Endocrine Abstracts

Introduction: Patients with Addison disease require lifelong glucocorticoid replacement treatment and it is recommended that glucocortiocoid therapy should be monitored in these patients to avoid over replacement and minimize long-term consequences of bone loss. The present study was carried out with the aim of evaluating bone turnover markers in patients with Addison disease.

Patients and methods: A cross sectional study including 50 patients who are followed for Addison disease, at the department of Endocrinology at Hedi Chaker hospital, sfax-Tunisia. Biochemical markers of bone metabolism (calcium, phosphorus, alkaline phosphatases, vitamin D and parathyroid hormone (PTH)) were measured and the average values were retrospectively analyzed.

Results: There were 40 females and 10 males. The average age of patients was 49,5±13,9 years (18–78 years). The majority (70%) were aged between 40 and 50 years old. Average duration of the disease was 13,9±8,7 years (5–35 years). Approximately 42,5% of females were menopausal. Two-thirds (66%) of patients were not physically active. All patients took no calcium oral supplementation nor oestrogen replacement. Only four patients received Vitamin D oral supplementation. Mean serum levels of calcium and phosphorus were 2,29±0,13 mmol/l (1,9–2,55 mmol/l) and 1,10±0,18 mmol/l (0,8–1,66 mmol/l), respectively. Hypocalcemia was observed in 9 (18%) patients after a mean duration of Addison disease of 11,9±7,1 years (4–26 years) and a mean cumulative hydrocortisone dose of 317,7±211,7 mg (75–702 mg). No significant statistically differences were found between hypocalcemia with regard to age, duration of glucocorticoid replacement or glucocorticoid dose. Mean alkaline phosphatase was 77,2±28,5 IU/l (15–190 IU/l). Patients presenting an increased alkaline phosphatase level (18%) received higher cumulative hydrocortisone dose but without statistical difference (413,4±348 mg versus 365,5±271 mg; P=0,7). Mean vitamin D level was 22,28±14,14 ng/ml (5,6–78,6 ng/ml).Hypovitaminosis D was observed in 33 (66%) patients. Mean PTH level was 51,79±23,84 pg/ml (16,36–139 pg/ml).An elevated PTH level was observed in 10 (20%) patients who had all vitamin D deficiency.

Conclusion: Long-term glucocorticoid replacement therapy in patients with Addison disease is associated with an increased risk of fractures and osteoporosis, which is not only identified by bone mineral density. Other markers as bone turnover markers may be useful. Markers of bone resorption seem to be higher in patients with Addison disease, particularly those who present hypovitaminosis D.