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In this issue of the Journal, Diamond et al.³ report a 20% mortality within six months of hip fracture among elderly men. While fracture-related complications in the men were comparable with those of randomly selected age-matched women with hip fracture, 14% of men died during admission, compared with only 6% of women. This difference was not statistically significant, and women were not followed after discharge, so further comparison of mortality was not possible. Interestingly, 32% of men and 28% of women were admitted from institutions where protein malnutrition, vitamin D deficiency, illness, falls and hip fractures are more common than in the community;⁴ 50% of men and 42% of women were discharged to institutions.

Despite important limitations of this study -- its small sample size (only 51 men, with 10 lost to follow-up) and the absence of control groups -- it does highlight the high morbidity and mortality associated with hip fractures in elderly Australians, and suggests that mortality may be higher in men than in women. In this, it concurs with the findings of Poor et al., who reported a mortality of 20.7% in men and 7.5% in women with hip fractures.^5,6 Among the 131 men they studied, hospital mortality was 11.5% and 30-day mortality was 16%, while 79% of the survivors resided in nursing homes at one year.

Fifty-eight per cent of these 131 men, compared with 94% of the age-matched community-residing male controls, were alive at one year, and the risk of death increased with higher levels of coexisting illness, age and with activity status at the time of fracture.⁶ Immediately after fracture, overall survival was similar for both patients and controls who had no pre-existing comorbid conditions. Survival was reduced for both groups with increasing numbers of coexisting illnesses, and was lower in the cases than controls at each level of comorbidity (see Box). Dementia, cerebrovascular disease, chronic lung disease, congestive heart failure and myocardial infarction significantly influenced survival. As neither fracture alone nor illness alone accounted for the excess mortality, it seems an interaction between fracture and its consequences with the coexisting illnesses may be responsible.

Bone strength is determined by bone size, mass and architecture. Men with fractures have smaller bones than controls: those with femoral neck fractures have reduced femoral neck width, and those with spinal fractures have reduced vertebral body width. Bones may be smaller because of reduced peak bone size and reduced periosteal appositional growth. Smaller bones have lower bone density because they have attained a lower peak bone mass or because bone has been lost.

Osteoporosis in old age is the result of genetic and environmental factors during growth and ageing, and both periods need to be studied. Hypogonadism during growth and delayed puberty may result in reduced peak bone size and bone density. Later in life, age-related hypogonadism and the resultant decline in testosterone levels may contribute to bone loss. Hypogonadism is present in around 20% of elderly men in the community (own unpublished data), and in around 50% of men with spine or hip fractures.⁷

There is no proven treatment for osteoporosis in men because there have been no appropriate randomised controlled trials. Calcium supplements are safe and may slow bone loss, at least in women.⁸ Vitamin D deficiency should be suspected in housebound or institutionalised elderly men and should be treated (after excluding malabsorption) with daily vitamin D supplements. The purported efficacy of 1 a ,25-dihydroxyvitamin D₃ for osteoporosis in women has led to it being approved in Australia for treating osteoporosis in men. Hypogonadism should be treated with testo sterone (which may increase bone mineral density [BMD] in eugonadal men, but only short term trials have been done). The possible increased risk of prostatic cancer associated with testosterone therapy needs to be considered in any cost-benefit analysis.

Several small short term trials in men with idiopathic or secondary osteoporosis suggest that bisphosphonates increase BMD and reduce bone turnover. Studies in women with primary osteoporosis, and in animals suggest that drugs such as alendronate and etidronate appear to be the best options at this time. However, as long term safety data are limited, these drugs must be given cautiously. The bisphosphonates may remain in bone indefinitely, alendronate can cause gastric irritation or oesophageal ulceration, and etidronate can cause focal osteomalacia when given for prolonged periods. Sodium fluoride increases BMD but not bone strength and should not be used in osteoporosis in men or women. There is no evidence for a favourable effect of anabolic steroids in men.

The problem of osteoporosis and fractures in men is likely to increase. To use drugs in men based on evidence from studies in women is not an appropriate long term solution. Drug therapy for men must be based on studies of efficacy, safety and quality of life in men. As with all measures in preventive medicine, potential drug therapy must be safe because most people who are treated derive no benefit. For example, if the incidence of fracture is two per 100 men per year, and a drug has a 50% antifracture efficacy, in any year 98 men will not have had a fracture with or without treatment, one will have a fracture anyway, and, in one, fracture will be prevented -- 99 will derive no benefit. Clearly, treatments must be safe.

Age-specific hip fracture incidence rates in men with low BMD must be determined prospectively to enable us to establish drug efficacy. For example, if the incidence of fracture is two per 100 men per year, 1260 men with hip fracture and 1260 controls will be needed to detect a 50% risk reduction by a drug in a three-year study. Smaller sample sizes may be adequate if high risk groups with low baseline BMD and fractures are recruited. Studies with endpoints such as BMD, histomorphometry, biochemical measurements of bone turnover and biomechanical testing of bone biopsy specimens may provide at least some clarification of appropriate drugs for use in men.

Ego Seeman
Associate Professor of Medicine, Austin & Repatriation Medical Centre, University of Melbourne, VIC

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3. Diamond TH, Thornley SW, Sekel R, Smerdley P. Hip fracture in elderly men: prognostic factors and outcomes. Med J Aust 1997; 167: 412-415.
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7. Stanley HL, Schmitt BP, Poses RM, Diess WP. Does hypogonadism contribute to the occurrence of a minimal trauma hip fracture in elderly men. J Am Geriatr Soc 1991; 39: 766-771.
8. Reid IR, Ames RW, Evans MC, et al. Long term effects of calcium supplementation on bone loss and fractures in post menopausal women -- a randomized controlled trial. Am J Med 1995; 98: 331-335.