Hip fracture incidence in nursing home residents and community-dwelling older people,Washington State, 1993-1995

OBJECTIVES: To establish and validate a method of linking data from the Minimum Data Set (MDS) and Medicare hospital claims, to estimate hip fracture incidence rates for Medicare beneficiaries aged 65 and older in Washington State, and to compare the incidence rates of hip fractures in nursing home and non-nursing home residents. DESIGN: Retrospective analysis of Medicare population-based enrollment, hospital claims, and nursing home administrative data sets. SETTING: Nursing home and non-nursing home setting. PARTICIPANTS: Medicare beneficiaries in Washington State residing in the community or in skilled nursing facilities. MEASUREMENTS: Crude age- and sex-specific and standardized age- and sex-adjusted hip fracture incidence for persons residing and not residing in nursing homes. RESULTS: From October 1, 1993, through September 30, 1995, 7,812 Medicare beneficiaries aged 65 or older were hospitalized for hip fractures (6,566 fractures for 1,155,234 person-years of exposure in non-nursing home residents and 1,246 fractures for 42,986 person-years of exposure in nursing home residents). The standardized age- and sex-adjusted hip fracture rate of nursing home residents (23.0 per 1,000 person-years) substantially exceeded that of non-nursing home residents (5.7 per 1,000 person-years) (incidence rate ratio = 4.0, 95% confidence interval = 3.7-4.5). CONCLUSION: The incidence of hip fracture in nursing home residents far exceeds that in noninstitutionalized older people. Linkage of MDS and Medicare hospital claims data is a useful tool for epidemiological surveillance regarding events in nursing homes that are likely to result in hospitalization.     

The new biology of aldosterone

Classically, aldosterone is synthesised in the adrenal zona glomerulosa and binds to specific mineralocorticoid receptors located in the cytosol of target epithelial cells. Translocation of the resulting steroid receptor complex to the cell nucleus modulates gene expression and translation of specific 'aldosterone-induced' proteins that regulate electrolyte and fluid balance. However, non-epithelial and rapid non-genomic actions of aldosterone have also been described that account for a variety of actions of aldosterone that contribute to blood pressure homeostasis. These include key actions on endothelial cells and on cardiac tissue. There is also evidence that aldosterone can be synthesised in other tissues; the most convincing evidence relates to the central nervous system. However, suggestions that aldosterone is produced in the heart remain controversial, and adrenal derived aldosterone is the principal source of circulating and locally available hormone. Recent studies have shown major therapeutic benefits of mineralocorticoid receptor antagonism in cardiac failure, which emphasise the importance of aldosterone in causing adverse cardiovascular pathophysiological effects. Additional evidence demonstrates that aldosterone levels predict development of high blood pressure in normotensive subjects, while it is now clear that increased aldosterone action contributes to hypertension and cardiovascular damage in approximately 10% of patients with established hypertension. These new findings highlight the role of aldosterone as a key cardiovascular hormone and extend our understanding of its role in determining adverse cardiovascular outcomes.