The high prevalence of low bone density in men aged 55 yr and over presenting with low trauma fractures to an accident and emergency department

T. A.-Z. K. Gaber, S. Love1 and A. J. Crisp1

Rehabilitation and elderly medicine Directorate, Leigh Infirmary and formerly Department of Rehabilitation Medicine, Addenbrooke's Hospital and
1 Metabolic Bone Diseases, Addenbrooke's Hospital, Cambridge CB2 2QQ, UK

SIR, About 30% of hip and 33% of vertebral fractures occur in males [1, 2]. The unbalanced focus on osteoporosis prevention as an issue of primarily women's health is therefore unjustified. Factors predisposing to the disease can be identified in up to 77% of male patients with osteoporosis [3]. It is not practical to screen men for these risk factors in order to identify a male population at high risk of first fracture. We planned to determine whether middle-aged and elderly men suffering unselected low trauma fractures, most commonly of distal limbs, might include a population with low bone mass requiring treatment to reduce their risk of suffering further fractures. We also attempted to identify lifestyle and biochemical factors that might be associated with osteoporosis. In particular we wished to investigate further the relationship between serum testosterone concentration, bone density and fracture rates [46].

Thirty seven men of 55 yr and over were recruited. All presented to the Accident and Emergency Department at Addenbrooke's Hospital, Cambridge with a low trauma fracture during a 1-month period. Exclusion criteria were a history of known osteoporosis or of malignant disease. Informed consent was obtained and subjects were interviewed. The following were recorded: age, fracture site, history of previous fractures, lifestyle factors (smoking, alcohol consumption and an estimate of physical activity), drug history and family history of osteoporosis. Blood samples were taken for full blood count, urea, electrolytes, liver function tests, calcium, phosphate, alkaline phosphatase, TSH, serum testosterone, FSH and LH.

Bone mineral density (BMD) measurements of L1–4 lumbar spine, total femur and distal forearm of the non-affected site were made on a Hologic DDR-4500A Dexa model and patients with abnormal investigations were referred to the Metabolic Bone Clinic (AJC) for further evaluation and treatment.

Full data were available on all 37 subjects. Ages ranged between 55 and 95 yr (mean age 68 yr, S.D. 9.6). Twenty six were smokers. Fourteen consumed more than 15 units of alcohol weekly. Twenty subjects took some regular daily exercise. Twenty two men had upper limb fractures, two had hip fractures and 13 had fractures in other sites (mainly distal lower limb). Fourteen subjects had a history of previous fracture. Urea, electrolytes, calcium, phosphate, alkaline phosphatase and TSH were normal in all subjects. Eleven subjects had minor abnormalities in full blood count (mild anaemia or leucocytosis) or minor liver dysfunction. Six subjects (16.2%) had low serum testosterone and all of them had low BMD.

Osteoporosis, as defined by WHO criteria [7], at any measured site was identified in 32.4% (T score worse than -2.5). Osteopenia at any site was present in 54% (T score -1.0–2.5). Normal BMD at all sites was found in only 13.6% of patients. The prevalence of osteoporosis at lumbar spine was 8.1%, at femur 5.4% and at distal forearm 29.7%. The prevalence of osteopenia was 37.8%, 56.8% and 35.1%, respectively.

Using linear regression analysis, no significant correlation was detected between BMD (adjusted for age in all cases) in any of the three sites tested and age, history of fractures or other lifestyle risk factors. Two approaches were used to examine the relationship between serum testosterone and BMD. First, subjects were stratified into those above and below the normal laboratory reference level of serum testosterone and, second, numerical testosterone levels were employed. No correlation with BMD was found by either method.

We report a 32.4% prevalence of previously undiagnosed osteoporosis in a cohort of men sustaining low impact fractures. The Dubbo study reported even higher prevalences in men with hip (66%) and upper limb (44%) fractures [8]. Epidemiological studies examining the relationships between osteoporosis and fractures in men have concentrated on vertebral body and hip fractures not only because of the proven strong association between osteoporosis and fractures at these sites [1, 9], but also because of the significant morbidity, mortality and economic consequences associated with these fractures [10]. Most of our subjects had distal upper and lower limb fractures and only two had hip fractures. These data suggest that low trauma fractures at any site may be associated with low bone mass.

Previous studies of male osteoporosis have reported likely contributory factors in 30–77% of patients. Most studies focused on vertebral fractures [3, 11] or hip fractures [12, 13]. No data on possible secondary causes of osteoporosis in men with distal limb fracture are available. A total of 16.2% of our fracture patients had low testosterone and this finding is consistent with previous studies [3, 12]. An even higher percentage of patients with low testosterone level cannot be ruled out as SHBG levels were not measured, and patients with high SHBG may have a falsely normal testosterone level. None of our subjects was taking corticosteroids or had evidence of abnormal calcium metabolism. Mild hepatic abnormalities could suggest a possible contribution of alcoholic bone toxicity in a minority of fracture patients.

We propose that the management of middle-aged and elderly men sustaining low traumatic fractures should routinely include a measurement of bone density and referral for medical treatment when indicated. If the diagnosis of low bone mass is missed at the time of fracture presentation, further fractures, perhaps including femur, may ensue.

We acknowledge the assistance of Mr R. Bathula, elective medical student, in assembling data for this project.

Notes

Correspondence to: T. A.-Z. K. Gaber, Rehabilitation Medicine, Leigh Infirmary, WN7 1HS, UK. E-mail: t_gaber{at}lycos.com; dobash{at}hotmail.com Back

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Accepted 11 November 2002





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