eMedicine Specialties > Pediatrics: General Medicine > Endocrinology

Androgen Insensitivity Syndrome

Author: Bruce E Wilson, MD, Associate Professor, Department of Pediatrics and Human Development, Michigan State University College of Human Medicine at East Lansing
Contributor Information and Disclosures

Updated: Jun 23, 2009

Introduction

Background

Androgen insensitivity syndrome (AIS), formerly known as testicular feminization, is an X-linked recessive condition resulting in a failure of normal masculinization of the external genitalia in chromosomally male individuals. This failure of virilization can be either complete androgen insensitivity syndrome (CAIS) or partial androgen insensitivity syndrome (PAIS), depending on the amount of residual receptor function.

Both individuals with partial androgen insensitivity syndrome and individuals with complete androgen insensitivity syndrome have 46,XY karyotypes. Individuals with complete androgen insensitivity syndrome have female external genitalia with normal labia, clitoris, and vaginal introitus.1,2,3 The phenotype of individuals with partial androgen insensitivity syndrome may range from mildly virilized female external genitalia (clitorimegaly without other external anomalies) to mildly undervirilized male external genitalia (hypospadias and/or diminished penile size).

Penoscrotal hypospadias is shown. Note the associ...

Penoscrotal hypospadias is shown. Note the associated ventral chordee and true urethral meatus located at the scrotal level.

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Penoscrotal hypospadias is shown. Note the associ...

Penoscrotal hypospadias is shown. Note the associated ventral chordee and true urethral meatus located at the scrotal level.



In either case, affected individuals have normal testes with normal production of testosterone and normal conversion to dihydrotestosterone (DHT), which differentiates this condition from 5-alpha reductase deficiency. Because the testes produce normal amounts of müllerian-inhibiting factor (MIF), also known as müllerian-inhibiting substance (MIS) or anti-müllerian hormone/factor (AMH/AMF), affected individuals do not have fallopian tubes, a uterus, or a proximal (upper) vagina.

Pathophysiology

The basic etiology of androgen insensitivity syndrome is a loss-of-function mutation in the androgen receptor (AR) gene. This AR gene has been localized to the long arm of the X chromosome (ie, Xq11-13). Over 200 such mutations have been described, including complete and partial gene deletions, point mutations, and small insertions/deletions. These mutations can cause a variety of functional defects, ranging from a complete loss of receptors on the cell surface because of incomplete protein synthesis to alterations in substrate binding affinity. Altered substrate binding affinity causes a signal transmission loss, despite normal cell surface receptor numbers. While the genotypes causing complete androgen insensitivity syndrome are consistent in phenotypic presentation, the genotype/phenotype relationships for the mutations causing partial androgen insensitivity syndrome remain unclear.

Loss of AR function means that, despite normal levels of androgen synthesis, the typical postreceptor events that mediate the effects of hormones on tissues do not occur. This results in the phenotype of prenatal undervirilization of external genitalia, absence of pubic and axillary hair, lack of acne, and absence of voice changes at puberty.

Frequency

United States

Data are currently not available on the specific incidence of complete androgen insensitivity syndrome and partial androgen insensitivity syndrome.

International

The best available data suggest an androgen insensitivity syndrome incidence of approximately 1 case per 20,400 liveborn males. This statistic is based on analysis of a Danish patient registry that included only hospitalized cases; thus, the true incidence of androgen insensitivity syndrome may be higher. Complete androgen insensitivity syndrome appears more common than partial androgen insensitivity syndrome, although exact figures are unavailable.

Mortality/Morbidity

Androgen insensitivity syndrome, either complete or partial, has little medical morbidity or mortality. Over time, untreated patients have a theoretical risk of malignant degeneration and development of gonadoblastoma of the testes. No documentation on the morbidity or mortality of these tumors specifically in individuals with androgen insensitivity syndrome is available. The tumor is considered cured without need for further therapy if it is removed while still limited to the interior of the testes capsule. The tumor is considered curable in most patients even when undetected at this early state.

In contrast to medical morbidity, psychological morbidity is common. Phenotypic females who are discovered to be genetic males may have psychosocial problems. These females require sensitive psychological support. Their psychosocial problems range from identity issues to problems dealing with the gender perceptions of the outside world and the style and sensitivity (or lack thereof) they encounter within the medical system.

Most affected individuals report psychological trauma at diagnosis. Their reactions to the diagnosis frequently are compounded by their interactions with the medical care system, in which they often are treated as oddities and forced to undergo multiple examinations and interviews with students and residents for teaching purposes. Even in nonteaching situations, women with androgen insensitivity syndrome report difficulties identifying offices where physicians and staff are familiar with their condition. Many of these patients have been told that they really are not women but actually are men because of the presence of a Y chromosome and testes. These difficulties and doubts often cause shame and self-doubt as well as anger and frustration with a medical system they had expected to take care of them.

Race

No racial differences in incidence or presentation of androgen insensitivity syndrome have been described.

Sex

All patients with androgen insensitivity syndrome are chromosomally and gonadally male. However, separating the concepts of sex and gender is crucial with these patients. The term sex is usually based on physical attributes, whereas the concept of gender is based on an individual's self-concept and self-identification as well as the role an individual assumes in society.

Most patients with complete androgen insensitivity syndrome have a female gender. This may be due, in part, to the patient's role assignment and upbringing before the diagnosis or to the patient's choice of female "sex/gender" at diagnosis. The significance of the androgen effect's absence is increasingly recognized for its influence on the maturing brain (and other systems) in terms of developing adult gender identity.

Partial androgen insensitivity syndrome is a more complicated problem for gender identity. Just as the genitalia may be highly varied in the degree of virilization, gender identity may be either female or male. At present, no reliable predictors of eventual gender identity have been identified, including genotype or degree of genital virilization at birth.

Clinical

History

Most cases of androgen insensitivity syndrome (AIS) are identified in the newborn period by the presence of inguinal masses, which later are identified as testes during surgery. Some patients are first seen in the teenage years for evaluation of primary amenorrhea. Many of these patients have a history of surgery for hernias and/or the presence of gonads in the inguinal canals, which were considered ovaries and returned to the abdomen.

Physical

In newborns with complete androgen insensitivity syndrome (CAIS), the most frequent initial finding is unilateral or bilateral masses in the inguinal canals that are found to be testes during surgery. Associated hernias may or may not be present.4

In adolescent patients, notable findings include inguinal masses. As with newborns, these masses may or may not be associated with hernias. In addition, adolescent patients have no pubic and axillary hair, with otherwise scanty body hair, and lack acne, although breast is normal as a result of conversion of testosterone to estradiol.

Newborn patients with partial androgen insensitivity syndrome (PAIS) can have a highly variable genital appearance. Adolescents may have pubic hair, although usually less than normal, and may have progressive clitoral enlargement and other signs of masculinization.

Causes

The basic etiology of androgen insensitivity syndrome is a loss-of-function mutation in the AR gene.5

More on Androgen Insensitivity Syndrome

Overview: Androgen Insensitivity Syndrome
Differential Diagnoses & Workup: Androgen Insensitivity Syndrome
Treatment & Medication: Androgen Insensitivity Syndrome
Follow-up: Androgen Insensitivity Syndrome
Multimedia: Androgen Insensitivity Syndrome
References
Further Reading
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Further Reading

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Keywords

androgen insensitivity syndrome, AIS, complete androgen insensitivity syndrome, CAIS, partial androgen insensitivity syndrome, PAIS, testicular feminization, androgen receptor deficiency, androgen resistance syndrome, feminizing testes syndrome, Reifenstein syndrome, Morris syndrome, Goldberg-Maxwell syndrome, hypospadias, clitorimegaly, diminished penile size, gonadoblastoma, hernias, acne, clitoral enlargement, masculinization, treatment, diagnosis

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Contributor Information and Disclosures

Author

Bruce E Wilson, MD, Associate Professor, Department of Pediatrics and Human Development, Michigan State University College of Human Medicine at East Lansing
Bruce E Wilson, MD is a member of the following medical societies: American Diabetes Association, Association of Clinical Scientists, Lawson-Wilkins Pediatric Endocrine Society, and New York Academy of Sciences
Disclosure: Nothing to disclose.

Medical Editor

Arlan L Rosenbloom, MD, Adjunct Distinguished Service Professor Emeritus of Pediatrics, University of Florida; Fellow of the American Academy of Pediatrics; Fellow of the American College of Epidemiology
Arlan L Rosenbloom, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Epidemiology, American Pediatric Society, Endocrine Society, Florida Pediatric Society, Lawson-Wilkins Pediatric Endocrine Society, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Lynne Lipton Levitsky, MD, Chief, Pediatric Endocrine Unit, Massachusetts General Hospital; Associate Professor, Department of Pediatrics, Harvard University Medical School
Lynne Lipton Levitsky, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Diabetes Association, American Pediatric Society, Endocrine Society, Lawson-Wilkins Pediatric Endocrine Society, and Society for Pediatric Research
Disclosure: Pfizer Grant/research funds P.I.; Tercica Grant/research funds PI, also occasional consultant

CME Editor

Merrily P M Poth, MD, Professor, Department of Pediatrics and Neuroscience, Uniformed Services University of the Health Sciences
Merrily P M Poth, MD is a member of the following medical societies: American Academy of Pediatrics, Endocrine Society, and Lawson-Wilkins Pediatric Endocrine Society
Disclosure: Nothing to disclose.

Chief Editor

Stephen Kemp, MD, PhD, Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas and Arkansas Children's Hospital
Stephen Kemp, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Pediatric Society, Endocrine Society, Phi Beta Kappa, Southern Medical Association, and Southern Society for Pediatric Research
Disclosure: Genentech, Inc. Honoraria Speaking and teaching; Pfizer, Inc. Honoraria Consulting

 
 
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