Bone formation markers in patients with glucocorticoid-induced osteoporosis
treated with teriparatide or alendronate.
Author(s): Eastell R, Chen P, Saag KG, Burshell AL, Wong M, Warner MR, Krege JH.
Affiliation(s): University of Sheffield Bone Metabolism Group, Metabolic Bone Centre, Sorby Wing,
Northern General Hospital, Herries Road, Sheffield, S5 7AU, UK.
r.eastell@sheffield.ac.uk
Publication date & source: 2010, Bone. , 46(4):929-34
Reduced osteoblast function is a primary defect in glucocorticoid-induced
osteoporosis (GIO), and is reflected by decreased biochemical markers of bone
formation, such as serum osteocalcin (OC) and procollagen type I N-terminal
propeptide (PINP). This analysis compared the effects of teriparatide and
alendronate on OC and PINP in patients with GIO. In a double-blind study, women
(N=159) and men (N=38) with GIO were randomized to either teriparatide 20 mug/day
by subcutaneous injection or to alendronate 10 mg/day orally. OC and PINP were
measured in fasting-state serum samples obtained at baseline and at 1, 6, 18, and
36 months. Baseline bone formation markers were below the reference interval
(low) in 33% of patients for OC and in 4% of patients for PINP. On teriparatide
therapy, the median OC and PINP levels increased by 92% and 108%, respectively,
and this resulted in only 12% and 1% of patients being low at 6 months. On
alendronate therapy, the median OC and PINP levels decreased by 40% and 53%,
respectively, and this resulted in 68% and 34% of patients being low at 6 months.
We conclude that bone formation as determined by surrogate markers was increased
in teriparatide-treated patients with GIO and decreased in alendronate-treated
patients with GIO.
|