As with other forms of CAH, the primary therapy of<unk><unk>  deficient CAH is lifelong glucocorticoid replacement in sufficient doses to prevent<unk>  insufficiency and suppress excess mineralocorticoid and androgen production. Salt-wasting in infancy responds to intravenous saline, dextrose, and high dose hydrocortisone, but prolonged fludrocortisone replacement is usually not necessary. The hypertension is ameliorated by glucocorticoid suppression of DOC. Long term glucocorticoid replacement issues are similar to those of 21-hydroxylase CAH, and involve careful balance between doses sufficient to suppress androgens while avoiding suppression of growth. Because the enzyme defect does not affect sex steroid synthesis, gonadal function at puberty and long-term fertility should be normal if<unk>  androgen production is controlled. See congenital<unk><unk>  for a more detailed discussion of androgen suppression and fertility potential in adolescent and adult women.
Congenital adrenal hyperplasia due to 11β-hydroxylase deficiency
Congenital adrenal hyperplasia due to 21-hydroxylase deficiency
Congenital adrenal hyperplasia due to 17α-hydroxylase deficiency
Congenital adrenal hyperplasia due to 3β-hydroxysteroid dehydrogenase deficiency
Primary pigmented nodular adrenocortical disease
Lipoid congenital adrenal hyperplasia
Pituitary ACTH hypersecretion
Cortisone reductase deficiency