Androgen insensitivity syndrome laboratory findings: Difference between revisions
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==Laboratory Findings== | ==Laboratory Findings== | ||
*Supportive laboratory findings:<ref name="pmid20301602">{{cite journal |vauthors=Pagon RA, Adam MP, Ardinger HH, Wallace SE, Amemiya A, Bean LJH, Bird TD, Ledbetter N, Mefford HC, Smith RJH, Stephens K, Gottlieb B, Trifiro MA |title= |journal= |volume= |issue= |pages= |year= |pmid=20301602 |doi= |url=}}</ref> | |||
*Normal 46,XY karyotype | *Normal 46,XY karyotype | ||
Revision as of 23:42, 6 July 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2]
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Overview
- Evidence of normal or increased synthesis of testosterone and its normal conversion to dihydrotestosterone, and normal or increased luteinizing hormone (LH) production by the pituitary gland AND/OR by the identification of a hemizygous pathogenic variant.
Laboratory Findings
- Supportive laboratory findings:[1]
- Normal 46,XY karyotype
- Evidence of normal or increased synthesis of testosterone (T) by the testes
- Evidence of normal conversion of testosterone to dihydrotestosterone (DHT)
- Evidence of normal or increased luteinizing hormone (LH) production by the pituitary gland
- In CAIS, but not in PAIS: possible reduction in postnatal (0-3 months) surge in serum LH and serum T concentrations.
- In the “predominantly male” phenotype:
- Less than normal decline of sex hormone-binding globulin in response to a standard dose of the anabolic androgen, stanozolol.
- Higher than normal levels of anti-müllerian hormone during the first year of life or after puberty has begun.