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Haugeberg et al recently published clinical decision rules to identify patients with rheumatoid arthritis (RA) at risk for osteoporosis.1 Included were patients treated with glucocorticoids, a subject that has been for a long time the interest of rheumatologists.2–,4
For example, the Dutch Society for Rheumatology has recently published guidelines for the prevention of glucocorticoid induced osteoporosis (GIOP).5 This document was prepared by a group of rheumatologists of the society and other experts to mark the occasion of the publication of the 3rd Osteoporosis Guideline, (the “CBO consensus”) which was, in turn, prepared at the request of the Dutch authorities by a multidisciplinary group who examined evidence based medicine.6
Figure 1⇓ is a stream diagram showing the diagnostic and therapeutic steps in making decisions for the prevention of GIOP.5 Factors that influence this decision include the dose of glucocorticoids and the presence of other risk factors such as age, sex, previous fracture, and bone mineral density (BMD). The main message is that treatment with bisphosphonates should be started immediately in patients at high risk (high dose of glucocorticoids, prevalent fracture, postmenopausal women, and elderly men).
The recommendations cover some uncertainties. Firstly, it is unclear what is the threshold value of BMD below which prevention is indicated if the intake of glucocorticoids is <7.5 mg prednisone equivalents/day in the absence of other risk factors. The CBO consensus suggested a T score <−2.5 or a Z score <−1.6 However, other groups have suggested different thresholds. The UK consensus group suggested a T score <−1.57 and the American College of Rheumatology suggested a T score <−1.3 The main reason for the absence of consensus is the uncertainty that the risk for osteoporosis is increased in a low risk group treated with low dose glucocorticoids, that fractures can be prevented in this group and, perhaps most relevant, that the fracture threshold is altered in GIOP.8 Indeed, bone loss is limited in patients chronically treated with low dose glucocorticoids if calcium and vitamin D supplements are given.9
Secondly, it is still unclear if these patients should have an x ray examination of the spine to document vertebral deformities. Although only one in three vertebral deformities is accompanied by acute symptoms of fractures, it has been recently shown that non-clinically manifest vertebral deformities also result in increased morbidity and an increased risk for new fractures.10,11 Introducing a new risk factor is a reason for increasing awareness: starting glucocorticoid treatment should be accompanied by treatment with bisphosphonates in high risk patients and by dual energy x ray absorptiometry (DXA) measurement in others.
Thirdly, specific risk factors of bone loss in conditions such as RA were not considered. Accelerated bone loss has been documented in patients with RA with high disease activity,12 immobility, and low body weight.13 However, no studies are available on the prevention of osteoporosis in patients with RA with these risk factors, and, thus, this information was lacking in the guidelines.
In conclusion, the guidelines on the prevention of GIOP, which have been approved by the Dutch Society for Rheumatology, should increase awareness about patients at high risk. The publication by Haugeberg et al draws our attention to patients with RA who are not treated with glucocorticoids who perhaps also should be a target for prevention of bone loss and osteoporosis. This proposal needs to be fully explored in future studies. Thus, guidelines may disclose not only our knowledge in specific clinical situations but also may open up areas for new research.
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