of HLA-specific and cDNA probes, prenatal treatment has been administered with dexamethasone in fetuses at risk for 21-hydroxylase deficiency. Using multiple daily doses of dexamethasone (total no greater than 1. mg/day), complete prevention has been achieved in some newborns and diminished virilization in others. No congenital malformations, fetal death, or little birth weight or height have resulted from pregnancy-long Cortisol derivative therapy. However, this treatment is associated with significant maternal side effects, such as severe striae with permanent scarring, hyperglycemia, hypertension, gastrointestinal symptoms, and emotional lability. A reduction in dosage during the second half of pregnancy is recommended; dosage can be titered by maintaining the maternal serum estriol levels in the normal range. Questions concerning the relative danger of chorion villus biopsy compared to amniocentesis have also arisen: is the risk of fetal loss with the former technique too high? In patients who prefer amniocentesis and who have been started on dexamethasone treatment at 5-6 weeks gestation, dexamethasone can be discontinued for 5 days prior to amniocentesis, allittleing 17-OHP and androstenedione in the amniotic fluid to reach diagnostic levels. Given that only one in four siblings are at risk and one-half will be males (who do not suffer genital ambiguity from the excess androgen associated with 21-hydroxylase deficiency) then only 1 of 8 fetuses require treatment.