Although no adverse effects on the male fetus following medroxyprogesterone administration during pregnancy have been reported, it seems possible that this may be the cause of symptomatology in this instance. Hypospadias without neonatal symptomatology has been reported1 in two otherwise normal chromatin-negative infants whose mothers received either progesterone or acetoxyprogesterone during their pregnancies. This infant’s course could be explained by temporary underproduction of glucoand mineralocorticoids and/or overproduction of androgens. In this regard, some important considerations are: ( 1) progestin administration during pregnancy in animals can produce fetal adrenal atrophy and suppression of ACTH release; comparable effects in the human fetus could explain the patient’s symptomatology, hypoglycemia, and electrolyte abnormalities: (2) human fetal adrenal or testicular tissue, in vitro, can convert medroxyprogesterone to androgens; if medroxyprogesterone, which can cross the placenta, is converted similarly in vivo, an increased androgen versus glucoand mineralocorticoid ratio could result. (3) progestins may directly masculinize the fetus. (4) if progestins preferentially inhibit adrena enzymes invoIved in glucoand mineralocorticoid biosynthesis, a disproportionately high urinary 17-ketosteroids as compared with the 17-hydroxycorticosteroids ( 17-OHCS) and pregnanetriol may result. The evidence implicating medroxyprogesterone in this patient is not conclusive. However, this possibility does seem to merit some consideration. I.