak around 1 month after birth and persist until approximately 6 months of age.[19] This mini-puberty phase is absent in patients with congenital hypogonadotropic hypogonadism—a rare genetic disorder affecting approximately 1 in 4000 to 1 in 15,000 male births annually.[17][18] (B3)

Congenital hypogonadotropic hypogonadism is characterized by a deficiency in hypothalamic GnRH production during both fetal and postnatal development.[17][18][96] Kallmann syndrome accounts for about 50% of all cases of male congenital hypogonadotropic hypogonadism.[96] Patients with this condition do not experience a normal mini-puberty, which further contributes to their penile size disorder. Diagnosis is established by measuring serum gonadotropin and testosterone levels within the first 2 months after birth.[18][97] (B3)

Evidence suggests that gonadotropin replacement therapy to mimic the natural "mini-puberty" period can help normalize penile size.[17][18][98][99][100][101] This approach may also reduce the incidence of cryptorchidism and enhance future male fertility.[18][98] Clinically, patients with congenital hypogonadotropic hypogonadism may present with both micropenis and cryptorchidism, although the condition is usually not diagnosed until puberty.[17][102](A1)

Treatment of congenital hypogonadotropic hypogonadism includes the administration of recombinant LH and FSH during infancy.[8][87] The recommended regimen is 21.3 IU of FSH and 20 to 40 IU of LH twice weekly for about 7 months.[8] Alternatively, a continuous infusion may also be used, as both protocols have yielded promising results.[8][18][80][86][87][103][104](B3)

Experimental studies have shown that reducing lysyl oxidase activity using anti-lysyl oxidase, combined with passive penile stretching via an external vacuum erection device (VED), can promote penile lengthening through tunica albuginea remodeling in a rat model.[105][106] This effect was more pronounced in prepubertal rats compared to adults.[107] Anti-lysyl oxidase therapy, with or without VED treatment, did not impact erectile function or alter the microscopic structure of the corpus cavernosum.[107] A maximum penile length increase of nearly 20% was observed.[107] The addition of hCG had no significant effect on penile growth.[106](B2)

Combining testosterone therapy with growth hormone supplementation produced normal-sized penises in an animal model of micropenis—an outcome neither therapy achieved individually.[108]

Surgical Treatment

Penile reconstruction may be considered when medical treatment fails to produce adequate results. However, most patients with micropenis achieve a normal penis size by adulthood without surgical intervention.[1][74] Although surgery can provide initially satisfactory outcomes, many treated patients later report dissatisfaction with penile appearance.[1][74] Therefore, surgical intervention for micropenis in children is rarely indicated, given the typically favorable outcomes without surgery, potential procedural risks, and inconsistent patient satisfaction.[1][8][74]

The suspensory support of the penis is provided by 4 pelvic ligaments—the arcuate, dense vertical, fundiform, and suspensory ligaments.[109] Of these, the fundiform and suspensory ligaments can be surgically released without compromising the stability of an erect penis.[109] This procedure typically increases the average flaccid stretched penile length from 7.4 cm to 10.7 cm without affecting erectile function or stability.[109][110] However, penile lengthening alone is generally insufficient to achieve a penis suitable for sexual intercourse, and phalloplasty is often required in adults to achieve satisfactory results.[111]

Complete penile reconstruction (phalloplasty)

Phalloplasty with urethroplasty can be successfully performed in adults with micropenis who have realistic expectations, with generally favorable outcomes reported.[81][112][113][114][115][116][117][118][119][120] The addition of a penile prosthesis can restore erectile function in the reconstructed penis.[121][122][123][124][125] Overall patient satisfaction following phalloplasty ranges from approximately 77% to 95%.[126][127][128][129][130][131](A1)

According to the American Urological Association and the Urology Care Foundation, phalloplasty is a surgical procedure to reconstruct the penis. This procedure is generally appropriate for adult men with severe micropenis when the condition causes significant distress, dysfunction, or negatively affects quality of life. Phalloplasty is particularly recommended for individuals with a stretched penile length of less than 7.5 cm (2.95 inches).[9]

Various surgical techniques for total phalloplasty, such as radial artery–based forearm skin flaps, can restore normal penile length, achieve favorable cosmetic outcomes, and enable acceptable sexual function when combined with a penile prosthesis.[112][113][114][115][116][117][132] Additional flap options include the sensate osteocutaneous fibular, free (septocutaneous) fibular, free scapular, suprapubic abdominal wall, pedicled anterolateral thigh, musculocutaneous latissimus dorsi, and vertical rectus abdominis flaps.[133][134] Among these, the radial forearm flap remains the most commonly used technique, followed by the anterolateral thigh flap.[133][134](A1)

Urethral reconstruction (urethroplasty)

Urethroplasty can be performed using various techniques, including the integrated (tube-in-tube) method, superficial circumflex iliac artery perforator flap, buccal mucosa grafts, radial forearm flap, or the "Big Ben" 2-stage approach for urethral lengthening.[120][128][135][136] However, phalloplasty and urethroplasty procedures are associated with a high rate of complications—such as scarring, penile insensitivity, fistula formation, urethral strictures, and patient dissatisfaction—often necessitating surgical repairs and modifications.[125][128][137][138][139][140] The primary goal of urethral reconstruction is to enable the patient to void while standing following phalloplasty.(B3)

Optimal results in adult patients with severe micropenis are achieved when expectations are realistic. Many men face significant psychological challenges that can interfere with sexual activity, including poor self-image and the effects of previous traumatic sexual experiences.[34][119][137] Psychological support is recommended and often essential for addressing these issues.[34][118][137] (B2)

An overall lack of systematic studies exists that compares the different treatment options for micropenis in terms of overall outcomes, patient satisfaction, genital appearance, quality of life, sexual function and enjoyment, and psychosocial development. Most existing studies include diverse sexually dysmorphic diagnoses, have small sample sizes, and lack long-term follow-up.[4]

Gender Assignment in Cases of Micropenis

Most prepubertal males with micropenis and bilaterally descended functional testes respond well to testosterone supplementation therapy.[4][34][76][78][132][141]

Gender reassignment to female with genitoplasty surgery is usually not recommended for isolated micropenis.[132][142][143] However, it may be considered in exceptional circumstances, such as in individuals with incomplete androgen insensitivity syndrome. Even in these cases, the decision remains a matter of controversy.[132][142][143]

The consensus among most experts and professional societies is that 46,XY male infants with isolated micropenis and functional testes should be raised as males, as they typically respond to testosterone therapy. An exception may be made in carefully selected cases involving incomplete androgen insensitivity syndrome.[132][142][143][144][145][146][147][148][149][150]

(B3)

Complete androgen insensitivity syndrome results in phenotypic females. The consensus is that individuals with this condition should be raised as females despite their 46,XY genotype.[146][150] The condition is typically diagnosed during evaluation for female infertility.[148] Please see StatPearls' companion resource, "Androgen Insensitivity Syndrome," for more information.

Children with 5α-reductase deficiency and micropenis are likely to experience spontaneous penile lengthening at puberty and are therefore raised as males.[146] The enzyme 5α-reductase converts testosterone into the more potent DHT, which is necessary for the early development of the male penis.[146] Please see StatPearls' companion resources, "5-Alpha Reductase Deficiency" and "Biochemistry, Dihydrotestosterone," for more information.

Differential Diagnosis

Accurate diagnosis of micropenis requires careful distinction from other conditions that cause the appearance of a small penis for appropriate management and the prevention of unnecessary interventions.

The most important differential diagnosis is pseudo-micropenis—a condition in which the penis appears small due to the unusual prominence of the surrounding peripubic tissue or the presence of a web that attaches the penis to the underlying scrotal skin.[2]

A meticulous and comprehensive physical examination is essential to rule out pseudo-micropenis and avoid unnecessary invasive diagnostic evaluation with significant psychosocial stress and anxiety for the patient and his family.

A buried penis can be mistaken for a micropenis.

Chordee of the penis and hypospadias are surgical conditions that cause abnormal curvature of the penile shaft, which can lead to underestimation of penile length.

Overly flaccid penile skin or foreskin, excessive fatty tissue, buried penis, and postoperative scarring from prior penile surgery can all interfere with obtaining an accurate measurement of stretched penile length.[2]

Prognosis

Micropenis carries a generally good prognosis, especially if detected and treated early.

Complications

Micropenis and phalloplasty surgery can be associated with various complications, including:

Dissatisfaction with penile size, girth, function, or appearance in adulthood (which is often related to a lack of social and psychological support, poor surgical outcomes, or unrealistic preoperative expectations)
Erectile dysfunction
Flap necrosis
Hematoma formation
High rate of reoperation
Infertility (often due to low sperm count or underlying hormonal disorders)
Loss of the phalloplasty flap due to tissue necrosis (reported in <7% of cases) [127]
Penile edema
Poor self-image
Postoperative scarring
Psychogenic sexual dysfunction
Unrecognized underlying pathologies
Unsatisfactory cosmetic appearance
Urethral fistulas (up to 50%) and strictures (up to 38%) [127]
Various psychological issues
Wound infection and dehiscence [127][151][152]

Deterrence and Patient Education

Early recognition of micropenis enables timely initiation of treatment, which can significantly improve the prognosis.[34] Notably, it is important to reassure families that the condition often resolves by adulthood, and if surgery is needed, it can be performed more safely and effectively at that time.

Young boys with micropenis may experience significant embarrassment and are at risk of bullying by peers. Therefore, healthcare providers should offer psychological support, counseling, and appropriate interventions to these individuals to help address emotional and social challenges.

Pearls and Other Issues

Key facts to keep in mind regarding micropenis include:

Circumcision is not recommended in children with micropenis.[8]

Elevated serum testosterone may indicate either androgen insensitivity syndrome (partial or incomplete) or 5-alpha reductase deficiency. The testosterone-to-DHT ratio can help differentiate between the two conditions.[8]
- The normal testosterone-to-DHT ratio is 2-3:1, but it can increase to as high as 26:1 following biochemical stimulation (hCG).
  - If the stimulated testosterone-to-DHT ratio is 27 or more, it suggests 5α-reductase deficiency. See the companion StatPearls' resource, "Biochemistry, Dihydrotestosterone" and "5-Alpha-Reductase Deficiency," for more information.
  - A stimulated testosterone-to-DHT ratio of 26 or lower is more consistent with partial androgen insensitivity syndrome. Please see StatPearls' companion resource, "Androgen Insensitivity Syndrome," for more information.[150]

Elevated 17-OH progesterone levels suggest virilizing congenital adrenal hyperplasia.[8]

An androstenedione-to-testosterone ratio greater than 20 indicate 17β-HSD type-3 deficiency.[8]

Elevated deoxycorticosterone levels are associated with 17α-hydroxylase deficiency.[153]

If hypogonadotropic hypogonadism is diagnosed, an MRI of the brain is suggested.[8]

In prepubertal males with normal testes, testosterone treatment for micropenis is likely to be successful.

Low levels of FSH, LH, and testosterone suggest the possibility of other hormonal abnormalities in the anterior pituitary. Evaluation should include growth hormone, insulin-like growth factor 1, cortisol, TSH, and free T4 levels, along with a brain MRI.[8]

Most cases of isolated micropenis resolve by the time the individual reaches adulthood.[1][74]

Testosterone therapy will be relatively ineffective in adult men and post-pubertal males.[81]

The simultaneous presentation of micropenis and cryptorchidism suggests a diagnosis of congenital hypogonadotropic hypogonadism.[8][154]

Topical DHT may be effective when topical testosterone therapy fails, particularly in patients with 5α-reductase deficiency.[2][79][84][155] Seethe companion StatPearls' resource, "5-Alpha-Reductase Deficiency," for more information.

Enhancing Healthcare Team Outcomes

Micropenis is a clinical finding that may indicate an underlying systemic hormonal abnormality or a genetic condition. As it can be a manifestation of various conditions, a comprehensive, multidisciplinary approach is essential for accurate diagnosis and effective management. The interdisciplinary healthcare team often includes adult and pediatric endocrinologists, urologists, plastic surgeons, and psychologists to address the medical, surgical, and psychosocial aspects of the condition.

Ancillary services, including those provided by geneticists, psychologists, social workers, and pharmacists, are essential for supporting families and maintaining the mental well-being of both patients and their families. As most cases of micropenis are identified during the early neonatal period, nursing assessments are often the first step in recognizing the condition and initiating further evaluation.

Although standardized evaluation and management guidelines have been proposed, the wide variability in presentation and underlying causes makes a comprehensive history and physical examination essential before initiating diagnostic testing. Medical and surgical treatments for micropenis generally yield satisfactory clinical outcomes; however, social and psychological dissatisfaction may persist, highlighting the need for ongoing psychosocial support.

Media

(Click Image to Enlarge)

Age-Specific Lower Limits (<2.5 SD Below the Mean) of Stretched Penile Lengths (in centimeters).

Contributed by M Alsaleem, MD

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