<?xml version="1.0" encoding="UTF-8"?>
<!DOCTYPE article PUBLIC "-//NLM//DTD JATS (Z39.96) Journal Publishing DTD v1.3 20210610//EN" "JATS-journalpublishing1-3.dtd">
<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">porozendo</journal-id><journal-title-group><journal-title xml:lang="ru">Остеопороз и остеопатии</journal-title><trans-title-group xml:lang="en"><trans-title>Osteoporosis and Bone Diseases</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2072-2680</issn><issn pub-type="epub">2311-0716</issn><publisher><publisher-name>Endocrinology Research Centre</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.14341/osteo12117</article-id><article-id custom-type="elpub" pub-id-type="custom">porozendo-12117</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>Научный обзор</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>Review</subject></subj-group></article-categories><title-group><article-title>Остеомаляция в практике эндокринолога: этиология, патогенез, дифференциальная диагностика с остеопорозом</article-title><trans-title-group xml:lang="en"><trans-title>Osteomalacia in practice of endocrinologist: etiology, pathogenesis, differential diagnosis with osteoporosis</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-2320-1051</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Голоунина</surname><given-names>Ольга Олеговна</given-names></name><name name-style="western" xml:lang="en"><surname>Golounina</surname><given-names>Olga O.</given-names></name></name-alternatives><bio xml:lang="ru"><p>cтудентка 3 курса Института клинической медицины</p></bio><bio xml:lang="en"><p>Student, Medical faculty</p></bio><email xlink:type="simple">olga.golounina@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-2144-8595</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Рунова</surname><given-names>Гюзель Евгеньевна</given-names></name><name name-style="western" xml:lang="en"><surname>Runova</surname><given-names>Gyuzel E.</given-names></name></name-alternatives><bio xml:lang="ru"><p>кандидат медицинских наук, ассистент кафедры эндокринологии №1</p></bio><bio xml:lang="en"><p>MD, PhD</p></bio><email xlink:type="simple">guzelvolkova@yandex.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-3026-6315</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Фадеев</surname><given-names>Валентин Викторович</given-names></name><name name-style="western" xml:lang="en"><surname>Fadeyev</surname><given-names>Valentin V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>д.м.н., профессор, член-корр. РАН</p></bio><bio xml:lang="en"><p>MD, PhD, Professor</p></bio><email xlink:type="simple">walfad@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru">ФГАОУ ВО «Первый Московский государственный медицинский университет им. И.М. Сеченова» Минздрава России (Сеченовский Университет)<country>Россия</country></aff><aff xml:lang="en">I.M. Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation (Sechenov University)<country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2019</year></pub-date><pub-date pub-type="epub"><day>07</day><month>02</month><year>2020</year></pub-date><volume>22</volume><issue>2</issue><fpage>23</fpage><lpage>31</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Голоунина О.О., Рунова Г.Е., Фадеев В.В., 2019</copyright-statement><copyright-year>2019</copyright-year><copyright-holder xml:lang="ru">Голоунина О.О., Рунова Г.Е., Фадеев В.В.</copyright-holder><copyright-holder xml:lang="en">Golounina O.O., Runova G.E., Fadeyev V.V.</copyright-holder><license license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://www.osteo-endojournals.ru/jour/article/view/12117">https://www.osteo-endojournals.ru/jour/article/view/12117</self-uri><abstract><p>Остеопороз – наиболее распространенная причина низкой минеральной плотности кости (МПК) и возникновения низкотравматичных переломов у взрослых. Однако при проведении дифференциальной диагностики с другими метаболическими заболеваниями скелета необходимо также учитывать другие возможные причины снижения МПК, в том числе остеомаляцию, поскольку схемы лечения при данных состояниях будут значимо различаться. Остеомаляция – системный патологический процесс, характеризующийся снижением прочности костной ткани в результате избыточного накопления неминерализованного остеоида и несоответствием между образованием костного матрикса и его минерализацией. Наиболее часто остеомаляция у взрослых развивается вследствие выраженного дефицита витамина D любой этиологии, реже – на фоне патологии почек, мезенхимальных опухолей, секретирующих фактор роста фибробластов 23, наследственных метаболических заболеваний скелета. Клинические симптомы остеомаляции неспецифичны, проявляются генерализованными диффузными болями в костях, мышечной слабостью, скелетными деформациями и часто остаются незамеченными на начальной стадии заболевания. Гистоморфометрическое исследование является наиболее точным методом для установления диагноза остеомаляции, позволяющим оценить скорость костеобразования и кальцификации. Основными задачами при лечении остеомаляции любой этиологии являются устранение дефицита витамина D, гипокальциемии, гипофосфатемии, предотвращение прогрессирования деформаций костей и мышечной гипотонии.</p></abstract><trans-abstract xml:lang="en"><p>Osteoporosis is the most common cause of low bone mineral density (BMD) and low-traumatic fractures in adults. However, differential diagnosis should also consider other causes of decreased BMD, including osteomalacia, as treatment for these conditions vary significantly. Osteomalacia is a systemic disorder characterized by decrease in bone strength due to of excessive accumulation of non-mineralized osteoid and uncoupling between bone matrix formation and mineralization. Osteomalacia in adults mostly develops due to severe vitamin D deficiency of any etiology, less often – along with kidney pathology, mesenchymal tumors secreting fibroblast growth factor 23 or hereditary metabolic bone diseases. Clinical symptoms of osteomalacia are nonspecific and mostly manifest by generalized diffuse bone pain, muscle weakness, skeletal deformities and often go unnoticed at initial stage of the disease. Histomorphometric examination is the most accurate method of the diagnosis, which allows assessment of bone formation rate and calcification. The utmost priority of the treatment of osteomalacia of any etiology is the elimination of vitamin D deficiency, hypocalcemia, hypophosphatemia and prevention of bone deformities progression and muscle hypotension.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>гипокальциемия</kwd><kwd>гипофосфатемия</kwd><kwd>витамин D</kwd><kwd>фактор роста фибробластов 23</kwd><kwd>минерализация</kwd><kwd>остеопороз</kwd><kwd>остеомаляция</kwd></kwd-group><kwd-group xml:lang="en"><kwd>hypocalcemia</kwd><kwd>hypophosphatemia</kwd><kwd>vitamin D</kwd><kwd>fibroblast growth factor 23</kwd><kwd>mineralization</kwd><kwd>osteoporosis</kwd><kwd>osteomalacia</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Bilezikian JP, Bouillon R, Clemens T, et al, eds. Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism. 1st ed. Wiley; 2018. doi: https://doi.org/10.1002/9781119266594</mixed-citation><mixed-citation xml:lang="en">Bilezikian JP, Bouillon R, Clemens T, et al, eds. Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism. 1st ed. Wiley; 2018. doi: https://doi.org/10.1002/9781119266594</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Whyte MP. Hypophosphatasia - aetiology, nosology, pathogenesis, diagnosis and treatment. Nat Rev Endocrinol. 2016;12(4):233-246. doi: https://doi.org/10.1038/nrendo.2016.14</mixed-citation><mixed-citation xml:lang="en">Whyte MP. Hypophosphatasia - aetiology, nosology, pathogenesis, diagnosis and treatment. Nat Rev Endocrinol. 2016;12(4):233-246. doi: https://doi.org/10.1038/nrendo.2016.14</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">Gifre L, Peris P, Monegal A, et al. Osteomalacia revisited : a report on 28 cases. Clin Rheumatol. 2011;30(5):639-645. doi: https://doi.org/10.1007/s10067-010-1587-z</mixed-citation><mixed-citation xml:lang="en">Gifre L, Peris P, Monegal A, et al. Osteomalacia revisited : a report on 28 cases. Clin Rheumatol. 2011;30(5):639-645. doi: https://doi.org/10.1007/s10067-010-1587-z</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Whyte MP, Thakker RV. Rickets and osteomalacia. Medicine. 2009;37(9):483-488. doi: https://doi.org/10.1016/j.mpmed.2009.06.004</mixed-citation><mixed-citation xml:lang="en">Whyte MP, Thakker RV. Rickets and osteomalacia. Medicine. 2009;37(9):483-488. doi: https://doi.org/10.1016/j.mpmed.2009.06.004</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Reginato AJ, Coquia JA. Musculoskeletal manifestations of osteomalacia and rickets. Best Pract Res Clin Rheumatol. 2003;17(6):1063-1080. doi: https://doi.org/10.1016/j.berh.2003.09.004</mixed-citation><mixed-citation xml:lang="en">Reginato AJ, Coquia JA. Musculoskeletal manifestations of osteomalacia and rickets. Best Pract Res Clin Rheumatol. 2003;17(6):1063-1080. doi: https://doi.org/10.1016/j.berh.2003.09.004</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Christakos S, Li S, De La Cruz J, Bikle DD. New developments in our understanding of vitamin metabolism, action and treatment. Metabolism. 2019;98:112-120. doi: https://doi.org/10.1016/j.metabol.2019.06.010</mixed-citation><mixed-citation xml:lang="en">Christakos S, Li S, De La Cruz J, Bikle DD. New developments in our understanding of vitamin metabolism, action and treatment. Metabolism. 2019;98:112-120. doi: https://doi.org/10.1016/j.metabol.2019.06.010</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Bove-Fenderson E, Mannstadt M. Hypocalcemic disorders. Best Pract Res Clin Endocrinol Metab. 2018;32(5):639-656. doi: https://doi.org/10.1016/j.beem.2018.05.006</mixed-citation><mixed-citation xml:lang="en">Bove-Fenderson E, Mannstadt M. Hypocalcemic disorders. Best Pract Res Clin Endocrinol Metab. 2018;32(5):639-656. doi: https://doi.org/10.1016/j.beem.2018.05.006</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">Khundmiri SJ, Murray RD, Lederer E. PTH and Vitamin D. Compr Physiol. 2016;6(2):561-601. doi: https://doi.org/10.1002/cphy.c140071</mixed-citation><mixed-citation xml:lang="en">Khundmiri SJ, Murray RD, Lederer E. PTH and Vitamin D. Compr Physiol. 2016;6(2):561-601. doi: https://doi.org/10.1002/cphy.c140071</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Aggarwal V, Seth A, Aneja S, et al. Role of calcium deficiency in development of nutritional rickets in Indian children: a case control study. J Clin Endocrinol Metab. 2012;97(10):3461-3466. doi: https://doi.org/10.1210/jc.2011-3120</mixed-citation><mixed-citation xml:lang="en">Aggarwal V, Seth A, Aneja S, et al. Role of calcium deficiency in development of nutritional rickets in Indian children: a case control study. J Clin Endocrinol Metab. 2012;97(10):3461-3466. doi: https://doi.org/10.1210/jc.2011-3120</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Adams JS, Hewison M. Extrarenal expression of the 25-hydroxyvitamin D-1-hydroxylase. Arch Biochem Biophys. 2012;523(1):95-102. doi: https://doi.org/10.1016/j.abb.2012.02.016</mixed-citation><mixed-citation xml:lang="en">Adams JS, Hewison M. Extrarenal expression of the 25-hydroxyvitamin D-1-hydroxylase. Arch Biochem Biophys. 2012;523(1):95-102. doi: https://doi.org/10.1016/j.abb.2012.02.016</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Margolis RN, Christakos S. The nuclear receptor superfamily of steroid hormones and vitamin D gene regulation. An update. Ann N Y Acad Sci. 2010;1192:208-214. doi: https://doi.org/10.1111/j.1749-6632.2009.05227.x</mixed-citation><mixed-citation xml:lang="en">Margolis RN, Christakos S. The nuclear receptor superfamily of steroid hormones and vitamin D gene regulation. An update. Ann N Y Acad Sci. 2010;1192:208-214. doi: https://doi.org/10.1111/j.1749-6632.2009.05227.x</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Morris HA. Vitamin D activities for health outcomes. Ann Lab Med. 2014;34(3):181-186. doi: https://doi.org/10.3343/alm.2014.34.3.181</mixed-citation><mixed-citation xml:lang="en">Morris HA. Vitamin D activities for health outcomes. Ann Lab Med. 2014;34(3):181-186. doi: https://doi.org/10.3343/alm.2014.34.3.181</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Pike JW, Meyer MB. The vitamin D receptor: new paradigms for the regulation of gene expression by 1,25-dihydroxyvitamin D(3). Endocrinol Metab Clin North Am. 2010;39(2):255-269, table of contents. doi: https://doi.org/10.1016/j.ecl.2010.02.007</mixed-citation><mixed-citation xml:lang="en">Pike JW, Meyer MB. The vitamin D receptor: new paradigms for the regulation of gene expression by 1,25-dihydroxyvitamin D(3). Endocrinol Metab Clin North Am. 2010;39(2):255-269, table of contents. doi: https://doi.org/10.1016/j.ecl.2010.02.007</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">Li YC, Bolt MJ, Cao LP, Sitrin MD. Effects of vitamin D receptor inactivation on the expression of calbindins and calcium metabolism. Am J Physiol Endocrinol Metab. 2001;281(3):E558-564. doi: https://doi.org/10.1152/ajpendo.2001.281.3.E558</mixed-citation><mixed-citation xml:lang="en">Li YC, Bolt MJ, Cao LP, Sitrin MD. Effects of vitamin D receptor inactivation on the expression of calbindins and calcium metabolism. Am J Physiol Endocrinol Metab. 2001;281(3):E558-564. doi: https://doi.org/10.1152/ajpendo.2001.281.3.E558</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">Van Cromphaut SJ, Dewerchin M, Hoenderop JG, et al. Duodenal calcium absorption in vitamin D receptor-knockout mice: functional and molecular aspects. Proc Natl Acad Sci U S A. 2001;98(23):13324-13329. doi: https://doi.org/10.1073/pnas.231474698</mixed-citation><mixed-citation xml:lang="en">Van Cromphaut SJ, Dewerchin M, Hoenderop JG, et al. Duodenal calcium absorption in vitamin D receptor-knockout mice: functional and molecular aspects. Proc Natl Acad Sci U S A. 2001;98(23):13324-13329. doi: https://doi.org/10.1073/pnas.231474698</mixed-citation></citation-alternatives></ref><ref id="cit16"><label>16</label><citation-alternatives><mixed-citation xml:lang="ru">Molin A, Wiedemann A, Demers N, et al. Vitamin D-Dependent Rickets Type 1B (25-Hydroxylase Deficiency): A Rare Condition or a Misdiagnosed Condition? J Bone Miner Res. 2017;32(9):1893-1899. doi: https://doi.org/10.1002/jbmr.3181</mixed-citation><mixed-citation xml:lang="en">Molin A, Wiedemann A, Demers N, et al. Vitamin D-Dependent Rickets Type 1B (25-Hydroxylase Deficiency): A Rare Condition or a Misdiagnosed Condition? J Bone Miner Res. 2017;32(9):1893-1899. doi: https://doi.org/10.1002/jbmr.3181</mixed-citation></citation-alternatives></ref><ref id="cit17"><label>17</label><citation-alternatives><mixed-citation xml:lang="ru">Al Mutair AN, Nasrat GH, Russell DW. Mutation of the CYP2R1 vitamin D 25-hydroxylase in a Saudi Arabian family with severe vitamin D deficiency. J Clin Endocrinol Metab. 2012;97(10):E2022-2025. doi: https://doi.org/10.1210/jc.2012-1340</mixed-citation><mixed-citation xml:lang="en">Al Mutair AN, Nasrat GH, Russell DW. Mutation of the CYP2R1 vitamin D 25-hydroxylase in a Saudi Arabian family with severe vitamin D deficiency. J Clin Endocrinol Metab. 2012;97(10):E2022-2025. doi: https://doi.org/10.1210/jc.2012-1340</mixed-citation></citation-alternatives></ref><ref id="cit18"><label>18</label><citation-alternatives><mixed-citation xml:lang="ru">Casella SJ, Reiner BJ, Chen TC, et al. A possible genetic defect in 25-hydroxylation as a cause of rickets. J Pediatr. 1994;124(6):929-932. doi: https://doi.org/10.1016/s0022-3476(05)83184-1</mixed-citation><mixed-citation xml:lang="en">Casella SJ, Reiner BJ, Chen TC, et al. A possible genetic defect in 25-hydroxylation as a cause of rickets. J Pediatr. 1994;124(6):929-932. doi: https://doi.org/10.1016/s0022-3476(05)83184-1</mixed-citation></citation-alternatives></ref><ref id="cit19"><label>19</label><citation-alternatives><mixed-citation xml:lang="ru">Tosson H, Rose SR. Absence of mutation in coding regions of CYP2R1 gene in apparent autosomal dominant vitamin D 25-hydroxylase deficiency rickets. J Clin Endocrinol Metab. 2012;97(5):E796-801. doi: https://doi.org/10.1210/jc.2011-2716</mixed-citation><mixed-citation xml:lang="en">Tosson H, Rose SR. Absence of mutation in coding regions of CYP2R1 gene in apparent autosomal dominant vitamin D 25-hydroxylase deficiency rickets. J Clin Endocrinol Metab. 2012;97(5):E796-801. doi: https://doi.org/10.1210/jc.2011-2716</mixed-citation></citation-alternatives></ref><ref id="cit20"><label>20</label><citation-alternatives><mixed-citation xml:lang="ru">Zhu JG, Ochalek JT, Kaufmann M, et al. CYP2R1 is a major, but not exclusive, contributor to 25-hydroxyvitamin D production in vivo. Proc Natl Acad Sci U S A. 2013;110(39):15650-15655. doi: https://doi.org/10.1073/pnas.1315006110</mixed-citation><mixed-citation xml:lang="en">Zhu JG, Ochalek JT, Kaufmann M, et al. CYP2R1 is a major, but not exclusive, contributor to 25-hydroxyvitamin D production in vivo. Proc Natl Acad Sci U S A. 2013;110(39):15650-15655. doi: https://doi.org/10.1073/pnas.1315006110</mixed-citation></citation-alternatives></ref><ref id="cit21"><label>21</label><citation-alternatives><mixed-citation xml:lang="ru">Jones G, Prosser DE, Kaufmann M. Chapter 5 - The Activating Enzymes of Vitamin D Metabolism (25- and 1α-Hydroxylases). In: Vitamin D. Volume 1: Biochemistry, Physiology and Diagnostics. 4th ed. Academic Press; 2018. p. 57-79. doi: https://doi.org/10.1016/b978-0-12-809965-0.00005-7</mixed-citation><mixed-citation xml:lang="en">Jones G, Prosser DE, Kaufmann M. Chapter 5 - The Activating Enzymes of Vitamin D Metabolism (25- and 1α-Hydroxylases). In: Vitamin D. Volume 1: Biochemistry, Physiology and Diagnostics. 4th ed. Academic Press; 2018. p. 57-79. doi: https://doi.org/10.1016/b978-0-12-809965-0.00005-7</mixed-citation></citation-alternatives></ref><ref id="cit22"><label>22</label><citation-alternatives><mixed-citation xml:lang="ru">Thambiah S, Roplekar R, Manghat P, et al. Circulating sclerostin and Dickkopf-1 (DKK1) in predialysis chronic kidney disease (CKD): relationship with bone density and arterial stiffness. Calcif Tissue Int. 2012;90(6):473-480. doi: https://doi.org/10.1007/s00223-012-9595-4</mixed-citation><mixed-citation xml:lang="en">Thambiah S, Roplekar R, Manghat P, et al. Circulating sclerostin and Dickkopf-1 (DKK1) in predialysis chronic kidney disease (CKD): relationship with bone density and arterial stiffness. Calcif Tissue Int. 2012;90(6):473-480. doi: https://doi.org/10.1007/s00223-012-9595-4</mixed-citation></citation-alternatives></ref><ref id="cit23"><label>23</label><citation-alternatives><mixed-citation xml:lang="ru">Evenepoel P, D’Haese P, Brandenburg V. Sclerostin and DKK1: new players in renal bone and vascular disease. Kidney Int. 2015;88(2):235-240. doi: https://doi.org/10.1038/ki.2015.156</mixed-citation><mixed-citation xml:lang="en">Evenepoel P, D’Haese P, Brandenburg V. Sclerostin and DKK1: new players in renal bone and vascular disease. Kidney Int. 2015;88(2):235-240. doi: https://doi.org/10.1038/ki.2015.156</mixed-citation></citation-alternatives></ref><ref id="cit24"><label>24</label><citation-alternatives><mixed-citation xml:lang="ru">Рожинская Л.Я., Белая Ж.Е., Луценко А.С. Новые возможности лечения вторичного гиперпаратиреоза у пациентов с терминальной стадией хронической болезни почек, получающих заместительную почечную терапию гемодиализом. // Остеопороз и остеопатии. — 2017. — Т. 20. — №1. — С. 32-38. [Rozhinskaya LY, Belaya ZE, Lutsenko AS. Novel treatment options for secondary hyperparathyroidism in end-stage kidney disease patients on hemodialysis therapy. Osteoporosis and bone diseases. 2017;20(1):32-38. (In Russ.)] doi: https://doi.org/10.14341/osteo2017126-33</mixed-citation><mixed-citation xml:lang="en">Рожинская Л.Я., Белая Ж.Е., Луценко А.С. Новые возможности лечения вторичного гиперпаратиреоза у пациентов с терминальной стадией хронической болезни почек, получающих заместительную почечную терапию гемодиализом. // Остеопороз и остеопатии. — 2017. — Т. 20. — №1. — С. 32-38. [Rozhinskaya LY, Belaya ZE, Lutsenko AS. Novel treatment options for secondary hyperparathyroidism in end-stage kidney disease patients on hemodialysis therapy. Osteoporosis and bone diseases. 2017;20(1):32-38. (In Russ.)] doi: https://doi.org/10.14341/osteo2017126-33</mixed-citation></citation-alternatives></ref><ref id="cit25"><label>25</label><citation-alternatives><mixed-citation xml:lang="ru">Barker SL, Pastor J, Carranza D, et al. The demonstration of alphaKlotho deficiency in human chronic kidney disease with a novel synthetic antibody. Nephrol Dial Transplant. 2015;30(2):223-233. doi: https://doi.org/10.1093/ndt/gfu291</mixed-citation><mixed-citation xml:lang="en">Barker SL, Pastor J, Carranza D, et al. The demonstration of alphaKlotho deficiency in human chronic kidney disease with a novel synthetic antibody. Nephrol Dial Transplant. 2015;30(2):223-233. doi: https://doi.org/10.1093/ndt/gfu291</mixed-citation></citation-alternatives></ref><ref id="cit26"><label>26</label><citation-alternatives><mixed-citation xml:lang="ru">Гребенникова Т.А., Белая Ж.Е., Цориев Т.Т., и др. Эндокринная функция костной ткани. // Остеопороз и остеопатии. — 2015. — Т. 18. — №1. — С. 28-37. [Grebennikova TA, Belaya ZE, Tsoriev TT, et al. The endocrine function of the bone tissue. Osteoporosis and bone diseases. 2015;18(1):28-37. (In Russ.)] doi: https://doi.org/10.14341/osteo2015128-37</mixed-citation><mixed-citation xml:lang="en">Гребенникова Т.А., Белая Ж.Е., Цориев Т.Т., и др. Эндокринная функция костной ткани. // Остеопороз и остеопатии. — 2015. — Т. 18. — №1. — С. 28-37. [Grebennikova TA, Belaya ZE, Tsoriev TT, et al. The endocrine function of the bone tissue. Osteoporosis and bone diseases. 2015;18(1):28-37. (In Russ.)] doi: https://doi.org/10.14341/osteo2015128-37</mixed-citation></citation-alternatives></ref><ref id="cit27"><label>27</label><citation-alternatives><mixed-citation xml:lang="ru">Fang Y, Ginsberg C, Seifert M, et al. CKD-induced wingless/integration1 inhibitors and phosphorus cause the CKD-mineral and bone disorder. J Am Soc Nephrol. 2014;25(8):1760-1773. doi: https://doi.org/10.1681/ASN.2013080818</mixed-citation><mixed-citation xml:lang="en">Fang Y, Ginsberg C, Seifert M, et al. CKD-induced wingless/integration1 inhibitors and phosphorus cause the CKD-mineral and bone disorder. J Am Soc Nephrol. 2014;25(8):1760-1773. doi: https://doi.org/10.1681/ASN.2013080818</mixed-citation></citation-alternatives></ref><ref id="cit28"><label>28</label><citation-alternatives><mixed-citation xml:lang="ru">Silver J, Rodriguez M, Slatopolsky E. FGF23 and PTH--double agents at the heart of CKD. Nephrol Dial Transplant. 2012;27(5):1715-1720. doi: https://doi.org/10.1093/ndt/gfs050</mixed-citation><mixed-citation xml:lang="en">Silver J, Rodriguez M, Slatopolsky E. FGF23 and PTH--double agents at the heart of CKD. Nephrol Dial Transplant. 2012;27(5):1715-1720. doi: https://doi.org/10.1093/ndt/gfs050</mixed-citation></citation-alternatives></ref><ref id="cit29"><label>29</label><citation-alternatives><mixed-citation xml:lang="ru">Klootwijk ED, Reichold M, Unwin RJ, et al. Renal Fanconi syndrome: taking a proximal look at the nephron. Nephrol Dial Transplant. 2015;30(9):1456-1460. doi: https://doi.org/10.1093/ndt/gfu377</mixed-citation><mixed-citation xml:lang="en">Klootwijk ED, Reichold M, Unwin RJ, et al. Renal Fanconi syndrome: taking a proximal look at the nephron. Nephrol Dial Transplant. 2015;30(9):1456-1460. doi: https://doi.org/10.1093/ndt/gfu377</mixed-citation></citation-alternatives></ref><ref id="cit30"><label>30</label><citation-alternatives><mixed-citation xml:lang="ru">Hall AM, Bass P, Unwin RJ. Drug-induced renal Fanconi syndrome. QJM. 2014;107(4):261-269. doi: https://doi.org/10.1093/qjmed/hct258</mixed-citation><mixed-citation xml:lang="en">Hall AM, Bass P, Unwin RJ. Drug-induced renal Fanconi syndrome. QJM. 2014;107(4):261-269. doi: https://doi.org/10.1093/qjmed/hct258</mixed-citation></citation-alternatives></ref><ref id="cit31"><label>31</label><citation-alternatives><mixed-citation xml:lang="ru">Foreman JW. Fanconi Syndrome. Pediatr Clin North Am. 2019;66(1):159-167. doi: https://doi.org/10.1016/j.pcl.2018.09.002</mixed-citation><mixed-citation xml:lang="en">Foreman JW. Fanconi Syndrome. Pediatr Clin North Am. 2019;66(1):159-167. doi: https://doi.org/10.1016/j.pcl.2018.09.002</mixed-citation></citation-alternatives></ref><ref id="cit32"><label>32</label><citation-alternatives><mixed-citation xml:lang="ru">Alexander RT, Bitzan M. Renal Tubular Acidosis. Pediatr Clin North Am. 2019;66(1):135-157. doi: https://doi.org/10.1016/j.pcl.2018.08.011</mixed-citation><mixed-citation xml:lang="en">Alexander RT, Bitzan M. Renal Tubular Acidosis. Pediatr Clin North Am. 2019;66(1):135-157. doi: https://doi.org/10.1016/j.pcl.2018.08.011</mixed-citation></citation-alternatives></ref><ref id="cit33"><label>33</label><citation-alternatives><mixed-citation xml:lang="ru">Bai XY, Miao D, Goltzman D, Karaplis AC. The autosomal dominant hypophosphatemic rickets R176Q mutation in fibroblast growth factor 23 resists proteolytic cleavage and enhances in vivo biological potency. J Biol Chem. 2003;278(11):9843-9849. doi: https://doi.org/10.1074/jbc.M210490200</mixed-citation><mixed-citation xml:lang="en">Bai XY, Miao D, Goltzman D, Karaplis AC. The autosomal dominant hypophosphatemic rickets R176Q mutation in fibroblast growth factor 23 resists proteolytic cleavage and enhances in vivo biological potency. J Biol Chem. 2003;278(11):9843-9849. doi: https://doi.org/10.1074/jbc.M210490200</mixed-citation></citation-alternatives></ref><ref id="cit34"><label>34</label><citation-alternatives><mixed-citation xml:lang="ru">Saleem S, Aslam HM, Anwar M, et al. Fahr’s syndrome: literature review of current evidence. Orphanet J Rare Dis. 2013;8:156. doi: https://doi.org/10.1186/1750-1172-8-156</mixed-citation><mixed-citation xml:lang="en">Saleem S, Aslam HM, Anwar M, et al. Fahr’s syndrome: literature review of current evidence. Orphanet J Rare Dis. 2013;8:156. doi: https://doi.org/10.1186/1750-1172-8-156</mixed-citation></citation-alternatives></ref><ref id="cit35"><label>35</label><citation-alternatives><mixed-citation xml:lang="ru">Lorenz-Depiereux B, Bastepe M, Benet-Pages A, et al. DMP1 mutations in autosomal recessive hypophosphatemia implicate a bone matrix protein in the regulation of phosphate homeostasis. Nat Genet. 2006;38(11):1248-1250. doi: https://doi.org/10.1038/ng1868</mixed-citation><mixed-citation xml:lang="en">Lorenz-Depiereux B, Bastepe M, Benet-Pages A, et al. DMP1 mutations in autosomal recessive hypophosphatemia implicate a bone matrix protein in the regulation of phosphate homeostasis. Nat Genet. 2006;38(11):1248-1250. doi: https://doi.org/10.1038/ng1868</mixed-citation></citation-alternatives></ref><ref id="cit36"><label>36</label><citation-alternatives><mixed-citation xml:lang="ru">Noonan ML, White KE. FGF23 Synthesis and Activity. Curr Mol Biol Rep. 2019;5(1):18-25. doi: https://doi.org/10.1007/s40610-019-0111-8</mixed-citation><mixed-citation xml:lang="en">Noonan ML, White KE. FGF23 Synthesis and Activity. Curr Mol Biol Rep. 2019;5(1):18-25. doi: https://doi.org/10.1007/s40610-019-0111-8</mixed-citation></citation-alternatives></ref><ref id="cit37"><label>37</label><citation-alternatives><mixed-citation xml:lang="ru">Sako S, Niida Y, Shima KR, et al. A novel PHEX mutation associated with vitamin D-resistant rickets. Hum Genome Var. 2019;6:9. doi: https://doi.org/10.1038/s41439-019-0040-3</mixed-citation><mixed-citation xml:lang="en">Sako S, Niida Y, Shima KR, et al. A novel PHEX mutation associated with vitamin D-resistant rickets. Hum Genome Var. 2019;6:9. doi: https://doi.org/10.1038/s41439-019-0040-3</mixed-citation></citation-alternatives></ref><ref id="cit38"><label>38</label><citation-alternatives><mixed-citation xml:lang="ru">Zhang S, Zhang Q, Cheng L, et al. [Analysis of PHEX gene mutations in three pedigrees affected with hypophosphatemic rickets]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi. 2018;35(5):644-647. doi: https://doi.org/10.3760/cma.j.issn.1003-9406.2018.05.005</mixed-citation><mixed-citation xml:lang="en">Zhang S, Zhang Q, Cheng L, et al. [Analysis of PHEX gene mutations in three pedigrees affected with hypophosphatemic rickets]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi. 2018;35(5):644-647. doi: https://doi.org/10.3760/cma.j.issn.1003-9406.2018.05.005</mixed-citation></citation-alternatives></ref><ref id="cit39"><label>39</label><citation-alternatives><mixed-citation xml:lang="ru">Avitan-Hersh E, Tatur S, Indelman M, et al. Postzygotic HRAS mutation causing both keratinocytic epidermal nevus and thymoma and associated with bone dysplasia and hypophosphatemia due to elevated FGF23. J Clin Endocrinol Metab. 2014;99(1):E132-136. doi: https://doi.org/10.1210/jc.2013-2813</mixed-citation><mixed-citation xml:lang="en">Avitan-Hersh E, Tatur S, Indelman M, et al. Postzygotic HRAS mutation causing both keratinocytic epidermal nevus and thymoma and associated with bone dysplasia and hypophosphatemia due to elevated FGF23. J Clin Endocrinol Metab. 2014;99(1):E132-136. doi: https://doi.org/10.1210/jc.2013-2813</mixed-citation></citation-alternatives></ref><ref id="cit40"><label>40</label><citation-alternatives><mixed-citation xml:lang="ru">Imel EA, Econs MJ. Fibrous dysplasia, phosphate wasting and fibroblast growth factor 23. Pediatr Endocrinol Rev. 2007;4 Suppl 4:434-439.</mixed-citation><mixed-citation xml:lang="en">Imel EA, Econs MJ. Fibrous dysplasia, phosphate wasting and fibroblast growth factor 23. Pediatr Endocrinol Rev. 2007;4 Suppl 4:434-439.</mixed-citation></citation-alternatives></ref><ref id="cit41"><label>41</label><citation-alternatives><mixed-citation xml:lang="ru">Hasani-Ranjbar S, Ejtahed HS, Amoli MM, et al. SLC34A3 Intronic Deletion in an Iranian Kindred with Hereditary Hypophosphatemic Rickets with Hypercalciuria. J Clin Res Pediatr Endocrinol. 2018;10(4):343-349. doi: https://doi.org/10.4274/jcrpe.0057</mixed-citation><mixed-citation xml:lang="en">Hasani-Ranjbar S, Ejtahed HS, Amoli MM, et al. SLC34A3 Intronic Deletion in an Iranian Kindred with Hereditary Hypophosphatemic Rickets with Hypercalciuria. J Clin Res Pediatr Endocrinol. 2018;10(4):343-349. doi: https://doi.org/10.4274/jcrpe.0057</mixed-citation></citation-alternatives></ref><ref id="cit42"><label>42</label><citation-alternatives><mixed-citation xml:lang="ru">Berman E, Nicolaides M, Maki RG, et al. Altered bone and mineral metabolism in patients receiving imatinib mesylate. N Engl J Med. 2006;354(19):2006-2013. doi: https://doi.org/10.1056/NEJMoa051140</mixed-citation><mixed-citation xml:lang="en">Berman E, Nicolaides M, Maki RG, et al. Altered bone and mineral metabolism in patients receiving imatinib mesylate. N Engl J Med. 2006;354(19):2006-2013. doi: https://doi.org/10.1056/NEJMoa051140</mixed-citation></citation-alternatives></ref><ref id="cit43"><label>43</label><citation-alternatives><mixed-citation xml:lang="ru">Vandyke K, Fitter S, Dewar AL, et al. Dysregulation of bone remodeling by imatinib mesylate. Blood. 2010;115(4):766-774. doi: https://doi.org/10.1182/blood-2009-08-237404</mixed-citation><mixed-citation xml:lang="en">Vandyke K, Fitter S, Dewar AL, et al. Dysregulation of bone remodeling by imatinib mesylate. Blood. 2010;115(4):766-774. doi: https://doi.org/10.1182/blood-2009-08-237404</mixed-citation></citation-alternatives></ref><ref id="cit44"><label>44</label><citation-alternatives><mixed-citation xml:lang="ru">O’Sullivan S, Lin JM, Watson M, et al. The skeletal effects of the tyrosine kinase inhibitor nilotinib. Bone. 2011;49(2):281-289. doi: https://doi.org/10.1016/j.bone.2011.04.014</mixed-citation><mixed-citation xml:lang="en">O’Sullivan S, Lin JM, Watson M, et al. The skeletal effects of the tyrosine kinase inhibitor nilotinib. Bone. 2011;49(2):281-289. doi: https://doi.org/10.1016/j.bone.2011.04.014</mixed-citation></citation-alternatives></ref><ref id="cit45"><label>45</label><citation-alternatives><mixed-citation xml:lang="ru">Addison WN, Azari F, Sorensen ES, et al. Pyrophosphate inhibits mineralization of osteoblast cultures by binding to mineral, up-regulating osteopontin, and inhibiting alkaline phosphatase activity. J Biol Chem. 2007;282(21):15872-15883. doi: https://doi.org/10.1074/jbc.M701116200</mixed-citation><mixed-citation xml:lang="en">Addison WN, Azari F, Sorensen ES, et al. Pyrophosphate inhibits mineralization of osteoblast cultures by binding to mineral, up-regulating osteopontin, and inhibiting alkaline phosphatase activity. J Biol Chem. 2007;282(21):15872-15883. doi: https://doi.org/10.1074/jbc.M701116200</mixed-citation></citation-alternatives></ref><ref id="cit46"><label>46</label><citation-alternatives><mixed-citation xml:lang="ru">Родионова С.С., Захарова Е.Ю., Буклемишев Ю.В., и др. Гипофосфатазия у взрослых: клинические случаи и обзор литературы. // Остеопороз и остеопатии. — 2015. — T. 18. — №2. — С. 25-28. [Rodionova SS, Zakharova EY, Buklemishev YV, et al. Hypophosphatasia in adults: clinical cases and literature review. Osteoporosis and bone diseases. 2015;18(2):25-28. (In Russ.)] doi: https://doi.org/10.14341/osteo2015225-28.</mixed-citation><mixed-citation xml:lang="en">Родионова С.С., Захарова Е.Ю., Буклемишев Ю.В., и др. Гипофосфатазия у взрослых: клинические случаи и обзор литературы. // Остеопороз и остеопатии. — 2015. — T. 18. — №2. — С. 25-28. [Rodionova SS, Zakharova EY, Buklemishev YV, et al. Hypophosphatasia in adults: clinical cases and literature review. Osteoporosis and bone diseases. 2015;18(2):25-28. (In Russ.)] doi: https://doi.org/10.14341/osteo2015225-28.</mixed-citation></citation-alternatives></ref><ref id="cit47"><label>47</label><citation-alternatives><mixed-citation xml:lang="ru">Glorieux FH, Pettifor JM. Vitamin D/dietary calcium deficiency rickets and pseudo-vitamin D deficiency rickets. Bonekey Rep. 2014;3:524. doi: https://doi.org/10.1038/bonekey.2014.19</mixed-citation><mixed-citation xml:lang="en">Glorieux FH, Pettifor JM. Vitamin D/dietary calcium deficiency rickets and pseudo-vitamin D deficiency rickets. Bonekey Rep. 2014;3:524. doi: https://doi.org/10.1038/bonekey.2014.19</mixed-citation></citation-alternatives></ref><ref id="cit48"><label>48</label><citation-alternatives><mixed-citation xml:lang="ru">Supornsilchai V, Hiranras Y, Wacharasindhu S, et al. Two siblings with a novel nonsense mutation, p.R50X, in the vitamin D receptor gene. Endocrine. 2011;40(1):62-66. doi: https://doi.org/10.1007/s12020-011-9450-9</mixed-citation><mixed-citation xml:lang="en">Supornsilchai V, Hiranras Y, Wacharasindhu S, et al. Two siblings with a novel nonsense mutation, p.R50X, in the vitamin D receptor gene. Endocrine. 2011;40(1):62-66. doi: https://doi.org/10.1007/s12020-011-9450-9</mixed-citation></citation-alternatives></ref><ref id="cit49"><label>49</label><citation-alternatives><mixed-citation xml:lang="ru">Malloy PJ, Tasic V, Taha D, et al. Vitamin D receptor mutations in patients with hereditary 1,25-dihydroxyvitamin D-resistant rickets. Mol Genet Metab. 2014;111(1):33-40. doi: https://doi.org/10.1016/j.ymgme.2013.10.014</mixed-citation><mixed-citation xml:lang="en">Malloy PJ, Tasic V, Taha D, et al. Vitamin D receptor mutations in patients with hereditary 1,25-dihydroxyvitamin D-resistant rickets. Mol Genet Metab. 2014;111(1):33-40. doi: https://doi.org/10.1016/j.ymgme.2013.10.014</mixed-citation></citation-alternatives></ref><ref id="cit50"><label>50</label><citation-alternatives><mixed-citation xml:lang="ru">Pang Q, Qi X, Jiang Y, et al. Clinical and genetic findings in a Chinese family with VDR-associated hereditary vitamin D-resistant rickets. Bone Res. 2016;4(1). doi: https://doi.org/10.1038/boneres.2016.18</mixed-citation><mixed-citation xml:lang="en">Pang Q, Qi X, Jiang Y, et al. Clinical and genetic findings in a Chinese family with VDR-associated hereditary vitamin D-resistant rickets. Bone Res. 2016;4(1). doi: https://doi.org/10.1038/boneres.2016.18</mixed-citation></citation-alternatives></ref><ref id="cit51"><label>51</label><citation-alternatives><mixed-citation xml:lang="ru">Koren R. Vitamin D receptor defects: the story of hereditary resistance to vitamin D. Pediatr Endocrinol Rev. 2006;3 Suppl 3:470-475.</mixed-citation><mixed-citation xml:lang="en">Koren R. Vitamin D receptor defects: the story of hereditary resistance to vitamin D. Pediatr Endocrinol Rev. 2006;3 Suppl 3:470-475.</mixed-citation></citation-alternatives></ref><ref id="cit52"><label>52</label><citation-alternatives><mixed-citation xml:lang="ru">Nakabayashi M, Tsukahara Y, Iwasaki-Miyamoto Y, et al. Crystal Structures of Hereditary Vitamin D-Resistant Rickets-Associated Vitamin D Receptor Mutants R270L and W282R Bound to 1,25-Dihydroxyvitamin D3and Synthetic Ligands. J Med Chem. 2013;56(17):6745-6760. doi: https://doi.org/10.1021/jm400537h</mixed-citation><mixed-citation xml:lang="en">Nakabayashi M, Tsukahara Y, Iwasaki-Miyamoto Y, et al. Crystal Structures of Hereditary Vitamin D-Resistant Rickets-Associated Vitamin D Receptor Mutants R270L and W282R Bound to 1,25-Dihydroxyvitamin D3and Synthetic Ligands. J Med Chem. 2013;56(17):6745-6760. doi: https://doi.org/10.1021/jm400537h</mixed-citation></citation-alternatives></ref><ref id="cit53"><label>53</label><citation-alternatives><mixed-citation xml:lang="ru">Malloy PJ, Feldman D. Genetic Disorders and Defects in Vitamin D Action. Endocrinol Metab Clin North Am. 2010;39(2):333-346. doi: https://doi.org/10.1016/j.ecl.2010.02.004</mixed-citation><mixed-citation xml:lang="en">Malloy PJ, Feldman D. Genetic Disorders and Defects in Vitamin D Action. Endocrinol Metab Clin North Am. 2010;39(2):333-346. doi: https://doi.org/10.1016/j.ecl.2010.02.004</mixed-citation></citation-alternatives></ref><ref id="cit54"><label>54</label><citation-alternatives><mixed-citation xml:lang="ru">Li YC, Amling M, Pirro AE, et al. Normalization of Mineral Ion Homeostasis by Dietary Means Prevents Hyperparathyroidism, Rickets, and Osteomalacia, But Not Alopecia in Vitamin D Receptor-Ablated Mice1. Endocrinology. 1998;139(10):4391-4396. doi: https://doi.org/10.1210/endo.139.10.6262</mixed-citation><mixed-citation xml:lang="en">Li YC, Amling M, Pirro AE, et al. Normalization of Mineral Ion Homeostasis by Dietary Means Prevents Hyperparathyroidism, Rickets, and Osteomalacia, But Not Alopecia in Vitamin D Receptor-Ablated Mice1. Endocrinology. 1998;139(10):4391-4396. doi: https://doi.org/10.1210/endo.139.10.6262</mixed-citation></citation-alternatives></ref><ref id="cit55"><label>55</label><citation-alternatives><mixed-citation xml:lang="ru">Izuora K, Twombly JG, Whitford GM, et al. Skeletal Fluorosis from Brewed Tea. J Clin Endocrinol Metab. 2011;96(8):2318-2324. doi: https://doi.org/10.1210/jc.2010-2891</mixed-citation><mixed-citation xml:lang="en">Izuora K, Twombly JG, Whitford GM, et al. Skeletal Fluorosis from Brewed Tea. J Clin Endocrinol Metab. 2011;96(8):2318-2324. doi: https://doi.org/10.1210/jc.2010-2891</mixed-citation></citation-alternatives></ref><ref id="cit56"><label>56</label><citation-alternatives><mixed-citation xml:lang="ru">Whyte MP, Totty WG, Lim VT, Whitford GM. Skeletal Fluorosis From Instant Tea. J Bone Miner Res. 2008;23(5):759-769. doi: https://doi.org/10.1359/jbmr.080101</mixed-citation><mixed-citation xml:lang="en">Whyte MP, Totty WG, Lim VT, Whitford GM. Skeletal Fluorosis From Instant Tea. J Bone Miner Res. 2008;23(5):759-769. doi: https://doi.org/10.1359/jbmr.080101</mixed-citation></citation-alternatives></ref><ref id="cit57"><label>57</label><citation-alternatives><mixed-citation xml:lang="ru">Kurland ES, Schulman RC, Zerwekh JE, et al. Recovery From Skeletal Fluorosis (an Enigmatic, American Case). J Bone Miner Res. 2006;22(1):163-170. doi: https://doi.org/10.1359/jbmr.060912</mixed-citation><mixed-citation xml:lang="en">Kurland ES, Schulman RC, Zerwekh JE, et al. Recovery From Skeletal Fluorosis (an Enigmatic, American Case). J Bone Miner Res. 2006;22(1):163-170. doi: https://doi.org/10.1359/jbmr.060912</mixed-citation></citation-alternatives></ref><ref id="cit58"><label>58</label><citation-alternatives><mixed-citation xml:lang="ru">Adams JE. Radiology of Rickets and Osteomalacia. In: Vitamin D. Volume 1: Biochemistry, Physiology and Diagnostics. 4th ed. Academic Press; 2018. p. 975-1006. doi: https://doi.org/10.1016/b978-0-12-809965-0.00054-9</mixed-citation><mixed-citation xml:lang="en">Adams JE. Radiology of Rickets and Osteomalacia. In: Vitamin D. Volume 1: Biochemistry, Physiology and Diagnostics. 4th ed. Academic Press; 2018. p. 975-1006. doi: https://doi.org/10.1016/b978-0-12-809965-0.00054-9</mixed-citation></citation-alternatives></ref><ref id="cit59"><label>59</label><citation-alternatives><mixed-citation xml:lang="ru">Bhan A, Qiu S, Rao SD. Bone histomorphometry in the evaluation of osteomalacia. Bone Rep. 2018;8:125-134. doi: https://doi.org/10.1016/j.bonr.2018.03.005</mixed-citation><mixed-citation xml:lang="en">Bhan A, Qiu S, Rao SD. Bone histomorphometry in the evaluation of osteomalacia. Bone Rep. 2018;8:125-134. doi: https://doi.org/10.1016/j.bonr.2018.03.005</mixed-citation></citation-alternatives></ref><ref id="cit60"><label>60</label><citation-alternatives><mixed-citation xml:lang="ru">Murshed M. Mechanism of Bone Mineralization. Cold Spring Harb Perspect Med. 2018;8(12):a031229. doi: https://doi.org/10.1101/cshperspect.a031229</mixed-citation><mixed-citation xml:lang="en">Murshed M. Mechanism of Bone Mineralization. Cold Spring Harb Perspect Med. 2018;8(12):a031229. doi: https://doi.org/10.1101/cshperspect.a031229</mixed-citation></citation-alternatives></ref><ref id="cit61"><label>61</label><citation-alternatives><mixed-citation xml:lang="ru">Cazalbou S, Bertrand G, Drouet C. Tetracycline-Loaded Biomimetic Apatite: An Adsorption Study. J Phys Chem B. 2015;119(7):3014-3024. doi: https://doi.org/10.1021/jp5116756</mixed-citation><mixed-citation xml:lang="en">Cazalbou S, Bertrand G, Drouet C. Tetracycline-Loaded Biomimetic Apatite: An Adsorption Study. J Phys Chem B. 2015;119(7):3014-3024. doi: https://doi.org/10.1021/jp5116756</mixed-citation></citation-alternatives></ref><ref id="cit62"><label>62</label><citation-alternatives><mixed-citation xml:lang="ru">Bitzan M, Goodyer PR. Hypophosphatemic Rickets. Pediatr Clin North Am. 2019;66(1):179-207. doi: https://doi.org/10.1016/j.pcl.2018.09.004</mixed-citation><mixed-citation xml:lang="en">Bitzan M, Goodyer PR. Hypophosphatemic Rickets. Pediatr Clin North Am. 2019;66(1):179-207. doi: https://doi.org/10.1016/j.pcl.2018.09.004</mixed-citation></citation-alternatives></ref><ref id="cit63"><label>63</label><citation-alternatives><mixed-citation xml:lang="ru">Fukumoto S, Ozono K, Michigami T, et al. Pathogenesis and diagnostic criteria for rickets and osteomalacia—proposal by an expert panel supported by the Ministry of Health, Labour and Welfare, Japan, the Japanese Society for Bone and Mineral Research, and the Japan Endocrine Society. J Bone Miner Metab. 2015;33(5):467-473. doi: https://doi.org/10.1007/s00774-015-0698-7</mixed-citation><mixed-citation xml:lang="en">Fukumoto S, Ozono K, Michigami T, et al. Pathogenesis and diagnostic criteria for rickets and osteomalacia—proposal by an expert panel supported by the Ministry of Health, Labour and Welfare, Japan, the Japanese Society for Bone and Mineral Research, and the Japan Endocrine Society. J Bone Miner Metab. 2015;33(5):467-473. doi: https://doi.org/10.1007/s00774-015-0698-7</mixed-citation></citation-alternatives></ref><ref id="cit64"><label>64</label><citation-alternatives><mixed-citation xml:lang="ru">John TJ, van der Made T, Conradie M, Coetzee A. Osteomalacia and looser zones. QJM. 2019;112(6):455-455. doi: https://doi.org/10.1093/qjmed/hcy293</mixed-citation><mixed-citation xml:lang="en">John TJ, van der Made T, Conradie M, Coetzee A. Osteomalacia and looser zones. QJM. 2019;112(6):455-455. doi: https://doi.org/10.1093/qjmed/hcy293</mixed-citation></citation-alternatives></ref><ref id="cit65"><label>65</label><citation-alternatives><mixed-citation xml:lang="ru">Kim S, Park CH, Chung Y-S. Hypophosphatemic Osteomalacia Demonstrated by Tc-99m MDP Bone Scan. Clin Nucl Med. 2000;25(5):337-340. doi: https://doi.org/10.1097/00003072-200005000-00003</mixed-citation><mixed-citation xml:lang="en">Kim S, Park CH, Chung Y-S. Hypophosphatemic Osteomalacia Demonstrated by Tc-99m MDP Bone Scan. Clin Nucl Med. 2000;25(5):337-340. doi: https://doi.org/10.1097/00003072-200005000-00003</mixed-citation></citation-alternatives></ref><ref id="cit66"><label>66</label><citation-alternatives><mixed-citation xml:lang="ru">Мельниченко Г.А., Белая Ж.Е., Рожинская Л.Я., и др. Федеральные клинические рекомендации по диагностике, лечению и профилактике остеопороза. // Проблемы эндокринологии. — 2017. — T. 63. — №6. — С. 392-426. [Melnichenko GA, Belaya ZE, Rozhinskaya LY, et al. Russian federal clinical guidelines on the diagnostics, treatment, and prevention of osteoporosis. Problems of endocrinology. 2018;63(6):392-426. (In Russ.)] doi: https://doi.org/10.14341/probl2017636392-426</mixed-citation><mixed-citation xml:lang="en">Мельниченко Г.А., Белая Ж.Е., Рожинская Л.Я., и др. Федеральные клинические рекомендации по диагностике, лечению и профилактике остеопороза. // Проблемы эндокринологии. — 2017. — T. 63. — №6. — С. 392-426. [Melnichenko GA, Belaya ZE, Rozhinskaya LY, et al. Russian federal clinical guidelines on the diagnostics, treatment, and prevention of osteoporosis. Problems of endocrinology. 2018;63(6):392-426. (In Russ.)] doi: https://doi.org/10.14341/probl2017636392-426</mixed-citation></citation-alternatives></ref><ref id="cit67"><label>67</label><citation-alternatives><mixed-citation xml:lang="ru">Пигарова Е.А., Рожинская Л.Я., Белая Ж.Е., и др. Клинические рекомендации Российской ассоциации эндокринологов по диагностике, лечению и профилактике дефицита витамина D у взрослых. // Проблемы эндокринологии. — 2016. — Т. 62. — №4. — С. 60-84. [Pigarova EA, Rozhinskaya LY, Belaya ZE, et al. Russian Association of Endocrinologists recommendations for diagnosis, treatment and prevention of vitamin D deficiency in adults. Problems of endocrinology. 2016;62(4):60-84. (In Russ.)] doi: https://doi.org/10.14341/probl201662460-84</mixed-citation><mixed-citation xml:lang="en">Пигарова Е.А., Рожинская Л.Я., Белая Ж.Е., и др. Клинические рекомендации Российской ассоциации эндокринологов по диагностике, лечению и профилактике дефицита витамина D у взрослых. // Проблемы эндокринологии. — 2016. — Т. 62. — №4. — С. 60-84. [Pigarova EA, Rozhinskaya LY, Belaya ZE, et al. Russian Association of Endocrinologists recommendations for diagnosis, treatment and prevention of vitamin D deficiency in adults. Problems of endocrinology. 2016;62(4):60-84. (In Russ.)] doi: https://doi.org/10.14341/probl201662460-84</mixed-citation></citation-alternatives></ref><ref id="cit68"><label>68</label><citation-alternatives><mixed-citation xml:lang="ru">Дедов И.И., Мельниченко Г.А. Эндокринология. Национальное Руководство. 2-е изд. — М.: ГЭОТАР-Медиа; 2018. [Dedov II, Mel’nichenko GA. Endokrinologiya. National guidelines. 2nd ed. Moscow; 2018. (In Russ.)]</mixed-citation><mixed-citation xml:lang="en">Дедов И.И., Мельниченко Г.А. Эндокринология. Национальное Руководство. 2-е изд. — М.: ГЭОТАР-Медиа; 2018. [Dedov II, Mel’nichenko GA. Endokrinologiya. National guidelines. 2nd ed. Moscow; 2018. (In Russ.)]</mixed-citation></citation-alternatives></ref><ref id="cit69"><label>69</label><citation-alternatives><mixed-citation xml:lang="ru">Basha B, Rao DS, Han Z-H, Parfitt AM. Osteomalacia due to vitamin D depletion: a neglected consequence of intestinal malabsorption. Am J Med. 2000;108(4):296-300. doi: https://doi.org/10.1016/s0002-9343(99)00460-x</mixed-citation><mixed-citation xml:lang="en">Basha B, Rao DS, Han Z-H, Parfitt AM. Osteomalacia due to vitamin D depletion: a neglected consequence of intestinal malabsorption. Am J Med. 2000;108(4):296-300. doi: https://doi.org/10.1016/s0002-9343(99)00460-x</mixed-citation></citation-alternatives></ref><ref id="cit70"><label>70</label><citation-alternatives><mixed-citation xml:lang="ru">Bhambri R, Naik V, Malhotra N, et al. Changes in bone mineral density following treatment of osteomalacia. J Clin Densitom. 2006;9(1):120-127. doi: https://doi.org/10.1016/j.jocd.2005.11.001</mixed-citation><mixed-citation xml:lang="en">Bhambri R, Naik V, Malhotra N, et al. Changes in bone mineral density following treatment of osteomalacia. J Clin Densitom. 2006;9(1):120-127. doi: https://doi.org/10.1016/j.jocd.2005.11.001</mixed-citation></citation-alternatives></ref></ref-list><fn-group><fn fn-type="conflict"><p>The authors declare that there are no conflicts of interest present.</p></fn></fn-group></back></article>
