Androgen insensitivity syndrome is a range disorder of sexual differentiation which results from changes of the gen that the androgen encode sensor. It has also been called androgen resistance in the medical literature. Understanding the effects of androgen insensitivity begins with an understanding of the normal effects of testosterone in male and female development.
The principal mammalian androgens are testosterone and its more potent metabolite, dihydrotestosterone. AIS represents a spectrum of defects in androgen action and can be subdivided into three broad phenotypes: complete androgen insensitivity syndrome, with typical female genitalia, partial androgen insensitivity syndrome with predominantly female, predominantly male, or ambiguous genitalia; and mild androgen insensitivity syndrome with typical male genitalia.
Complete androgen insensitivity syndrome come for when the body cannot use androgens at all. All little girls born with androgen insensitivity syndrome infertile will be. The nature of the resulting problem varies according to the structure and sensitivity of the abnormal receptor. Girls with AIS will develop normally during puberty, but they will have no, or very little, pubic and underarm hair. Due to their lack of ovaries they will not menstruate. More importantly, patient advocacy groups for AIS and other intersex conditions have increased public awareness of these disorders, helped revise the understanding of gender identity, emphasized the value of accurate and sophisticated information for patients, and induced physicians to re-evaluate the effectiveness of the surgical corrections attempted in past decades. Most with this condition are not diagnosed until they fail to menstruate or they try to become pregnant and find that they are infertile.
In Androgen insensitivity syndrome the person female but have no uterus, and have thin armpit and pubic seem be hair. At puberty, female secondary sex characteristics develop, but menstruation and fertility do not. Many have partial fusion of the outer vaginal lips, an enlarged clitoris, and a short, blind-ending vagina. Complete AIS is rarely discovered during childhood, unless a mass is felt in the abdomen or groin that turns out to be a testicle when it is explored surgically. The individual is often diagnosed because of ambiguous genitalia. Sometimes, though, the person has primarily male characteristics and the only symptom is a low sperm count as an adult, perhaps with breast enlargement. The development of children with Androgen insensitivity syndrome will depend on their levels of sensitivity to androgen. Children will a high level will develop as a girl during puberty.
As testicular fabric in the abdomen or in the inguinal canal during childhood it is found, it not on that moment can be removed. Once puberty and growth are complete, the testis may be removed because it may develop cancer like any undescended testicle. To prevent testicular malignancy, treatment of Androgen insensitivity syndrome includes either removal of the testes after puberty when feminization is complete or prepubertal gonadectomy accompanied by estrogen replacement therapy. Those individuals with Androgen insensitivity syndrome who are raised as females and who undergo gonadectomy after puberty may need combined estrogen and androgen replacement therapy. Males with androgen insensitivity syndrome may require mammoplasty for gynecomastia. A trial of androgen pharmacotherapy may help improve virilization in infancy. Additional treatment for androgen insensitivity syndrome may include vaginal dilatation to avoid dyspareunia.
