LETTER
Relation of Osteopenia to Glucocorticoid Replacement Therapy in Addison Disease
J.P Devogelaer, MD;
J. Crabbe, MD; and
C. Nagant Deuxchaisnes, MD
1 August 1994 | Volume 121 Issue 3 | Pages 235-237
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].
1. Zelissen PM, Croughs RJ, van Rijk PP, Raymakers JA. Effect of glucocorticoid replacement therapy on bone mineral density in patients with Addison disease. Ann Intern Med. 1994; 120:207-10.
2. Devogelaer JP, Crabbe J, Nagant de Deuxchaisnes C. Bone mineral density in Addison's disease: evidence for an effect of adrenal androgens on bone mass. Br Med J. 1987; 294:798-800.
3. Devogelaer JP, Crabbe J, Nagant de Deuxchaisnes C. Trabecular bone mass in postmenopausal addisonians: a clue to postmenopausal osteoporosis? In: Christiansen C, Johansen JS, Riis BJ, eds. Osteoporosis 1987. Viborg: Norhaven; 1987:623-4.
4. Winter JS, Couch RM. Modern medical therapy of congenital adrenal hyperplasia. Ann N Y Acad Sci. 1985; 458:165-73.
5. Migeon CJ. Diagnosis and treatment of adrenogenital disorders. In: DeGroot LJ, ed. Endocrinology. 2d ed. Philadelphia: W.B. Saunders; 1989:1676-704.
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