|
Home
|
Issues
|
MJA shop
|
MJA Careers
|
Contact
|
Topics
|
Search
|
RSS |
→ Contents list for this issue
→ More articles on Rheumatology
→ More articles on Pharmacology
→ More articles on Endocrinology
Click to Login
Hide the Login Box
→ Click here for subscription options
To the Editor: Nordin and colleagues raised important issues about prescribing for osteoporosis.1 We agree that the Pharmaceutical Benefits Schedule guidelines for therapy are imperfect, but they do not necessarily lead, as Nordin et al claim, to inappropriate prescribing. For historical reasons, osteoporosis is held to be synonymous with vertebral fractures, but this misrepresents the epidemiology of fractures. Non-vertebral fractures account for 80% of all fractures and 90% of the loss of quality of life and economic costs. Vertebral fractures contribute only 20% of the burden.2 Most fractures arise in the large population at moderate risk with osteopenia — the “bell” of the Gaussian bone mineral density (BMD) distribution, not its “tail”, which comprises those with osteoporosis (defined by a bone densitometry T-score less than – 2.5). Concentrating on vertebral fractures and screening for osteoporosis with bone densitometry, as recommended by Nordin et al, is no solution to this public health problem.
Nutritional change and exercise are appealing because they are safe and cost-effective approaches for early intervention, but are supported only by level D evidence (expert opinion).3 Although these approaches are plausible, no trials demonstrate their antifracture efficacy. There are no means of early identification of individuals who will sustain a fracture. Densitometry is neither sensitive nor specific for fracture; most people with osteoporosis do not sustain a fracture, and most fractures arise in people without osteoporosis, who would, paradoxically, be excluded from treatment by screening.4 Bone densitometry should be more accessible for case finding, but its use for screening does not reduce the fracture burden because of this screening paradox. However, Medicare reimbursement for densitometry is available for high-risk individuals (those with premature menopause, other illnesses or who are taking corticosteroids), not just for those aged over 70 years or those with fractures. Restricting treatment on the basis of BMD results is not advocated by the Australian and New Zealand Bone and Mineral Society precisely because it excludes this moderate-risk group from treatment, particularly those with fractures and osteopenia.
There is level A evidence (meta-analysis of multiple randomised trials)5 for the antifracture efficacy of bisphosphonates in patients with osteoporosis, and evidence based on single trials6 of their antifracture efficacy in those with osteopenia and prevalent fractures, whose fracture risk is similar to that of people with osteoporosis and no prevalent fracture. There is limited evidence of antifracture efficacy of bisphosphonates in individuals with osteopenia alone.6 Preventing the first fracture is important, and guidelines are deficient in this way. Case finding to estimate absolute risk is the best approach available at this time, using risk factors, remodelling markers and, more recently, microstructural analysis to improve sensitivity and specificity.
Rather than inappropriate or overprescribing, evidence suggests underutilisation of drug therapy for osteoporosis.7,8 Osteoporosis remains underdiagnosed, underinvestigated and undertreated, and limiting access to bone densitometry is not supported by the Australian and New Zealand Bone and Mineral Society.
Competing interests: Ego Seeman serves on the medical advisory committees of and has received speaker fees from Amgen, Eli Lilly, Merck Sharp and Dohme, Novartis, Procter and Gamble, Sanofi-Aventis and Servier. Mark Kotowicz serves on the Novartis Alcast medical advisory board and has received speaker fees and travel assistance from Merck Sharp and Dohme, Sanofi-Aventis and Servier. Peter Nash received research funding for clinical trials, and honoraria for advice from Eli Lilly, Merck Sharp and Dohme, Novartis, Sanofi and Servier, and has also lectured on their behalf. Philip Sambrook serves on the medical advisory boards of and has received speaker fees from Amgen, Merck Sharp and Dohme, Novartis, Sanofi-Aventis and Servier.
1 Australian and New Zealand Bone and Mineral Society, Sydney, NSW.
2 Department of Medicine, University of Melbourne, Melbourne, VIC.
3 School of Medicine, University of Queensland, Brisbane, QLD.
4 Institute of Bone and Joint Research, Royal North Shore Hospital, Sydney, NSW.
In reply: Seeman and colleagues agree that most patients with minimal trauma fractures do not have osteoporosis. The figures are clear: only 13% of patients with a peripheral fracture have a hip bone mineral density (BMD) T-score less than or equal to − 2.5 and only 25% have a score less than or equal to − 1.5. The corresponding figures for vertebral fractures are 25% and 38%, respectively.1 We do not argue that the − 2.5 T-score threshold for defining osteoporosis is sacrosanct, but simply that some bone density threshold be defined for subsidised therapy, for which virtually all the supporting evidence is based on treatment of patients with established osteoporosis. Osteopenia is an artificial concept with an arbitrary definition, but we agree that the T-score threshold for subsidised therapy need not be as low in those with prevalent adult fracture as in those without — perhaps − 1.5, which is the threshold recently adopted for patients receiving corticosteroid therapy.
We disagree about the predictive power of bone densitometry; it is comparable to that of blood cholesterol level for heart attacks and blood pressure for stroke.2 It therefore makes sense to measure BMD in all women at menopause and all men at age 60 years to identify those with osteoporosis before they sustain fractures, as well as those with normal but negative T-scores, who have a fracture risk twice that of those with positive T-scores.3 Those with proven osteoporosis could receive subsidised therapy, and those with low normal values could be advised on lifestyle measures, such as calcium supplementation (which significantly delays or prevents bone loss in postmenopausal women).4 People with positive T-scores can be reassured. To suggest that no trials have demonstrated the antifracture efficacy of nutritional measures is to argue against three large meta-analyses showing significant prevention of fractures with vitamin D and calcium supplementation.5-7
The additional cost of confirming low bone density before providing subsidised therapy in fracture cases is likely to be more than offset by the savings from reduced inappropriate therapy; bone densitometry costs about $80 per test, but bisphosphonate therapy costs about $50 a month for each patient. The extra cost of bone densitometry for every woman at menopause and every man at age 60 years could be $20 million a year, but even with subsidised therapy for those without fracture but proven osteoporosis (with a T-score less than or equal to − 2.5, for instance), the cost is also likely to be more than offset in the long term by reducing the enormous cost of osteoporotic fractures ($8 billion annually8). We find it hard to understand why any of our colleagues would not support proposals that would transfer treatment from those who do not need it to those who do.
1 Endocrine and Metabolic Unit, Royal Adelaide Hospital, Adelaide, SA.
2 SA Health Working Party on Prevention of Osteoporosis and Fractures, Adelaide, SA.
christopher.nordinATimvs.sa.gov.au
|
Home
|
Issues
|
MJA shop
| Terms of use
|
MJA Careers
|
More...
|
Contact
|
Topics
|
Search
|
RSS |
©The Medical Journal of Australia 2009 www.mja.com.au PRINT ISSN: 0025-729X ONLINE ISSN: 1326-5377