Virilization
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In biology and medicine, virilization refers to the biological development of sex differences, changes which make a male body different from a female body. Most of the changes of virilization are produced by androgens. Virilization is most commonly used in three medical and biology of gender contexts: prenatal sexual differentiation, the postnatal changes of normal male puberty, and excessive androgen effects in girls or women.
Prenatal virilization
In the prenatal period, virilization refers to closure of the perineum, thinning and rugation of the scrotum, growth of the phallus, and closure of the urethral groove to the tip of the penis. In this context masculinization is synonymous with virilization. Prenatal virilization of genetic females and undervirilization of genetic males are common causes of ambiguous genitalia and intersex conditions.
Undervirilization can occur if a genetic male cannot produce enough androgen or the body tissues cannot respond to it. Extreme undervirilization occurs when no significant androgen can be produced or the body is completely insensitive to it, and results in a female body. Partial undervirilization produces ambiguous genitalia part way between male and female. The mildest degree of undervirilization may be a slightly small penis with hypospadias. Examples of undervirilization are androgen insensitivity syndrome, 5 alpha reductase deficiency, and some forms of congenital adrenal hyperplasia.
Prenatal virilization (or masculinization) of a genetically female fetus can occur when an excessive amount of androgen is produced by the fetal adrenal glands or is present in maternal blood. In the severest form of congenital adrenal hyperplasia complete masculinization of a genetically female fetus results in an apparently normal baby boy with no palpable testes. More often, the virilization is partial and the genitalia are ambiguous.
Normal virilization
In common as well as medical usage, virilization often refers to the process of normal male puberty, in which testosterone changes a boy's body into a man's. These effects include growth of the penis and testes, accelerated growth, development of pubic hair and other androgenic hair of face, torso, and limbs, deepening of the voice, increased musculature, thickening of the jaw, prominence of the neck cartilage, and broadening of the shoulders.
Abnormal childhood virilization
Virilization can occur in childhood in either boys or girls due to excessive amounts of androgens. Typical effects of virilization in children are pubic hair, accelerated growth and bone maturation, increased muscle strength, acne, adult body odor, and sometimes growth of the penis. In a boy, virilization may signal precocious puberty, while congenital adrenal hyperplasia and androgen producing tumors (usually) of the gonads or adrenals are occasional causes in both sexes.
virilization in adolescent or adult women
Virilization in a woman can manifest as clitoral enlargement, increased muscle strength, acne, hirsutism, frontal hair thinning, deepening of the voice, and menstrual disruption due to anovulation. Some of the possible causes of virilization in women are:
- Polycystic ovary syndrome
- Androgen-producing tumors of the
- Hypothyroidism
- Anabolic steroid exposure
- Congenital adrenal hyperplasia due to 21-hydroxylase deficiency (late-onset)
See also
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
