Secondary osteoporosis: a disease with serious consequences

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Secondary osteoporosis (OP) develops as a result of somatic pathologies (endocrine, genetic diseases, kidney damage, gastrointestinal tract, etc.), lifestyle habits or medications. Any patient with suspected secondary OP must undergo a series of laboratory tests (full clinical blood test, biochemical blood test, blood test for 25-hydroxyvitamin D, parathyroid hormone, etc.). The “gold standard” for instrumental diagnosis of OP is dual-energy X-ray densitometry of the lumbar spine and proximal femur to assess bone mineral density.

Treatment of secondary OP is etiological, aimed at identifying and eliminating the underlying cause of the disease, which usually involves discontinuation of medications (if possible) and correction of modifiable risk factors.

If it is impossible to influence the cause of secondary OP, pathogenetic therapy is used, including antiresorptive drugs, agents that enhance bone formation, and monoclonal antibodies. It is important to remember that the effectiveness of treatment of OP is influenced by indicators of phosphorus-calcium metabolism, therefore, before starting pathogenetic therapy, it is necessary to determine the levels of calcium, phosphorus and 25-hydroxyvitamin D in the blood, bring these indicators to normal values, and then continue taking these drugs along with pathogenetic therapy. To do this, they recommend a diet balanced in calcium, phosphorus and proteins, and the prescription of vitamin D supplements and calcium salts. One of the effective means for normalizing phosphorus-calcium metabolism is the drug Osteomed Forte.

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作者简介

M. Sergeeva-Kondrachenko

Penza Institute for Postgraduate Medical Education

Email: marserkon@mail.ru

MD

俄罗斯联邦, Penza

N. Terina

Penza Institute for Postgraduate Medical Education

编辑信件的主要联系方式.
Email: marserkon@mail.ru
俄罗斯联邦, Penza

参考

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2. Fig. 1. Bone tissue in normal and in the development of postmenopausal osteoporosis

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3. Fig. 2. The most frequent localizations of osteoporotic fractures

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4. Fig. 3. Example of results of fracture risk assessment according to the FRAX calculator

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5. Fig. 4. Scheme of the pathogenesis of glucocorticoid-induced osteoporosis (cited from Canalis E. et al., 2007)

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6. Fig. 5. Possible consequences of low vitamin D levels

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