Osteomalacia: from clinical suspicion to treatment: topic review
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Keywords

osteomalacia
vitamin D deficiency
hypophosphatemia
hypocalcemia
physiologic calcification

How to Cite

Duque, V., Barrera, N., Gómez, J., Guerra, V., Ceballos, L., & Aristizábal, N. (2019). Osteomalacia: from clinical suspicion to treatment: topic review. Revista Colombiana De Endocrinología, Diabetes &Amp; Metabolismo, 6(4), 298–305. https://doi.org/10.53853/encr.6.4.548

Abstract

This review it´s proposed to explore updated bibliography taking in a count the epidemiology, physiopathology, clinical manifestations and treatment of Osteomalacia to achieve a better comprehension about the disease and a proper specific treatment to this condition. It’s known that for a correct mineralization it’s necessary an appropriate input of vitamin D and it´s metabolic processes must remain unscathed. Vitamin D role in the human body is to maintain the homeostatic balance of calcium and the bone health; vitamin D deficit can cause Rickets in childhood and Osteomalacia in adults; this way, the most frequent cause of Osteomalacia it´s the vitamin D deficiency and in Colombia it´s prevalence is around 55,3%. Vitamin D is provided to the organism through two ways: endogenously from the solar exposition of the skin or exogenously from the diet. Any condition that alterate one of the two ways and produce a significant deficit of vitamin D or a detriment of its physiological effects can manifestate as osteomalacia. The clinical manifestations of osteomalacia, considering the wide variety of signs and symptoms, can be referred to jointly as Osteomalacia Syndrome. On the grounds that a multiple causes can produce osteomalacia, it’s advisable to identify the etiology of the clinical manifestations to establish an effective therapeutic scheme.

https://doi.org/10.53853/encr.6.4.548
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References

1. Weinstein R. Osteomalacia y raquitismo. En: Elsevier, editor: Goldman L, Schafer AI. Goldman-Cecil: tratado de medicina interna. 2017. p. 1645- 1649.
2. Sud K, Parashar A, Chauhan V. Clinical Syndromes of Vitamin D and Phosphate Dysregulation. En: Williams R. Williams textbook of endocrinology. 13th edition. Melmed S, Polonsky KS, Larsen PR, Kronenberg H, editores. Philadelphia, PA: Elsevier; 2016. p. 373-388.
3. MeSH Browser [Internet]. [citado 7 de octubre de 2019]. Disponible en: https://meshb.nlm.nih.gov/search
4. Mazanec DJ, Khalaf T, Orr R. Metabolic bone disease. En: Benzel EC, Steinmetz MP. Benzel’s spine surgery: techniques, complication avoidance, and management. 2017. p. 893-903.
5. Sundaram M, Schils J. Hyperparathyroidism, renal osteodystrophy, osteomalacia and rickets. En: Pope TL, Bloem HL, Beltran J, Morrison WB, Wilson DJ. Musculoskeletal imaging [Internet]. 2015 [citado 7 de octubre de 2019]. Disponible en: https://www.clinicalkey.com/dura/browse/bookChapter/3-s2.0-C20100686676.p.889-889.
6. Moreno AQ, González MDS, Calleja CH, Morales CM, Pino-Montes J del. Osteomalacia. Med - Programa Form Médica Contin Acreditado. 2016;12(16):909-14.
7. Forrest KYZ, Stuhldreher WL. Prevalence and correlates of vitamin D deficiency in US adults. Nutr Res. 2011;31(1):48-54.
8. Marazuela M. Déficit de vitamina D en el adulto: clínica, diagnóstico y tratamiento. Endocrinol Nutr. 2005;52(5):215-23.
9. Bringhurst FR, Demay MB, Krane SM, Kronenberg HM. Bone and mineral metabolism in health and disease. En: Kasper D, Fauci A, Hauser S, Longo D, Jameson JL, Loscalzo J, editores. Harrison’s Principles of Internal Medicine [Internet]. 19.a ed. New York, NY: McGraw-Hill Education; 2015 [citado 5 de mayo de 2018]. Disponible en:
accessmedicine.mhmedical.com/content.aspx?aid=1120816741
10. Binkley N, Ramamurthy R, Krueger D. Low Vitamin D Status: Definition, Prevalence, Consequences, and Correction. Endocrinol Metab Clin North Am. 2010;39(2):287-301.
11. Christakos S, Ajibade DV, Dhawan P, Fechner AJ, Mady LJ. Vitamin D: Metabolism. Endocrinol Metab Clin North Am. 2010;39(2):243-53.
12. Rosen CJ. Vitamin D Insufficiency. N Engl J Med. 2011;364(3):248-54.
13. Espinosa NAZ, Velásquez JMA, González VB, Blanco KEJ, Maya GC. Vitamina D: nuevos paradigmas. Med Lab. 2011;17(05-06):211-46.
14. Goltzman D. Functions of vitamin D in bone. Histochem Cell Biol. abril de 2018;149(4):305-12.
15. Manzano G, Vega MEA de la, Calleja CH, Morales CM, Montes J del P. Protocolo diagnóstico y tratamiento de la osteomalacia. Med Programa Form Médica Contin Acreditado. 2018;12(60):3542-6.
16. Bhan A, Rao AD, Rao DS. Osteomalacia as a result of vitamin D deficiency. Endocrinol Metab Clin North Am. junio de 2010;39(2):321-31, table of contents.
17. Walker J. Pathogenesis, diagnosis and management of osteomalacia. Nurs Older People. 2014;26(6):32-7.
18. Chong WH, Molinolo AA, Chen CC, Collins MT. Tumor-induced osteomalacia. Endocr Relat Cancer. 2011;18(3):R53-77.
19. Rader CP, Corsten N, Rolf O. Osteomalacia and vitamin D deficiency. Orthopade. 2015;44(9):695-702.
20. Sahebari M, Sigari SY, Heidari H, Biglarian O. Osteomalacia can still be a point of attention to celiac disease. Clin Cases Miner Bone Metab. 2011;8(3):14-5.
21. Vaishya R. Bilateral protrusio acetabuli of the hip. BMJ Case Rep. 2014;2014. pii: bcr2013201784.
22. Riancho J. Osteomalacia y raquitismo. REEMO. 2004;13(4):77-9.
23. Potts JT, Jüppner H. Trastornos de las glándulas paratiroides y la homeostasis de calcio. En: Kasper DL, Hauser SL, Jameson LJ, Fauci AS, Longo DL, Loscalzo J, editores. Harrison Principio de Medicina Interna (19.ª edición). New York: Mc Graw Hill; 2015. p. 2466-88.
24. Bringhurst RF, Demay MB, Kronenberg HM. Hormonas y trastornos del metabolismo mineral. En: Elsevier, editor. Williams. Tratado de endocrinología (13.ª edición). Barcelona: Elsevier; 2017. p. 1254-322.
25. Imel EA, Zhang X, Ruppe MD, Weber TJ, Klausner MA, Ito T, et al. Prolonged Correction of Serum Phosphorus in Adults With X-Linked Hypophosphatemia Using Monthly Doses of KRN23. J Clin Endocrinol Metab. 2015;100(7):2565-73.
26. Insogna KL, Briot K, Imel EA, Kamenický P, Ruppe MD, Portale AA, et al. A Randomized, Double-Blind, Placebo-Controlled, Phase 3 Trial Evaluating the Efficacy of Burosumab, an Anti-FGF23 Antibody, in Adults With XLinked Hypophosphatemia: Week 24 Primary Analysis. J Bone Miner Res Off J Am Soc Bone Miner Res. 2018;33(8):1383-93.
27. Lamb YN. Burosumab: First Global Approval. Drugs. 2018;78(6):707-14.
28. Portale AA, Carpenter TO, Brandi ML, Briot K, Cheong HI, Cohen-Solal M, et al. Continued Beneficial Effects of Burosumab in Adults with X-Linked Hypophosphatemia: Results from a 24-Week Treatment Continuation Period After a 24-Week Double-Blind Placebo-Controlled Period. Calcif Tissue Int. 2019;105(3):271-84.
29. Cheong HI, Yoo H-W, Adachi M, Tanaka H, Fujiwara I, Hasegawa Y, et al. First-in-Asian Phase I Study of the Anti-Fibroblast Growth Factor 23 Monoclonal Antibody, Burosumab: Safety and Pharmacodynamics in Adults With X-linked Hypophosphatemia. JBMR Plus. 2019;3(2):e10074.
30. Lyseng-Williamson KA. Burosumab in X-linked hypophosphatemia: a profile of its use in the USA. Drugs Ther Perspect Ration Drug Sel Use. 2018;34(11):497-506.
31. Clinical manifestations, diagnosis, and treatment of osteomalacia [Internet]. Base de datos UptoDate: Peter J Snyder; 2017 [modificado en Abril 2018; citado Mayo 2018]. Disponible en: https://bit.ly/2roolXT.

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