eMedicine Specialties > Pediatrics: General Medicine > Endocrinology

Androgen Insensitivity Syndrome: Treatment & Medication

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

Treatment

Medical Care

Medical care for a patient with androgen insensitivity syndrome (AIS) has 2 aspects: hormone replacement therapy (HRT) and psychological support.

  • HRT
    • HRT is the first and less complex aspect. All patients with complete androgen insensitivity syndrome (CAIS) and most patients with all but the mildest forms of partial androgen insensitivity syndrome (PAIS) undergo gonadectomy at some point in their treatment (see Surgical Care). Adolescent and adult patients with androgen insensitivity syndrome require hormone replacement.
    • For patients with complete androgen insensitivity syndrome, hormone therapy almost always consists of estrogen replacement. The general belief is that these women do not require progesterone because they have no uterus. Some evidence suggests that progesterone therapy combined with estrogen replacement may lessen the long-term risk of breast cancer, although this type of therapy is debatable. More recent meta-analyses suggest progesterone administration may have little or no advantage for patients without a uterus. Therapy usually is initiated with a low dose of estrogen alone, then is increased to routine adult dosing. Progesterone is added, if considered appropriate, after maintenance therapy with estrogen is established.
    • For individuals with partial androgen insensitivity syndrome , traditional therapy has mirrored therapy for individuals with complete androgen insensitivity syndrome. Patients with partial androgen insensitivity syndrome who have a male gender identity, however, may be treated with testosterone and/or dihydrotestosterone (DHT). The advantage of DHT is that it cannot be aromatized to estrogen. No medical consensus has been reached about this therapy; no dosage schedules have been established. Therapy may vary depending on the nature of the gene defect.
  • Psychological support
    • Psychological support is probably the most important aspect of medical care from the patient's point of view. In a family with an affected infant, the parents are the primary clients. Parents need genetic counseling to understand the nature of the condition and the risk of recurrence (25% for each subsequent pregnancy) as well as to identify other potential carriers. In addition, parents often benefit from the services of a pediatric psychologist or child and adolescent psychiatrist to help adjust to their child's condition, including support on how to inform the child, over time and in an age-appropriate manner, about the condition. Genetic counselors do not provide this type of ongoing family support.
    • In a family with an affected older child, the patient is the primary client, although family members also may require psychological services. In these cases, too, pediatric psychologists or child and adolescent psychiatrists are the preferred clinicians because of their medical background and ability to help address medical, emotional, and psychological issues or questions. If at all possible, the therapist also should have experience dealing with patients who have intersex conditions, even if this experience is not specific to androgen insensitivity syndrome. The patient needs to establish a long-term relationship with the therapist to discuss new issues that arise as the child matures. (At times, these visits will be infrequent.) For adults with androgen insensitivity syndrome and other intersex conditions, lack of emotional and psychological support has been a major criticism of the medical care system.
    • The primary care practitioner can coordinate medical care for a child with androgen insensitivity syndrome, or coordination may be performed by a pediatric endocrinologist, especially as part of a multidisciplinary team. Carefully maintain communication and coordination among primary care, genetic, endocrinologic, and surgical services to avoid trauma to the child and family.
    • Contact with other individuals who have androgen insensitivity syndrome is another source of psychological and emotional support for the patient. The Androgen Insensitivity Syndrome Support Group (AISSG) has constituent organizations in the United States, United Kingdom, and Australia, as well as contacts and/or smaller groups in many European countries. AISSG maintains an excellent Web site at www.medhelp.org/www/ais that provides a large amount of medical information, AISSG contact points, and patients' accounts of their experiences with AIS. This type of contact can markedly decrease feelings of "freakishness" and "being the only one," which patients and families frequently experience.

Surgical Care

  • For individuals with androgen insensitivity syndrome, the standard of care is an orchidectomy to prevent possible malignant degeneration of the testes.6 The timing of such surgery has been debated. Historically, early surgery was assumed preferable to avoid raising uncomfortable psychosexual issues during adolescence or young adulthood. More recently, surgery during the late teenage years or early 20s has been preferred. Later orchidectomy allows pubertal development to occur spontaneously with the production of estrogen from the aromatization of the high levels of testosterone normally produced.
  • In addition, many women with androgen insensitivity syndrome require vaginal lengthening procedures. Orchidectomy and vaginal lengthening procedures may be performed concurrently if surgery is postponed until the patient matures. Ultrasound examination of the gonads can monitor potential tumor development.
  • Vaginal lengthening procedures have stirred ongoing debate. In the past, many vaginal lengthening procedures were performed before or at onset of puberty. Many patient advocates now support delaying these procedures until the patient is sufficiently mature to participate actively in treatment decisions (ie, whether to undergo surgery, what type of procedure).
  • Similarly, in female gender patients with partial androgen insensitivity syndrome who have some degree of masculinization of the genitalia at birth, cosmetic reconstructive surgery traditionally has been performed in infancy. Patient advocates, including medical ethicists and intersex advocates, now endorse delaying this reconstructive surgery until children are old enough to decide for themselves. Medical practice and court decisions appear to be moving in this direction as the new standard of care.

Consultations

  • Initial consultation for the child with androgen insensitivity syndrome should include a geneticist and a pediatric endocrinologist. These individuals order and interpret the tests required to confirm the diagnosis. Additionally, these clinicians can provide appropriate information about the child's condition. An endocrinologist helps set the future course for medical and surgical therapy.
  • Because this is a particularly stressful diagnostic possibility for many families, consult an appropriate mental health professional to provide psychological and emotional support. Part of the mental health professional's role is to facilitate communication between the medical team and the family.

Medication

Hormone replacement therapy (HRT) with estrogens has been the standard of practice for postorchidectomy patients with androgen insensitivity syndrome (AIS). Although most physicians prescribe estrogen alone, some physicians have begun adding progesterone to the regimen, based upon a relatively small amount of data that suggests progesterone may lower the risk of breast cancer, have a role in the ductal development of the breast, or have some role in bone mineral accretion. (These potential benefits are hypothetical.)

Administration of androgens in more masculinized patients with partial androgen insensitivity syndrome (PAIS) has been suggested but remains highly controversial. Because some patients now are assigned male gender and are identifying as males in adulthood, this treatment probably will be described more extensively soon. No data currently describe dosage, administration, benefits, or adverse effects of androgen administration to patients with androgen insensitivity syndrome. Dosage and response likely depends on the severity of the receptor defect. Dihydrotestosterone (DHT) or androgen analogues that cannot be aromatized to estrogen appear to be the treatments of choice.

Estrogens

These agents are used as hormone replacement for women with androgen insensitivity syndrome who are postgonadectomy to support development and maintenance of secondary sexual characteristics and to prevent osteoporosis.


Conjugated estrogens (Premarin)

Represents the average composition of estrogens in pregnant mare urine. Composed of estrone, equilin, 17-alpha estradiol, equilenin, and 17-alpha dihydroequilenin (in small amount). Rapidly biotransformed after administration.

Adult

0.3-0.625 mg PO qd
If cycling with progesterone, administer on days 1-21 of cycle

Pediatric

In girls who are orchidectomized prepubertally, start estrogens at lowest available dose, preferably when bone age is at least 13 y
Appropriate beginning dose: 0.3 mg qod; then gradually increase dose to mimic normal female puberty until adult levels achieved

May reduce hypoprothrombinemic effect of anticoagulants; coadministration of barbiturates, rifampin, and other agents that induce hepatic microsomal enzymes may reduce estrogen levels; increased pharmacologic and toxicologic effects of corticosteroids may occur via inactivation of hepatic P450 enzyme; loss of seizure control has been observed when administered concurrently with hydantoins

Documented hypersensitivity; avoid in patients diagnosed with breast cancer, undiagnosed abnormal genital bleeding, active thrombophlebitis or thromboembolic disorders, or in patients with history of such disorders with previous estrogen use (except when used in treatment of breast or prostatic malignancy)

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

May cause some degree of fluid retention and require careful observation; certain patients may develop undesirable manifestations of excessive estrogenic stimulation


Ethinyl estradiol (Estinyl)

Bioequivalence of various estrogens is quite unclear, but 5-10 mcg of ethinyl estradiol equals approximately 300 mcg of conjugated estrogens in terms of quantifiable metabolic effects on sex hormone binding globulin and gonadotropins.

Adult

20 mcg PO qd

Pediatric

20 mcg PO qod

May reduce hypoprothrombinemic effect of anticoagulants; coadministration of barbiturates, rifampin, and other agents that induce hepatic microsomal enzymes may reduce estrogen levels; increased pharmacologic and toxicologic effects of corticosteroids may occur via inactivation of hepatic P450 enzyme; loss of seizure control has been observed when administered concurrently with hydantoins

Documented hypersensitivity; avoid in patients diagnosed with breast cancer, undiagnosed abnormal genital bleeding, active thrombophlebitis or thromboembolic disorders, or in patients with history of such disorders with previous estrogen use (except when used in treatment of breast or prostatic malignancy)

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

May cause some degree of fluid retention and require careful observation; certain patients may develop undesirable manifestations of excessive estrogenic stimulation

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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References

  1. Ohba K, Hayashida Y, Hakariya H, Ichinose S, Naitou S. [A case of complete androgen insensitivity syndrome]. Hinyokika Kiyo. May 2009;55(5):277-80. [Medline].

  2. Oakes MB, Eyvazzadeh AD, Quint E, Smith YR. Complete androgen insensitivity syndrome--a review. J Pediatr Adolesc Gynecol. Dec 2008;21(6):305-10. [Medline].

  3. Hashmi A, Hanif F, Hanif SM, Abdullah FE, Shamim MS. Complete Androgen Insensitivity Syndrome. J Coll Physicians Surg Pak. Jul 2008;18(7):442-4. [Medline].

  4. Solari A, Groisman B, Bidondo MP, Cinca C, Alba L. [Complete androgen insensitivity syndrome: diagnosis and clinical characteristics]. Arch Argent Pediatr. Jun 2008;106(3):265-8. [Medline].

  5. Philibert P, Audran F, Pienkowski C, et al. Complete androgen insensitivity syndrome is frequently due to premature stop codons in exon 1 of the androgen receptor gene: an international collaborative report of 13 new mutations. Fertil Steril. May 20 2009;[Medline].

  6. Winterborn MH, France NE, Raiti S. Incomplete testicular feminization. Arch Dis Child. Dec 1970;45(244):811-2. [Medline].

  7. Consortium on the Management of Disorders of Sex Development. Handbook for Parents. ISNA; 2006.

  8. Garrett CC, Kirkman M. Being an XY female: an analysis of accounts from the website of the androgen insensitivity syndrome support group. Health Care Women Int. May 2009;30(5):428-46. [Medline].

  9. [Guideline] Wierman ME, Basson R, Davis SR, et al. Androgen therapy in women: an Endocrine Society Clinical Practice guideline. J Clin Endocrinol Metab. Oct 2006;91(10):3697-710. [Medline]. [Full Text].

  10. [Guideline] Tekgul S, Riedmiller H, Gerharz E, et al. Micropenis. Guidelines on paediatric urology. Mar 2009;[Full Text].

  11. Amrhein JA, Meyer WJ 3d, Jones HW Jr, Migeon CJ. Androgen insensitivity in man: evidence for genetic heterogeneity. Proc Natl Acad Sci U S A. Mar 1976;73(3):891-4. [Medline]. [Full Text].

  12. Bals-Pratsch M, Schweikert HU, Nieschlag E. Androgen receptor disorder in three brothers with bifid prepenile scrotum and hypospadias. Acta Endocrinol (Copenh). Sep 1990;123(3):271-6. [Medline].

  13. Batch JA, Evans BA, Hughes IA, Patterson MN. Mutations of the androgen receptor gene identified in perineal hypospadias. J Med Genet. Mar 1993;30(3):198-201. [Medline].

  14. Boczkowski K, Teter J. FAmilial male pseudohermaphroditism. Acta Endocr. 1965;49:497-509.

  15. Bullock LP, Bardin WC. Androgen receptors in testicular feminization. J Clin Endocrinol Metab. Dec 1972;35(6):935-7. [Medline].

  16. Charest NJ, Zhou ZX, Lubahn DB, et al. A frameshift mutation destabilizes androgen receptor messenger RNA in the Tfm mouse. Mol Endocrinol. Apr 1991;5(4):573-81. [Medline].

  17. Consortium on the Management of Disorders of Sex Development. Clinical Guidelines for the Management of the Patient with a Disorder of Sex Development. ISNA; 2006.

  18. Davies HR, Hughes IA, Savage MO, et al. Androgen insensitivity with mental retardation: a contiguous gene syndrome?. J Med Genet. Feb 1997;34(2):158-60. [Medline].

  19. Edwards A, Hammond HA, Jin L, et al. Genetic variation at five trimeric and tetrameric tandem repeat loci in four human population groups. Genomics. Feb 1992;12(2):241-53. [Medline].

  20. Eil C. Familial incomplete male pseudohermaphroditism associated with impaired nuclear androgen retention. Studies in cultured skin fibroblasts. J Clin Invest. Apr 1983;71(4):850-8. [Medline].

  21. French FS, Baggett B, Van Wyk J. Testicular feminization: clinical, morphological and biochemical studies. J Clin Endocr. 1965;25:661-77.

  22. French FS, Van Wyk JJ, Baggett B, et al. Further evidence of a target organ defect in the syndrome of testicular feminization. J Clin Endocrinol Metab. May 1966;26(5):493-503. [Medline].

  23. Galli-Tsinopoulou A, Hiort O, Schuster T, et al. A novel point mutation in the hormone binding domain of the androgen receptor associated with partial and minimal androgen insensitivity syndrome. J Pediatr Endocrinol Metab. Feb 2003;16(2):149-54. [Medline].

  24. Gaspar ML, Meo T, Bourgarel P, et al. A single base deletion in the Tfm androgen receptor gene creates a short-lived messenger RNA that directs internal translation initiation. Proc Natl Acad Sci U S A. Oct 1 1991;88(19):8606-10. [Medline]. [Full Text].

  25. Gerli M, Migliorini G, Bocchini V, et al. A case of complete testicular feminisation and 47,XXY karyotype. J Med Genet. Dec 1979;16(6):480-3. [Medline].

  26. German J, Vesell M. Testicular feminization in monozygotic twins with 47 chromosomes (XXY). Ann Genet. 1966;9(1):5-8. [Medline].

  27. Goldstein JL, Wilson JD. Studies on the pathogenesis of the pseudohermaphroditism in the mouse with testicular feminization. J Clin Invest. Jul 1972;51(7):1647-58. [Medline].

  28. Griffin JE. Testicular feminization associated with a thermolabile androgen receptor in culutred human fibroblasts. J Clin Invest. Dec 1979;64(6):1624-31. [Medline].

  29. Griffin JE, Wilson JD. The syndromes of androgen resistance. N Engl J Med. Jan 24 1980;DA - 19800228(4):198-209. [Medline].

  30. Grino PB, Griffin JE, Cushard WG Jr, Wilson JD. A mutation of the androgen receptor associated with partial androgen resistance, familial gynecomastia, and fertility. J Clin Endocrinol Metab. Apr 1988;66(4):754-61. [Medline].

  31. Hughes IA, Evans BA. Complete androgen insensitivity syndrome characterized by increased concentration of a normal androgen receptor in genital skin fibroblasts. J Clin Endocrinol Metab. Aug 1986;63(2):309-15. [Medline].

  32. Imperato-McGinley J, Ip NY, Gautier T, et al. DNA linkage analysis and studies of the androgen receptor gene in a large kindred with complete androgen insensitivity. Am J Med Genet. May 1990;36(1):104-8. [Medline].

  33. Irvine RA, Yu MC, Ross RK, Coetzee GA. The CAG and GGC microsatellites of the androgen receptor gene are in linkage disequilibrium in men with prostate cancer. Cancer Res. May 1 1995;55(9):1937-40. [Medline].

  34. Jagiello G, Atwell JD. Prevalence of testicular feminisatioon. Lancet. 1962;1:329.

  35. Jukier L, Kaufman M, Pinsky L, Peterson RE. Partial androgen resistance associated with secondary 5 alpha-reductase deficiency: identification of a novel qualitative androgen receptor defect and clinical implications. J Clin Endocrinol Metab. Oct 1984;59(4):679-88. [Medline].

  36. Kaufman M, Pinsky L, Baird PA, McGillivray BC. Complete androgen insensitivity with a normal amount of 5 alpha- dihydrotestosterone-binding activity in labium majus skin fibroblasts. Am J Med Genet. 1979;4(4):401-11. [Medline].

  37. Kaufman M, Pinsky L, Bowin A, Au MW. Familial external genital ambiguity due to a transformation defect of androgen-receptor complexes that is expressed with 5 alpha- dihydrotestosterone and the synthetic androgen methyltrienolone. Am J Med Genet. Jul 1984;18(3):493-507. [Medline].

  38. Kaufman M, Pinsky L, Feder-Hollander R. Defective up-regulation of the androgen receptor in human androgen insensitivity. Nature. Oct 29 1981;293(5835):735-7. [Medline].

  39. Kaufman M, Straisfeld C, Pinsky L. Male pseudohermaphroditism presumably due to target organ unresponsiveness to androgens. Deficient 5alpha-dihydrotestosterone binding in cultured skin fibroblasts. J Clin Invest. Aug 1976;58(2):345-50. [Medline].

  40. Keenan BS, Meyer WJ 3d, Hadjian AJ, et al. Syndrome of androgen insensitivity in man: absence of 5 alpha- dihydrotestosterone binding protein in skin fibroblasts. J Clin Endocrinol Metab. Jun 1974;38(6):1143-6. [Medline].

  41. Kovacs WJ, Griffin JE, Weaver DD, et al. A mutation that causes lability of the androgen receptor under conditions that normally promote transformation to the DNA-binding state. J Clin Invest. Apr 1984;73(4):1095-104. [Medline]. [Full Text].

  42. Liao S, Witte D. Autoimmune anti-androgen-receptor antibodies in human serum. Proc Natl Acad Sci U S A. Dec 1985;82(24):8345-8. [Medline].

  43. Lin SY, Ohno S. The binding of androgen receptor to DNA and RNA. Biochim Biophys Acta. Jul 27 1981;654(2):181-6. [Medline].

  44. Long SE, David JS. Testicular feminisation in an Ayrshire cow. Vet Rec. Aug 8 1981;109(6):116-8. [Medline].

  45. Lubs HA, Vilar O, Bergenstal DM. Familial male pseudohermaphroditism with labial testes and partial feminization: endocrine studies and genetic aspects. J Clin Endocr. 1959;19:1110-1120.

  46. Lyon MF, Hawkes SG. X-linked gene for testicular feminization in the mouse. Nature. Sep 19 1970;227(5264):1217-9. [Medline].

  47. Madden JD, Walsh PC, MacDonald PC, Wilson JD. Clinical and endocrinologic characterization of a patients with the syndrome of incomplete testicular feminization. J Clin Endocrinol Metab. Oct 1975;41(4):751-60. [Medline].

  48. Mauvais-Jarvis P, Bercovici JP, Crepy O, Gauthier F. Studies on testosterone metabolism in subjects with testicular feminization syndrome. J Clin Invest. Jan 1970;49(1):31-40. [Medline]. [Full Text].

  49. Meyer WJ 3d, Migeon BR, Migeon CJ. Locus on human X chromosome for dihydrotestosterone receptor and androgen insensitivity. Proc Natl Acad Sci U S A. Apr 1975;72(4):1469-72. [Medline]. [Full Text].

  50. Muller U, Schneider NR, Marks JF, et al. Maternal meiosis II nondisjunction in a case of 47,XXY testicular feminization. Hum Genet. Feb 1990;84(3):289-92. [Medline].

  51. Northcutt RC, Island DP, Liddle GW. An explanation for the target organ unresponsiveness to testosterone in the testicular feminization syndrome. J Clin Endocrinol Metab. - Liddle GW;29(3):422-5. [Medline].

  52. Ohno S. The Y-linked H-Y antigen locus and the X-linked Tfm locus as major regulatory genes of the mammalian sex determining mechanism. J Steroid Biochem. May 1977;8(5):585-92. [Medline].

  53. Ono S. Simplicity of mammalian regulatory systems inferred by single gene determination of sex phenotypes. Nature. Nov 19 1971;234(5325):134-7. [Medline].

  54. Opitz JM, Simpson JL, Sarto GE, et al. Pseudovaginal perineoscrotal hypospadias. Clin Genet. 1972;3(1):1-26. [Medline].

  55. Perez-Palacios G, Ortiz S, Lopez-Amor E, et al. Familial incomplete virilization due to partial end organ insensitivity to androgens. J Clin Endocrinol Metab. Nov 1975;41(5):946-52. [Medline].

  56. Philip J, Trolle D. Familial male hermaphroditism with delayed and partial masculinization. Am J Obstet Gynecol. Dec 15 1965;93(8):1076-83. [Medline].

  57. Pinsky L, Kaufman M, Killinger DW, et al. Human minimal androgen insensitivity with normal dihydrotestosterone- binding capacity in cultured genital skin fibroblasts: evidence for an androgen-selective qualitative abnormality of the receptor. Am J Hum Genet. Sep 1984;36(5):965-78. [Medline].

  58. Pinsky L, Kaufman M, Levitsky LL. Partial androgen resistance due to a distinctive qualitative defect of the androgen receptor. Am J Med Genet. Jun 1987;27(2):459-66. [Medline].

  59. Pinsky L, Kaufman M, Summitt RL. Congenital androgen insensitivity due to a qualitatively abnormal androgen receptor. Am J Med Genet. 1981;10(1):91-9. [Medline].

  60. Purves JT, Miles-Thomas J, Migeon C, Gearhart JP. Complete androgen insensitivity: the role of the surgeon. J Urol. Oct 2008;180(4 Suppl):1716-9. [Medline].

  61. Quigley CA, De Bellis A, Marschke KB, et al. Androgen receptor defects: historical, clinical, and molecular perspectives. Endocrine Reviews. 1995;16:271-321.

  62. Shapiro BH, Levine DC, Adler NT. The testicular feminized rat: a naturally occurring model of androgen independent brain masculinization. Science. Jul 18 1980;209(4454):418-20. [Medline].

  63. Stenchever MA, Jones GK, Jarvis JA. Testicular feminization syndrome. Chromosomal, histologic, and genetic studies in a large kindred. Obstet Gynecol. May 1969;33(5):649-57. [Medline].

  64. Strickland AL, French FS. Absence of response to dihydrotestosterone in the syndrome of testicular feminization. J Clin Endocrinol Metab. Sep 1969;29(9):1284-6. [Medline].

  65. Takeda H, Lasnitzki I, Mizuno T. Change of mosaic pattern by androgens during prostatic bud formation in XTfm/X+ heterozygous female mice. J Endocrinol. Jul 1987;114(1):131-7. [Medline].

  66. Takeda H, Suzuki M, Lasnitzki I, Mizuno T. Visualization of X-chromosome inactivation mosaicism of Tfm gene in XTfm/X+ heterozygous female mice. J Endocrinol. Jul 1987;114(1):125-9. [Medline].

  67. Wilson BE, Reiner WG. Management of intersex: a shifting paradigm. J Clin Ethics. Winter 1998;9(4):360-9. [Medline].

  68. Wilson JD, Carlson BR, Weaver DD, et al. Endocrine and genetic characterization of cousins with male pseudohermaphroditism: evidence that the Lubs phenotype can result from a mutation that alters the structure of the androgen receptor. Clin Genet. Oct 1984;26(4):363-70. [Medline].

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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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