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Towards the end of the 20th century, the problems of diagnosis have not
really changed. These remain how to evaluate the risk of disease, and
then how to explain risk reduction clearly to patients. What has
changed is our ability to predict risk, and to reduce that risk by the
powerful public health, pharmacological or surgical interventions
now available.
What has this to do with osteoporosis, a microarchitectural disorder
leading to fragility fracture? Osteoporosis is a classic chronic
disorder in which the actual individual risk of clinical
disease (in this case future fracture) is often difficult to
quantify. The situation is similar for hypertension and
hypercholesterolaemia. A few statistics may aid risk evaluation. A
risk of 5%-10% or greater over five years of any osteoporotic fracture
(arms, legs, pelvis, spine or rib) is generally regarded as requiring
intervention. Interventions can reduce fracture risk by about
15%-50%.1,2 To prevent one fracture in
such a population, between 20 and 133 patients need to be treated for
five years. The risk of osteoporotic fracture depends on age. In women
over the age of 65 years, the five-year risk rises dramatically from
5%, and to 20% in women over the age of 90 years.3 The presence of a previous
osteoporotic fracture at least doubles the risk of future
fracture.4-6
What does bone densitometry have to do with risk evaluation? It is
this: when bone density is measured by dual energy x-ray
absorptiometry (DEXA), then, for each standard deviation that the
result falls below the mean for the individual's age (the Z score), the
future risk of fracture doubles. Thus, an individual with a Z score of
22 has a fourfold greater risk of fracture than the average person of
the same age. In a 65-year-old, this would give an actual five-year
risk of fracture of about 30%. Because the bone density of fracture
populations is independent of age, the concept of a standard
deviation unit with respect to a fixed, low-risk population --
healthy 20-30-year-olds -- has been introduced (the T score) (see
Figure). Significant microarchitectural deterioration
(osteoporosis) is defined in bone density terms as a T score of -2.5 or
less. Patients with a T score in this range have at least 5.65 times the
risk of fracture relative to normal young individuals. However,
their absolute five-year risk of fracture is related to the actual
population risk at their age; for women aged 65-70 years this is about
18%.2
Factors other than age and bone density contribute to calculation of
absolute fracture risk. Particularly important is a
previous history of osteoporotic fracture.
Currently, bone density risk evaluation by DEXA or quantitative
computed tomography is supported by rebates from the Health
Insurance Commission (HIC) for patients at high risk based on
clinical information. Rebates are for evaluation of individuals who
have had an osteoporotic fracture; who have clinical risk factors,
such as corticosteroid treatment or premature menopause; or
who have had osteoporosis diagnosed on a previous bone density test.
The HIC will not fund the first bone density test in unselected
individuals, otherwise known as population screening. This is
because it is currently considered that bone density testing and the
interventions consequent on finding high-risk individuals do not
fulfil Australian cost-effectiveness criteria. However,
individuals who do not meet current HIC criteria for bone density
testing often decide to pay for the test themselves.
How should we advise the HIC or the individual patient about the most
effective screening for osteoporosis? Based on the epidemiology of
fracture in Australia, it could be argued that, as well as the
categories of high risk patients already outlined, all women aged
65-75 years should have bone density testing. This is because the
population risk of future fracture rises dramatically in this age
group. If screening is performed at an earlier age, the benefits are
diluted by the small number of patients with detectable osteoporosis
and the lack of controlled trial evidence that treatment prevents
fracture at these ages when event rates are low.
Could ultrasound become a "front end" to DEXA testing? In this issue of
the Journal, the article by Naganathan et
al7 is
a useful contribution to the debate, providing a framework for
considering the value of ultrasound screening. Naganathan et al
report a simple method for calculating the benefits of testing bone
structure by ultrasound compared with the current "gold standard" of
DEXA. They achieved this by comparing the pre- and post-test
probabilities of DEXA-defined osteoporosis (T score  -2.5 at
spine or hip sites) after ultrasound testing. Interestingly, they
showed that 37% of their selected population had a normal combined
quantitative ultrasound score, and that this finding completely
excluded DEXA-defined osteoporosis. However, based on these data,
an ultrasound test does not seem to be a good deal either for the
individual patient or for the HIC, should it fund screening. The cost
of screening 100 patients with ultrasound ($40 each) plus DEXA for
those with abnormal ultrasound results ($80 x 63) would be $9040; the
cost of screening with DEXA alone would be only $8000. Thus, both
patients and the HIC should be advised not to pay for
commercial ultrasound testing as a "front end" to DEXA at
present.
What about the future -- could ultrasound replace DEXA as the "gold
standard" for predicting fracture? The answer is yes, possibly. The
evidence-based approach would demand large prospective studies
showing that ultrasound is better and cheaper than DEXA in predicting
fracture, and that patients treated on the basis of ultrasound
testing have a reduced risk of fracture compared with those who are not
treated. To date, a couple of studies have taken the first steps to show
effective fracture prediction in elderly women.8,9 It has taken 20
years to validate DEXA as a clinically useful predictor of patients
who should be treated to prevent fracture, so don't hold your breath
over ultrasound!
Richard L Prince
Associate Professor, University Department of Medicine
Sir Charles Gairdner Hospital, Perth, WA
Reprints: Associate Professor R L Prince, University Department of
Medicine, Sir Charles Gairdner Hospital, Nedlands, WA 6009.
-
Eddy DM, Johnston CC, Cummings SR, et al. Osteoporosis: review of
the evidence for prevention, diagnosis and treatment and
cost-effectiveness analysis. Osteoporos Int 1998; 8 Suppl
4: S7-S80.
-
Cummings SR. Effect of alendronate on risk of fracture in women with
low bone density but without vertebral fracture: Results from the
Fracture Intervention Trial. JAMA 1998; 280: 2077-2082.
-
Sanders KM, Seeman E, Ugoni AM, et al. The age- and gender-specific
rate of fractures in Australia: a population based study.
Osteoporos Int 1999. In press.
-
Ross PD, Genant HK, Davis JW, et al. Predicting vertebral fracture
incidence from prevalent fractures and bone density among
non-black, osteoporotic women. Osteoporos Int 1993; 3:
120-126.
-
Wasnich RD, Davis JW, Ross PD. Spine fracture risk is predicted by
non-spine fractures. Osteoporos Int 1994; 4: 1-5.
-
Cummings SR, Nevitt MC, Browner WS, et al. Risk factors for hip
fracture in white women. N Engl J Med 1995; 332: 767-773.
-
Naganathan V, March L, Hunter D, et al. Quantitative heel
ultrasound as a predictor of osteoporosis. Med J Aust 1999;
171: 297-300.
-
Bauer DC, Gluer CC, Cauley JA, et al. Broadband ultrasound
attenuation predicts fractures strongly and independently of
densitometry in older women. Arch Intern Med 1997; 157:
629-634.
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Porter RW, Miller C, Grainger D, Palmer SB. Prediction of hip
fracture in elderly women: a prospective study. BMJ 1990;
301: 638-641.
©MJA 1999
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