Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2010) 22 S10.3

ECE2010 Symposia Novel aspects in the treatment of bone disease (3 abstracts)

Teriparatide and parathyroid hormone in the treatment of ostoporosis

Marius E Kraenzlin

Division of Endocrinology, Diabetology and Clinical Nutrition, University Hospital Basel, Basel, Switzerland.

The pharmacologic armamentarium available to clinicians to reduce fracture risk in women with postmenopausal osteoporosis consists essentially of antiresorptive agent. Recently, peptides from the parathyroid hormone (PTH) family, which under specific modalities of administration act as anabolic agents have become available. The interest generated by these alternatives to antiresorptive treatment resides in their greater potential for restauration of bone mass and possibly also bone structure in osteoporotic subjects who have already suffered substantial skeletal deterioration.

The anabolic effects of intermittent administration of low dose PTH are exerted through stimulation of the PTH-PTHrP recpeptor. The anabolic actions involve augmentation of the number of osteoblasts through stimulation of cell replication and inhibition of osteoblast apoptosis, and probably also stimulation of osteoblast activity. The molecular mechanisms underlying these anabolic effects are still poorly understood, but appear to include both direct actions on osteoblastic cells as well as indirect effects such as through stimulation of IGF1 production and down-regulation of sclerostin, a physiologic antagonist of the important anabolic Wnt-β-catenin pathway.

The anabolic effects of intermittently administered PTH (PTH1–34 or PTH1–84) are manifest as increases in skeletal mass, bone turnover markers, and bone strength. The effects of teriparatide (PTH1–34) on bone have been studied in postmenopausal women and men with advanced osteoporosis. The administration of teriparatide (PTH1–34) 20 μg daily in postmenopausal women increased BMD by 8–9% at the spine and by about 3% at the hip. There was an associated reduction in vertebral fracture incidence by 65% and incidence of non-vertebral fractures by 54%. The full length molecule of PTH, PTH1–84, reduced the risk of new vertebral fracture by 58%. Regarding non-vertebral fracture, a non significant reduction of the risk was observed in the patients with BMD <−3.0 T-score and one prevalent fracture.

Treatment with PTH might also be particularly effective in glucocorticoid-induced osteoporosis, because impaired bone formation is a important pathogenetic feature. The results of a controlled trial comparing teriparatide with alendronate, over an 18-month period, in patients with glucocorticoid induced osteoporosis showed greater increases in vertebral BMD and a greater reduction in new vertebral fractures with teriparatide than with alendronate.

The most common adverse effects associated with teriparatide include injection-site pain, nausea, headaches, leg cramps, and dizziness.

After a maximum of 2 years of PTH therapy, the drug should be discontinued and antiresorptive therapy begun to preserve the gains achieved during PTH treatment, as there is rapid bone loss after stopping PTH treatment. On the other hand, patients who are candidate for treatment with PTH have often previously been treated with an antiresorptive agent. Available data suggest that prior treatment with antiresorptive drugs does not compromise the treatment effects of teriparatide.

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