Endocrine Abstracts

Introduction: The treatment of Primary Adrenal Insufficiency involves the chronic use of glucocorticoids. The balance between the dose needed to supply the cortisol deficit and the possible consequences of overtreatment is a challenge. In patients with Addison disease (AD), androgens deficiency is an additional factor for osteoporosis.

Objective: To evaluate if there are differences in bone mineral density (BMD) in patients with Addison’s disease versus congenital adrenal hyperplasia (CAH) – classic form.

Methods: We included patients with a diagnosis of Addison’s disease or CAH, with follow-up in a tertiary center. Patient’s characteristics and cumulative doses of glucocorticoid (in hydrocortisone converted doses) were recorded and calculated by body surface area (HC/BSA). BMD was evaluated by dual-energy X-ray absorptiometry (DXA), at lumbar spine, femoral neck, and distal radius. Excluded patients with secondary causes of osteoporosis.

Results: 27 patients were included: 16 with AD and 11 with CAH. Sex and age distribution were similar between groups. Patients with Addison had a lower BMI (26.34±4.17 vs 31.47±6.4, P=0.030), and shorter disease duration (17,75±12.27 vs 31.63±11.47, P=0.007). Daily doses of HC/BSA were similar between groups (15.91±4.48 for AD vs 11.22±4.17, P=0.061), but cumulative yearly doses of HC/BSA were higher in patients with Addison (5672±1621 vs 3480±1885, P=0.027). Lumbar T-score was significantly inferior in patients with Addison (−2.00±1.20, vs −0.69±0.93, P=0.022), with no differences in femoral or radius T-score between groups. There was a non-significant correlation between lumbar T-score and cumulative yearly doses of HC/BSA (r=−0.321, P=0.208).

Conclusion: The significantly difference found in lumbar T-score between AD and CAH my be explained by the higher cumulative yearly dose of HC/BSA of the AD group which is associated to high risk of BMD reduction. Also, the AD group had lower BMI, which is known to be a protective factor against bone mineral loss. Androgen deficiency, typical of Addison disease, is also a reasonable explanation for this discrepancy, since androgens are known to increase bone formation markers.