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Alan Malabanan, Commentary, Clinical Chemistry, Volume 64, Issue 1, 1 January 2018, Page 51, https://doi.org/10.1373/clinchem.2017.281857
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This case highlights the need to identify and correct secondary causes of low bone mass before considering osteoporosis therapy. Osteoporosis can be diagnosed on the basis of low bone density, typical fragility fractures, or increased fracture risk, but in all instances, metabolic bone diseases such as osteomalacia must be ruled out (1). Distinguishing osteomalacia from osteoporosis is not possible with bone density alone and requires a careful history, physical, and judicious selection of laboratory tests. In this case presentation, there are multiple likely contributory etiologies and clues to secondary osteoporosis—a history of bariatric surgery, bony pain, uncorrected vitamin D deficiency, hypocalcemia, secondary hyperparathyroidism, increased alkaline phosphatase, and proton pump inhibitor therapy. Serum magnesium, necessary for adequate parathyroid hormone action, and a fasting serum phosphate, a necessary component along with calcium for normal bone mineralization, will also be useful. The ongoing high-dose estrogen therapy and mildly osteopenic bone density also argue against postmenopausal osteoporosis as an etiology for her fractures. If the bone density is not the cause of skeletal fragility, then the bone quality must be the issue. As the author mentions, bisphosphonate therapy is harmful and not helpful in those with vitamin D deficiency, hypocalcemia, and esophageal ulcerations.
