Search:
Menopause Live - IMS Updates
InFocus

Date of release: 28 January, 2009

Vertebral fracture risk reduction in women who lose femoral neck bone mineral density on teriparatide treatment


In a recent paper, Watts and colleagues examined the clinical significance in non-responders of bone mineral density (BMD) measured at the femoral neck after 12-month treatment with teriparatide, a parathyroid hormone analogue, compared to placebo in terms of vertebral fracture risk reduction [1]. A BMD change from baseline of > 4% was considered to be clinically significant. Women on teriparatide who lost femoral neck BMD still had significant reductions in vertebral fracture risk compared with placebo (relative risk 0.11; 95% confidence interval, 0.03–0.45). Vertebral fracture risk reduction with teriparatide compared with placebo was similar across categories of femoral neck BMD change from baseline at 12 months (loss > 4%, ‘loss’ 0–4%, ‘gain’ 0–4%, or gain > 4%) (interaction, p = 0.40). Irrespective of femoral neck BMD loss or gain, it was concluded that loss of femoral neck BMD at 12 months in postmenopausal women with osteoporosis treated with teriparatide is nevertheless consistent with a good treatment response in terms of vertebral fracture risk reduction.

Comment

The message is clear. Serial measurement of BMD in the patient on anti-fracture treatment is not of much help in judging response to treatment and is a poor parameter to use in clinical decisions regarding future treatment options. This should not be confused with the important role of BMD as an indicator of risk in the untreated patient. As long as the patient is compliant with therapy, she will have better fracture protection than the patient without treatment, irrespective of BMD changes. Although this was known for patients on anti-resorptive therapy (alendronate and raloxifene), this is the first report in patients on anabolic treatment [2]. In patients on anti-resorptive therapy, serial measurement of femoral neck BMD after 12 months is inappropriate, considering that the expected change in BMD on treatment is less than the least significant change, considering the precision error of machine and operator. This is not so for the anabolic agent teriparatide, where larger increases are expected after 12 months. Nevertheless, a longer follow-up period of, say, 24 months in this study would have been preferred, especially to look at possible regression to the mean. This means that patients who are the largest losers of BMD in the first year tend to gain the most in the second year. In conclusion, present methods of monitoring response to treatment (including BMD and markers of bone metabolism) are not of much help in making clinical decisions in the non-responder. Increases of BMD may be helpful to enhance compliance. The most important aim of the follow-up visit should be to assess whether the patient is compliant to therapy and to detect the presence of any new fractures by DXA vertebral fracture assessment or conventional radiography.

Comentario

Tobie de Villiers
Consultant Gynaecologist, Panorama MediClinic and University of Stellenbosch, Cape Town, South Africa

    References

  1. Watts N, Miller PD, Kohlmeier LA, et al. Vertebral fracture risk is reduced in women who lose femoral neck bone mineral density with teriparatide treatment. J Bone Min Res 2008 Dec 29. [Epub ahead of print].
    http://www.ncbi.nlm.nih.gov/pubmed/19113918

  2. Sebba AI. Significance of a decline in bone mineral density while receiving oral bisphosphonate therapy. Clin Ther 2008;30:443-52. Published March, 2008.
    http://www.ncbi.nlm.nih.gov/pubmed/18405784