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Relation of Osteopenia to Glucocorticoid Replacement Therapy in Addison Disease
- J.P Devogelaer, MD;
- J. Crabbe, MD; and
- C. Nagant Deuxchaisnes, MD
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TO THE EDITOR:
The interesting study by Zelissen and colleagues [1] on bone mineral density in patients with Addison disease seems to confirm our published findings, that it is the lack of adrenal androgens in patients with Addison disease rather than the glucocorticoid replacement therapy that is responsible for low bone mineral density [2, 3]. Thus, the title of their article is misleading. Furthermore, their Table 1 is somewhat confusing, particularly because of the failure to distinguish postmenopausal from premenopausal women. In our experience [2, 3] only postmenopausal women with Addison disease have a decreased bone mineral density both at the forearm and at the lumbar spine. Zelissen and colleagues' Table 2 indicates that in women, bone mass was related to plasma androstenedione levels with a correlation coefficient (called a regression coefficient) reaching statistical significance for the femoral neck only. Hydrocortisone or cortisone treatment seems an unlikely cause of osteopenia because the daily doses did not exceed 37.5 mg of cortisone acetate (that is, 20 to 30 mg of hydrocortisone). These doses are in the range used to treat adults with Addison disease, as well as levels recognized by pediatric endocrinologists to have no detrimental effect on statural growth (10 to 20 mg/m2 per 24 h) while preventing undue virilization in children with the congenital adrenogenital syndrome [4, 5]. We believe that the osteopenia is not caused by glucocorticoid replacement therapy by itself. The deficient production of adrenal androgens in patients with Addison disease leads to osteopenia in postmenopausal women with Addison disease who are not receiving hormonal replacement therapy. In premenopausal women with the disease, however, bone mass is maintained because of ovarian estrogen production. Other factors, such as concomitant diabetes mellitus or associated autoimmune endocrinopathies or a history of tuberculosis, which lead to immobilization and inactivity, could be partly responsible for a low bone mineral density in men, as we have previously shown [2].
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
•Include no more than 300 words of text, three authors, and five references
•Type with double-spacing
•Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.
Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.
Annals welcomes electronically submitted letters.
- Copyright ©2004 by the American College of Physicians
