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Authors’ Response: Pheochromocytoma, Steroids, & Myocardial Infarction

Section of Cardiovascular Medicine, Yale University School of Medicine, New Haven, Connecticut 06520

Address correspondence to: John F. Setaro, M.D., Yale University School of Medicine, Section of Cardiovascular Medicine, 333 Cedar Street, P.O. Box 208017, New Haven, Connecticut 06520. E-mail: john.setaro{at}yale.edu.

To the editor:

We thank Dr. Balkin (1) for his thoughtful letter, in which he offers an intelligent and plausible alternative explanation for our patient’s labile clinical course (2). However, we would like to comment on one specific point raised in his letter. Although it seems true that in states of adrenal cortical insufficiency, subnormal epinephrine responses are not corrected by exogenous glucocorticoids (3), the effect of supraphysiological glucocorticoid exposure on adrenal medullary function is less clear. In our patient, who received 6 mg dexamethasone daily, glucocorticoid levels (even in the adrenal medulla) were presumably nearly 10-fold higher than normal. The local threshold level of glucocorticoid required to sustain adrenal medullary epinephrine production is worthy of further study and discussion.

Received April 7, 2005.

References

1. Balkin MS 2005 Pheochromocytoma, steroids, & myocardial infarction. J Clin Endocrinol Metab 90:3803–3804 (Letter)[Free Full Text]
2. 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]
3. 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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