A problem of control of treatment in a boy with salt‐losing congenital adrenal hyperplasia (21‐hydroxylation defect)

Abstract Inadequate mineralocorticoid replacement is shown to have been the cause of elevated levels of plasma ACTH and 17α‐hydroxyprogesterone and of urinary steroids in a boy with salt‐losing congenital adrenal hyperplasia who was receiving more than adequate glucocorticoid replacement.