Osteoporosis (cont.)

The long-term use of corticosteroids (such as prednisone, cortisone, and prednisolone) can lead to osteoporosis. Corticosteroids cause decreased calcium absorption from the intestines, increased loss of calcium through the kidneys in urine, and increased calcium loss from the bones. To prevent bone loss while on long-term corticosteroids, patients should

1. have an adequate calcium (1,000 mg daily if premenopausal, 1,500 mg daily if postmenopausal) and vitamin D intake (the actual level of Vitamin D can be measured with a simple blood test); however, calcium alone or combined with vitamin D cannot be relied upon to prevent bone loss from corticosteroids unless other prescription medications are added;
2. discuss with their doctor the use of either alendronate, risedronate, and zoledronate, which have been approved for the prevention and treatment of corticosteroid-induced osteoporosis;
3. discuss with their doctor about having a DXA bone density scan prior to beginning therapy and careful monitoring for osteoporosis during therapy.

The controversy of bone density testing in patients already taking osteoporosis medication

The American Medical Association and other reputable medical organizations recommend that repeat bone density testing (DXA scans) not be done for monitoring osteoporosis treatment or prevention on a routine basis; it is scientifically premature to measure bone density as a way of monitoring the effects of treatment. Doctors simply do not know how to use repeated bone density measurements during therapy. Here are a few of the most important reasons:

1. Bone density changes so slowly with treatment that the changes are smaller than the measurement error of the machine. In other words, repeat DXA scans cannot distinguish between a real increase in bone density due to treatment or a mere variation in measurement from the machine itself.
2. The real purpose of osteoporosis treatment is to decrease future bone fractures. There is no good correlation between increases in bone density with decreases in fracture risks with treatment. For example, alendronate has been shown to decrease fracture risk by 50% but only to increase bone density by a few percent. In fact, most of the fracture reduction with raloxifene is not explained by raloxifene's effects on bone mineral density.
3. One density measurement taken during treatment will not help the doctor plan or modify treatment. For example, even if the DXA scan shows continued deterioration in bone density during treatment, there is not yet research data demonstrating that changing a medication, combining medications, or doubling medication doses will be safe and helpful in decreasing the future risk of fractures.
4. Even if bone density deteriorates during treatment, it is quite likely that the patient would have lost even more bone density without treatment.
5. Recent research has shown that women who lose bone density after the first year of HRT will gain bone density in the next two years of therapy, whereas women who gain in the first year will tend to lose density in the next two years of therapy. Therefore, bone density during treatment fluctuates naturally, and these fluctuations may not correlate with the prevention of fractures due to the medication.

For all of these reasons, as surprising as it may sound to many people (and even some doctors!), rechecking bone density is not at all like checking blood pressure during treatment of high blood pressure (hypertension). Routine bone density testing during treatment is unlikely to be helpful. In the future, however, if ongoing research brings new technology or new therapies, testing decisions may change.

Source: MedicineNet.com
http://www.medicinenet.com/osteoporosis/article.htm