Bronzing of the skin and patchy melanosis of the oral mucosa are signs of Addison’s disease and pituitary-based Cushing’s syndrome.In both of these endocrine disorders, the cause of hyperpigmentation is oversecretion of ACTH, a hormone with melanocyte-stimulating properties. In Addison’s
disease, adrenocortical insufficiency evolves as a consequence of granulomatous infection of the cortex or autoimmune cortical destruction. As steroid hormones decrease, the feedback loop is stimulated with excess secretion of ACTH by the neurohypophysis. With a decrease in mineralocorticoids and glucocorticoids, the patient develops hypotension and hypoglycemia, respectively.
In Cushing’s syndrome, adrenocortical hyperactivity is observed, and if such activity is caused by a cortical secretory adenoma or cortical hyperplasia of adrenal origin, ACTH secretion will be shut down. Alternatively, if the hypercorticism is the consequence of a pituitary ACTH-secreting tumor that secondarily induces an adrenal hypersecretion, then melanocyte-stimulating effects may evolve. Patients with Cushing’s syndrome may be hypertensive and hyperglycemic and may show facial edema (“moon face”).
In both cases, the skin may appear tanned, and the gingiva, palate, and buccal mucosa may be blotchy. These changes in pigmentation are due to an accumulation of melanin granules as a consequence of increased hormone-dependent melanogenesis. Endocrinopathic disease should be suspected whenever oral melanotic pigmentation is accompanied by cutaneous bronzing. Serum steroid and ACTH determinations will aid the diagnosis, and the pigment will disappear once appropriate therapy for the endocrine problem is initiated.