Based on animal studies, statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) have been suggested as potential agents in the treatment of osteoporosis. In some epidemiological studies, statins have been associated with a reduced fracture risk. Our objective was to examine associations between statin treatment and risk of hip fracture in a population-based case-control study. A total of 6660 subjects with hip fracture and 33,274 gender- and age-matched population controls were identified from 1 January 1994 to 31 December 2001 using the Hospital Patient Register in North Jutland County, Denmark, and the Danish Central Personal Registry, respectively. Data on redeemed prescriptions for statins within the last 5 years before the index date were retrieved from a population-based prescription database. We used conditional logistic regression to estimate odds ratios (OR) for hip fracture according to use of statin prescriptions adjusted for potential confounding factors, i.e. gender, other diseases, and use of other drugs known to affect bone metabolism and fracture risk. After adjustment for potential confounders, statin treatment was associated with a reduced risk of hip fracture (OR=0.68; 95% confidence interval: 0.50-0.93) for those who had redeemed more than three prescriptions for a statin drug. We found that risk of hip fracture decreased with the number of statin prescriptions. Stratified analyses on gender and age did not reveal any major differences between men and women or among different age groups on the estimates between use of statins and hip fracture risk. Our findings support an association between statin treatment and a reduced hip fracture risk. However, it is unclear whether this association is causal.

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Abstract. Vestergaard P, Olsen ML, Paaske Johnsen S, Rejnmark L, Toft Sørensen H, Mosekilde L

1. The present study examined how uptake of lactate and H+ in resting muscle is affected by blood flow, arterial lactate concentration and muscle metabolism. 2. Six male subjects performed intermittent arm exercise in two separate 32 min periods (Part I and Part II) and in one subsequent 20 min period in which one leg knee-extensor exercise was also performed (Part III). The exercise was performed at various intensities in order to obtain different steady-state arterial blood lactate concentrations. In the inactive leg, femoral venous blood flow (draining about 7-7 kg of muscles) was measured and femoral arterial and venous blood was collected frequently. Biopsies were taken from m. vastus lateralis of the inactive leg at rest and 10 and 30 min into both Part I and Part II as well as 10 min into recovery from Part II.3. The arterial plasma lactate concentrations were 7, 9 and 16 mmol F' after 10 min of Parts I, II and III, respectively, and the corresponding arterial-venous difference (a-vdiff) for lactate in the resting leg was 1-3, 1-4 and 2 0 mmol F1. The muscle lactate concentration was 2-8 mmol (kg wet wt)-' after 10 min of Part I and remained constant throughout the experiment. During Parts I and II, a-vdiff lactate decreased although the arterial lactate concentration and plasma-muscle lactate gradient were unaltered throughout each period. Thus, membrane transport of lactate decreased during each period. 4. Blood flow in the inactive leg was about 2-fold higher during arm exercise compared to the rest periods, resulting in a 2-fold higher lactate uptake. Thus, lactate uptake by inactive muscles was closely related to blood flow.5. Throughout the experiment a-vdiff for actual base excess and for lactate were of similar magnitude.Thus, in inactive muscles lactate uptake appears to be coupled to the transport of H+.