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More than 10% of HIVers are now over 50. And physicians are starting to see the overlap between what naturally happens as people get older and what could already be happening to the body because of HIV. For example, around age 35 men and women start losing 0.5% to 1% of their bone mass each year; this increases in women after menopause. There are different causes for this bone loss, and that is why there is a fairly wide variation in the amount of this loss in any one age group. Factors include cigarette smoking, low body weight, corticosteroid use, arthritis, alcohol use, low testosterone, overactive thyroid or parathyroid, inadequate calcium intake, kidney disease, family history, or long-term bed rest from a chronic illness. It's not hard to see that HIV can contribute to some of these factors. The way bone mineral density is measured is by a dual X-ray absorptiometry, or DEXA, scan. The results are then compared to the peak bone density in a population of 30-year-olds adjusted for race and sex, arriving at a T-score. Osteoporosis is defined as a T-score more than 2H standard deviations below the peak bone density and carries an increase of four to five times in the risk of fractures. Osteopenia is one to 2H standard deviations below the peak and has two times the risk of fracture. Bone mineral loss is caused by a shift in the balance in the bone between the cells building new bone and the cells destroying or remodeling old bone. In addition, HIV alone can cause bone demineralization. In a Gilead study 600 treatment-naive patients with an average age of 36 had baseline DEXA scans. Osteopenia was already found in 23% to 28%, far above the national norm. Over the study there was continued bone loss, but most of it occurred early on and then stabilized. There was also slightly more bone loss in the tenofovir arm of the study. However, there are no studies indicating that tenofovir is more harmful to bone than any other antiretroviral. Current practice guidelines have no recommendations on when and for whom to order DEXA scans. At a minimum, though, any patient with a fracture or multiple risk factors should be studied. Treatment should start with addressing any of the risk factors along with the addition of at least 1,000 milligrams of calcium and 400 international units of vitamin D daily. Fosamax, which reduces bone destruction, can also be safely used by HIVers. The second bony issue is osteonecrosis, formerly known as avascular necrosis. This occurs when loss of blood supply to part of a bone causes death of its tissue. The exact cause is not understood but is probably multifactorial. Contributors may include prolonged corticosteroid use, alcohol use, elevated lipids or the use of lipid-lowering agents, smoking, and testosterone or steroid use. The first report of osteonecrosis in HIV occurred in 1990. Then in the late 1990s there seemed to be an increase in cases. In a study in 1999 by the National Institutes of Health, 4.4% of 339 HIV-positive patients had osteonecrosis versus none in 118 matched HIV-negative controls. Concern initially focused on protease inhibitors as a possible cause, but no clear association with their use has been found. Patients usually see their physician because of a deep aching pain in the hip. Any X-rays are almost always negative, except in advanced disease. Diagnosis is made by magnetic resonance imaging. Far less commonly, osteonecrosis can be found in the shoulders, knees, or wrists. Initial treatment is to take the weight off the joint; in very early cases calcium, vitamin D, and Fosamax might help. However, hip replacement is the eventual treatment in most patients. Newer, less radical surgical treatments are being tried in less advanced cases, but results are mixed. Meanwhile, none of us is getting any younger, so now is the time to exercise more, stop smoking, reduce alcohol intake, and add a little calcium to your life.
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