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Pheochromocytoma, Steroids, & Myocardial Infarction

Department of Medicine, Nassau University Medical Center, East Meadow, New York 11554

Address correspondence to: Michael S. Balkin, M.D., Department of Medicine, Nassau University Medical Center, East Meadow, New York 11554. E-mail: mbalkin{at}mac.com.

To the editor:

Brown et al. (1) describe a patient with a hemorrhagic pheochromocytoma who suffered a definite exacerbation of symptoms after initiation of therapeutic glucocorticoids. The authors suggest that this effect might be due to the augmentation of either synthesis or release of catecholamines induced by glucocorticoids or to the permissive effects of glucocorticoids on catecholamine action. I wish to offer an alternative explanation.

High-dose glucocorticoids are required to activate the epinephrine-synthesizing enzyme phenylethanolamine N-methyltransferase (2). The intimate relationship of the adrenal cortex to the adrenal medulla ensures that the medullary chromaffin cells are bathed in a sufficiently high level of glucocorticoids to produce epinephrine, provided the adrenal cortex is producing cortisol (3, 4). Therefore, states of primary and secondary adrenal cortical insufficiency, even when not congenital in origin, have been associated with reduced levels of epinephrine that are not corrected by the administration of exogenous glucocorticoids (5).

The importance of epinephrine in antagonizing the action of unregulated norepinephrine production in this patient was suggested by the dramatic rise in her blood pressure to 260/165 mm Hg when she received iv metoprolol. This individual’s ACTH was undoubtedly suppressed by the administration of a daily dose of 6 mg of dexamethasone; in turn, her adrenal production of cortisol and, secondarily, epinephrine would have dropped, thereby potentially leaving her unprotected from the vasoconstricting effects of unopposed norepinephrine. In summary, I suggest that a glucocorticoid-induced decline in epinephrine, rather than a glucocorticoid-induced augmentation of catecholamine effect, was the cause of this patient’s acute clinical presentation.

Received February 18, 2005.

References

1. Brown H, Goldberg PA, Selter JG, Cabin HS, Marieb NJ, Udelsman R, Setaro JF 2005 Clinical case seminar: hemorrhagic pheochromocytoma associated with systemic corticosteroid therapy and presenting as myocardial infarction with severe hypertension. J Clin Endocrinol Metab 90:563–569[Abstract/Free Full Text]
2. Axelrod J 1966 Methylation reactions in the formation and metabolism of catecholamines and other biogenic amines. Pharmacol Rev 18:95–113[Free Full Text]
3. Wurtman RJ, Axelrod J 1966 Control of enzymatic synthesis of adrenaline in the adrenal medulla by adrenal cortical steroids. J Biol Chem 241:2301–2305[Abstract/Free Full Text]
4. Mannelli M, Lanzillotti R, Pupilli C, Ianni L, Conti A, Serio M 1994 Adrenal medulla secretion in Cushing’s syndrome. J Clin Endocrinol Metab 78:1331–1335[Abstract]
5. Stewart PM 2004 Adrenal replacement therapy: time for an inward look to the medulla? J Clin Endocrinol Metab 89:3677–3678[Free Full Text]

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