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In Australia (as in other developed countries), fractures of the
proximal femur are one of the major hazards of old age, particularly in
women, in whom the incidence reaches about 3% per annum in the ninth
decade.1 Hip fracture, with its
associated significant mortality and high rate of residual
disability,2 is widely regarded as the
ultimate expression of osteoporosis. In fact, this fracture is as
much due to more frequent falls in the elderly as to reduced bone
density.2,3 As hip fracture is so
clearly a function of ageing, its prevalence is bound to increase with
increasing longevity, but the scale of this increase is not widely
appreciated. In this issue of the Journal, two reports, one by Sanders
et al 4 and the other by Pocock et al
5, predict an alarming virtual
doubling in hip fracture incidence in Australia (from about 15 000 to
30 000 per annum) in the next 20 years, assuming age-specific rates
remain constant.
The scenario presented by these authors is made even more disturbing
by Pocock and colleagues' assessment of the scope for a preventive
screening program.5 Applying optimistic
assumptions of 60% of the target population screened, 60% complying
with therapy, and the therapy being 50% effective, they found that the
number of hip fractures would still increase by over 50% in the next 20
years.
This is not surprising in view of the diversity of risk factors
involved in both bone fragility and falls in the elderly. Bone
fragility is a function not only of bone density (in which there is a
major genetic component6), but also of bone
turnover7 and bone
architecture.8 Falls are subject to even
more risk factors, including impaired vision, muscle weakness,
postural hypotension (including the use of diuretics, because of
their hypotensive action) and long-acting sedatives. Other risk
factors for low bone density or frequent falls include smoking,
physical inactivity, low body weight and inadequate exposure to
sunlight.9
Most preventive measures for hip fractures in the elderly have been
directed at the bone itself, and oestrogens,10
bisphosphonates11 and
calcitriol12 have all been shown to
reduce fracture rates. However, even if increasing use of these
potent and relatively expensive agents could reverse fracture risk
in selected individuals, this would have only a limited impact at the
population level.9
In this rather bleak scenario, there is one relatively simple
approach that should perhaps be pursued more actively than it is at
present, namely the greater use of vitamin D and calcium in the
elderly, particularly in those who are housebound or in
institutions. It is 30 years since histological evidence of vitamin D
deficiency in hip fracture patients was first reported in
England,13 and over 20 years since
this histological evidence was confirmed by demonstrating low serum
levels of 25-hydroxyvitamin D in these patients.14
After confirmation of these findings in many other countries,
vitamin D insufficiency (ie, a low serum level of 25-hydroxyvitamin D
without overt evidence of rickets/osteomalacia) was uncovered in
women with hip fractures and in nursing home residents in sunny South
Australia.15 Subsequent studies
confirmed the poor vitamin D status of nursing home residents in New
South Wales16 and Victoria,17 and it is now
generally accepted that vitamin D insufficiency, and associated
secondary hyperparathyroidism16 with high bone
turnover,18 are as common among
elderly citizens in Australia as elsewhere, both because physical
infirmity reduces exposure to sunlight and because age-related
thinning of the skin reduces its capacity to synthesise
cholecalciferol.19 Although there is some
disagreement about the threshold level of 25-hydroxyvitamin D in
plasma that triggers secondary hyperparathyroidism (we find the
threshold to be at about 40-50 nmol/L, but thresholds as high as 100
nmol/L have been suggested20), there is consensus that
quite mild vitamin D insufficiency stimulates parathyroid hormone
secretion.
These observations might be regarded as academic were it not for a
French trial in which 800 units of vitamin D and 1200 mg of calcium daily
for 18 months normalised serum 25-hydroxyvitamin D and parathyroid
hormone levels and reduced the hip fracture incidence by 43% in 877
female nursing home residents (compared with 888
controls).21 Although the rapidity of
this therapeutic effect could hardly have been due to a change in bone
density, it might be explained by a reduction in bone turnover from
reduced parathyroid activity, combined with improved muscle
strength and a consequent reduction in falls from the action of
vitamin D on muscle.22 A subsequent Dutch study,
showing that 400 units of vitamin D without calcium given daily for
three years had no effect on hip fracture rate in subjects not in
institutions,23 does not vitiate the
French trial, which used more vitamin D, combined it with calcium and
targeted a vitamin D-insufficient population.
We do not wish to imply that vitamin D (with calcium) is the be-all and
end-all of hip fracture prevention, or to deny that aged-care
services need to be strengthened to cope with an ageing population. We
do suggest, however, that vitamin D (with calcium) -- a preventive
measure that is not only cheap and safe but simultaneously targets
both bone and muscle -- is an attractive but neglected weapon in the
campaign against hip fractures. Perhaps the time has come to set up
task forces at Federal and/or State levels to consider this and other
options.
Howard A Morris
Chief Medical Scientist
Allan G Need
Divisional Head, and Senior Visiting Physician, Division of
Clinical Biochemistry
Institute of Medical and Veterinary Science,
and
Department of Medicine, University of Adelaide, SA
B E Christopher Nordin
Senior Specialist and Visiting Professor
Division of Clinical Biochemistry, Institute of Medical and
Veterinary Science, and
Department of Pathology, University of Adelaide, SA
- March L, Chamberlain A, Cameron I, et al. Prevention, treatment and
rehabilitation of fractured neck of femur. Health Outcomes Project
1996. Sydney: Public Health Unit, Northern Sydney Area Health
Service, 1996. (ISBN 07310 9633 9). Also on the internet
<http://www.mja.com.au/public/issues/iprs2/march/fnof.pdf>
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Brockelhurst JC, Exton-Smith AN, Lempert Barber SM, et al.
Fracture of the femur in old age: a two-centre study of associated
clinical factors and the cause of the fall. Age Ageing 1978; 7:
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Dargent-Molina P, Favier F, Grandjean H, et al. Fall-related
factors and risk of hip racture: the EPIDOS prospective study.
Lancet 1996; 348: 145-149.
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Sanders KM, Nicholson GC, Ugoni AM, et al. Health burden of hip and
other fractures in Australia beyond 2000. Projections based on the
Geeong Osteoporosis Study. Med J Aust 1999; 170: 467-470.
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Pocock NA, Culton NL, Harris ND. The potential effect on hip
fracture incidence of mass screening for osteoporosis. Med J
Aust 1999; 170: 486-488.
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Slemenda CW, Christian JC, Williams CJ, et al. Genetic
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Melton LJ, Khosla S, Atkinson EJ, et al. Relationship of bone
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Faulkner KG, Cummings SR, Black D, et al. Simple measurement of
femoral geometry predicts hip fracture: the study of osteoporotic
fractures. J Bone Miner Res 1993; 8: 1211-1217.
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Cummings SR. Prevention of hip fractures in older women: a
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Weiss NS, Ure CI, Ballard JH, et al. Decreased risk of fractures of
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Liberman UA, Weiss SR, Broll J, et al. Effect of oral alendronate on
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Tilyard M, Spears GFS, Thomson J, Dovey S. Treatment of
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Aaron JE, Gallagher JC, Anderson J, et al. Frequency of
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Lancet 1974; 2: 229-233.
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Baker MR, McDonnell H, Peacock M, Nordin BEC. Plasma
25-hydroxyvitamin D concentrations in patients with fractures of
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Morris HA, Morrison GW, Burr M, et al. Vitamin D and femoral neck
fractures in elderly South Australian women. Med J Aust 1984;
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Brock K, Reid J, Fraser D. Effect of type of accommodation on the
vitamin D status of the elderly in Sydney, Australia. In: Norman AW,
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Stein MS, Scherer SC, Walton SL, et al. Risk factors for secondary
hyperparathyroidism in a nursing home population. Clin
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Gallagher JC, Kinyamu HK, Fowler SE, et al. Calciotropic hormones
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Need AG, Morris HA, Horowitz M, Nordin BEC. Effects of skin
thickness, age, body fat, and sunlight on serum 25-hydroxyvitamin D.
Am J Clin Nutr 1993; 58: 882-885.
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McKenna MJ, Freaney R. Secondary hyperparathyroidism in the
elderly: means to defining hypovitaminosis D. Osteoporos
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Chapuy MC, Arlot ME, Duboeuf F, et al. Vitamin D3 and
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Boland R. Role of vitamin D in skeletal muscle function.
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©MJA 1999
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