Normally, the adrenal gland converts cholesterol to cortisone and other hormones through a series of enzyme mediated reactions that are regulated through feed-back loops. In some individuals, however, enzyme deficiencies can lead to a build-up of certain intermediate hormones along the pathway toward cortisol, a condition called congenital adrenal hyperplasia. The most common of these enzyme deficiencies, 21-hydroxylase, causes acculumlation of 17-hydroxy progesterone and other hormones with androgenic properties. Twenty-one hydroxylase deficiency in female embryos causes androgenic stimulation that results in enlargement of the genital tubercle, fusion of the internal and external urethral folds and fusion of the labio-scrotal folds just as normal production of testosterone does in male embryos. This can result in a female infant having marked enlargement of the clitoris and fusion of the labioscrotal folds. This 'virilization' can cause an infant with a 46-XX karyotype to have the appearance of having hypospadias and cryptrochidism..