Does Parathyroid Hormone Treatment Affect Fracture Risk or Bone Mineral Density in Patients with Osteoporosis?

Juliet Compston


Nat Clin Pract Rheumatol. 2007;3(6):324-325. 

In This Article


Background: The effects of parathyroid hormone (PTH) peptide therapy for osteoporosis, including the optimum treatment dose, duration of treatment and hormone type (PTH [1−34] vs PTH [1−84]) are unknown.
Objective: To assess the effect of PTH on risk of fracture and on bone mineral density (BMD), and whether such an effect is altered by the combination of PTH with antiresorptive agents, or by PTH type.
Design and Intervention: A search of PubMed, Embase, the Science Citation Index, the Cochrane Central Database of Controlled Trials and abstracts from the publications Journal of Bone Mineral Research, Calcified Tissue International and Osteoporosis was carried out to identify studies with outcome measures of fracture occurrence or change in BMD. The search and medical subject heading terms included 'parathyroid hormone' and 'fracture', and the limiting terms were 'human' and 'randomized controlled trial'. Original randomized studies included in the analysis met the following criteria: duration longer than 6 months, patient age >18 years, active arm of study included treatment with PTH (1−34 or 1−84), and recorded spine fractures verified by X-ray. Data extracted for the analysis comprised number of patients with one or more vertebral or nonvertebral fractures and reduced lumbar spine and hip areal BMD. Relative risks (RRs) were compared directly by logarithmic transformation and t-test for comparison between different treatments.
Outcome Measures: Weighted risk values, calculated on the basis of RRs. BMD changes were measured by the weighted mean difference for both Z-score changes and percentage changes.
Results: A total of 13 studies were included in the analysis. PTH treatment alone or in combination with antiresorptive agents reduced vertebral fracture risk by 64% (RR 0.36, 95% CI 0.28−0.47) and nonvertebral fracture risk by 38% (RR 0.62, 95% CI 0.48−0.82), compared with controls. The reduction in risk for both vertebral and nonvertebral fracture was unaffected by duration of PTH treatment. There was no significant difference between the RRs of fracture with PTH treatment in combination with antiresorptive agents versus PTH alone, or between the RRs of fracture with PTH (1−84) versus PTH (1−34) treatment. PTH therapy increased spine BMD by 6.6% (95% CI 5.2−8.1) during 11−36 months follow-up, but had no significant effect on hip BMD (1.0%, 95% CI -0.1 to 2.1). The improvements in both spine and hip BMD correlated significantly (P = 0.01 for both variables) with treatment duration <18 months. There was no difference in the BMD improvement observed with PTH treatment in combination with alendronate or hormone replacement therapy compared with PTH alone, although PTH combined with hormone replacement therapy caused a greater gain in BMD than PTH combined with alendronate. Differences in study characteristics precluded a comparison of the effects of PTH dose and type on BMD.
Conclusion: PTH therapy alone or in combination with antiresorptive agents reduces the risk of vertebral or nonvertebral fracture and increases spine, and potentially hip, BMD in patients with osteoporosis.