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Disorders of sexual differentiation have proven difficult to treat not only because of physicians' lack of understanding regarding the determinants of sexual orientation, but also because of the psychological impact associated with sexual dysfunction. Patients with complete androgen insensitivity syndrome not only must undergo gonadectomy after puberty, requiring post-gonadectomy hormonal replacement, but also can suffer from underdeveloped, blind vaginal pouches. As a result, sexual intercourse is compromised. Many attempts have been made throughout medical history to correct the vaginal defect, including surgical and nonsurgical approaches, each with its own technical difficulties and complications. Presently, consensus regarding the optimal time for intervention is when the patient is ready to begin sexual life. However, the optimal surgical approach has not been established. In general, nonsurgical vaginal dilatation, like the Frank and Ingram methods, should be followed by surgical interventions, such as described by McIndoe, Vecchietti, and intestinal transplantation, in case of failure of the more conservative procedures.
DISORDERS OF SEXUAL DIFFERENTIATION, although obscure topics in society and even the medical community, have been studied for decades. A wellknown example is the androgen insensitivity syndrome or testicular feminization. Historical anecdotes suggest the possibility that Queen Elizabeth I and Joan of Arc may have suffered from this disorder.1 There are different variations in the genetic penetrance of this condition (e.g., complete ví partial), but it is an X-linked recessive disorder affecting 1 in 13,000 to 40,000 individuals,2 in which mutated androgen receptors are rendered nonfunctional and thus nonresponsive to the effects of androgens (i.e., testosterone).1 The result is a newborn, who is genetically a male (XY), with male gonads (testicles) in the abdomen, but female external genitalia. The presence of Mullerian inhibiting factor, produced by die male gonads, inhibits the development of female internal genitalia (i.e., Fallopian tubes, uterus, and upper two thirds of vagina); however, most of these infants do have a blind pouch, which constitutes the lower one third of the vagina.1 The latter was thought to have originated from the urogenital sinus, which is insensitive to sex hormones, such as Mullerian inhibiting factor and testosterone.3 Subsequent investigation has shown that the lower one third of the vagina may be a residual segment from the caudal migration of the Mullerian ducts.3 Interestingly, Drews3 demonstrated that Wolffian...