AbstractsEarth & Environmental Science

Growth hormone increases bone formation and linear growth while glucocorticoids inhibit bone formation. Growth hormone modulates the metabolism of glucocorticoids by inhibiting the activity and expression of 11-beta-hydroxysteroid dehydrogenase type 1, the enzyme that converts the inactive metabolite cortisone to the active hormone cortisol. The aim of this project was to study bone mineral density before and after two years on growth hormone replacement therapy in patients with hypopituitarism. The main hypothesis was that patients on glucocorticoid replacement demonstrate greater improvement in bone mineral density when treated with growth hormone than glucocorticoid sufficient patients. This was a retrospective study on 175 adult patients with hypopituitarism due to non-functioning pituitary adenoma. All patients were growth hormone deficient. Bone mineral density was measured before growth hormone replacement therapy started and after two years of therapy. Of 175 patients, 77 (44%) were glucocorticoid sufficient and 98 (56%) were glucocorticoid insufficient, receiving a mean ± SD hydrocortisone equivalent dose of 20.9 ± 5.0 mg/day. Bone mineral density at baseline did not differ between glucocorticoid sufficient and insufficient patients, neither at lumbar spine nor proximal femur neck. Both groups improved their bone mineral density significantly after two years on growth hormone replacement. However, no significant difference between the two groups regarding change in bone mineral density was observed. Growth hormone replacement therapy for 2 years increases bone mineral density in hypopituitary patients, but the treatment response is not influenced by glucocorticoid insufficiency and its replacement therapy.