HIV-positive people taking rosuvastatin for 48 weeks had significantly greater gains in bone mineral density than people taking placebo, according to results of a 150-person trial.1 Statins are used to treat high cholesterol in people with and without HIV, but this is the first comparative trial to show that statins have a positive impact on bone density in people with HIV.
HIV-positive people have higher rates of heart disease than people without HIV.2 Because statins lower "bad" low-density lipoprotein (LDL) cholesterol, they could help prevent heart disease in HIV-positive people. A recent study found that -- besides lowering LDL cholesterol -- a statin also cut the number and size of coronary artery plaques (fatty build-ups) in people with HIV (see the preceding article in this issue of HIV Treatment Alerts).3 That could be another way statins prevent heart disease in HIV-positive people.
Like heart disease, osteoporosis (low bone mineral density, Figure 1) has become more common in people with HIV as they grow older. Some studies of older people with HIV suggest that statins have a positive impact on bone mineral density and body composition, but research has not firmly established these benefits. To address those questions, US researchers planned a trial to compare daily rosuvastatin with placebo (a dummy pill) in HIV-positive adults.
Figure 1. People with HIV infection may have several risk factors for severe loss of bone mineral density -- osteoporosis. (Illustrations from Servier PowerPoint image bank.)
The trial involved HIV-positive adults invited to join the study between March 2011 and August 2012. The researchers randomly assigned half of them to take 10 mg of rosuvastatin daily and half to take placebo, an inactive pill made to look like rosuvastatin. The prime use of rosuvastatin and all statins is to lower LDL cholesterol and thus prevent heart disease. Neither study participants nor study investigators knew which people got rosuvastatin and which got placebo. This is the strongest trial design for determining the impact of a treatment in a given group of people.
All study participants were at least 18 years old, were taking antiretroviral therapy for at least 6 months, and had a viral load below 1000 copies. Everyone had a "bad" LDL cholesterol at or below 130 mg/dL, which is a healthy LDL level. Everyone also had certain signals of inflammation or immune-cell activation.
No one had an active or ongoing inflammatory condition (except HIV infection), and no one had an earlier fracture suggesting low bone mineral density or an earlier heart attack. No one was taking bone therapy drugs, cancer chemotherapy, steroids, or more than 81 mg of aspirin daily (the low dose taken to prevent heart disease).
When people entered the study and 48 weeks later, they had a DXA scan of their whole body, their lower spine, and their left hip. Researchers used initial DXA findings to see who had osteopenia (low bone density) or osteoporosis (very low bone density) and to measure limb fat, trunk fat, and lean mass. The researchers defined lean mass as DXA-measured mass not including fat or bone. They also measured blood markers of inflammation and immune-cell activation.
The main goals were to measure changes in bone mineral density, fat, and lean mass from study entry to week 48 and to compare changes in people taking rosuvastatin and people taking placebo. The research team used accepted statistical methods to make these comparisons.
This analysis of changes in bone mineral density, fat, and lean mass after 48 weeks was a planned part of the SATURN-HIV trial, which is also testing the impact of rosuvastatin on cholesterol, inflammation, and activation of immune system cells.4-7
The researchers randomly assigned 72 people to take rosuvastatin and 75 to take placebo. The study group had a median age of 47 years, about three quarters were men, and about 70% were black. When the study began, median CD4 count stood at 613, and 78% of participants had an undetectable viral load. Almost one quarter of participants had osteopenia or osteoporosis when the study started.
After 48 weeks of treatment, average hip bone mineral density rose 0.6% in people taking rosuvastatin and fell 0.6% in people taking placebo (Figure 2). The difference between groups was statistically significant, meaning chance cannot explain the difference. At the trochanter (the top of the thigh bone), average bone mineral density rose 0.9% in the rosuvastatin group and fell 0.7% in the placebo group (Figure 2). This difference between rosuvastatin and placebo was also statistically significant. Average bone mineral density in the lower spine changed little through 48 weeks in either group.
Figure 2. In a trial that randomly assigned HIV-positive adults to take rosuvastatin or placebo (a dummy pill), people taking rosuvastatin for 48 weeks gained bone mineral density in the total hip and trochanter, while people taking placebo lost bone mineral density at these sites. (Bone illustration from Servier PowerPoint image bank.)
The researchers then performed a statistical analysis that assessed the potential impact of age, race, sex, and smoking on hip bone mineral density. (Older age, white rate, female sex, and smoking can contribute to lower bone density.) In this analysis, the estimated average difference in hip bone mineral density between the rosuvastatin group and the placebo group was almost 1% (0.92%).
Leg lean mass increased significantly by 1.5% in the rosuvastatin group, and there was a trend toward increased total lean mass with rosuvastatin (+0.8%). Changes in total, leg, or arm lean mass did not differ significantly between people taking rosuvastatin and people taking placebo. Total body fat, trunk fat, and limb fat did not change significantly during 48 weeks of treatment with rosuvastatin. And fat changes did not differ significantly between people taking rosuvastatin and people taking placebo.
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