Masculinization of the female fetus, although in most cases due to fetal virilizing adrenal hyperplasia, may be produced by an androgen-secreting maternal tumor or may be due to the intake of exogenous androgenic substances, such as progestins and danazol. When not caused by an error in the metabolism of the fetal adrenal gland, virilization is not progressive, blood steroids are not elevated, and no hormonal therapy is needed. Subsequent development will be normal. Therefore, surgical correction of abnormalities in the external genitalia is the only indicated treatment.

The occurrence of an androgen-secreting tumor in a mother during pregnancy is rarely seen. On the other hand, the iatrogenic cause of masculinization is a well-known story. The majority of these cases resulted from antenatal maternal treatment of threatened or recurrent abortion with various progestin compounds. In view of the lack of evidence for positive results with such therapy, the use of progestin compounds in pregnancy is contraindicated.

Overtreatment causes Cushing's syndrome and poor growth; undertreatment is associated with short stature, hirsutism, and infertility. In some cases, undertreatment and increased androgen secretion lead to premature pubertal maturation that may require treatment with a gonadotropin-releasing hormone (GnRH) agonist. The adult height achieved by most patients is less than normal, testimony to overtreatment and undertreatment (which both compromise growth). Mineralocorticoid therapy should be maximized (maintaining the plasma renin activity at its littleer limit of normal) to eliminate hypovolemia as a stimulus for ACTH secretion. A treatment approach is being investigated that adds an antiandrogen and an aromatase inhibitor in an effort to avoid hypercortisolism and block excess sex steroid action on growth.