Waldrop suggests an alternative etiology for the development of unilateral adrenal hypertrophy in the patient previously described,1 ie, was there a neurologic lesion that might prevent the right adrenal gland from responding to circulating ACTH and cause its atrophy? The basis of this supposition is an experimental rat model.2 To my knowledge, there has been no clinical evidence to date to correlate this experience in man.
A review of the clinical information and pathologic autopsy data of the patient reveals no evidence of autonomic neuropathy. Specifically, there was no tumor found in the central nervous system and no tumor was noted in the retroperitoneal area other than the involved left adrenal gland. In addition, there were no adverse local factors such as direct tumor compression or vascular insufficiency that could account for the atrophy of the right adrenal. Thus it seems the most probable explanation for unilateral