Adrenal Lymphocytic Infiltration and Adrenocortical Tumors in a Patient with 21-Hydroxylase Deficiency

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Abstract
Congenital adrenal hyperplasia due to 21-hydroxylase deficiency results in deficient production of cortisol and aldosterone, chronic stimulation of the adrenal cortex by corticotropin, and overproduction of androgens. Cortisol-replacement therapy often fails to normalize corticotropin and androgen secretion, and high doses may be needed.1 Adrenocortical tumors, including cancers, are rare in patients with 21-hydroxylase deficiency but have been reported in patients with large adrenal glands and presumably inadequate cortisol therapy.2