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Current Osteoporosis Reports

Erschienen in:

29.08.2019 | Therapeutics and Medical Management (S Jan de Beur and B Clarke, Section Editors)

When Low Bone Mineral Density and Fractures Is Not Osteoporosis

verfasst von: Smita Jha, Marquis Chapman, Kelly Roszko

Erschienen in: Current Osteoporosis Reports | Ausgabe 5/2019

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Abstract

Purpose of Review

To review the differential diagnosis of low bone mineral density (BMD).

Recent Findings

Osteoporosis is the most common cause of low BMD in adults; however, non-osteoporotic causes of low BMD should be considered in the differential diagnosis of patients with low BMD. Mild osteogenesis imperfecta, osteomalacia, and mineral and bone disorder of chronic kidney disease as well as several other rare diseases can be characterized by low BMD.

Summary

This review summarizes the differential diagnosis of low BMD. It is important to differentiate osteoporosis from other causes of low BMD since treatment regimens can vary tremendously between these different disease processes. In fact, some treatments for osteoporosis could worsen or exacerbate the mineral abnormalities in other causes of low BMD.

Kanis JA. Assessment of fracture risk and its application to screening for postmenopausal osteoporosis: synopsis of a WHO report. WHO Study Group Osteoporos Int. 1994;4(6):368–81.CrossRef

Kanis JA, McCloskey EV, Johansson H, Oden A, Melton LJ 3rd, Khaltaev N. A reference standard for the description of osteoporosis. Bone. 2008;42(3):467–75. https://doi.org/10.1016/j.bone.2007.11.001.CrossRefPubMed

2013 ISCD Official Position - Adults. Internation Society of Clinical Densitometry. 2013. http://www.iscd.org/official-positions/2013-iscd-official-positions-adult/. Accessed November 11th, 2018 2018.

Bhambri R, Naik V, Malhotra N, Taneja S, Rastogi S, Ravishanker U, et al. Changes in bone mineral density following treatment of osteomalacia. J Clin Densitom. 2006;9(1):120–7. https://doi.org/10.1016/j.jocd.2005.11.001.CrossRefPubMed

Saghafi M, Azarian A, Hashemzadeh K, Sahebari M, Rezaieyazdi Z. Bone densitometry in patients with osteomalacia: is it valuable? Clinical Cases in Mineral and Bone Metabolism : the official journal of the Italian Society of Osteoporosis, Mineral Metabolism, and Skeletal Diseases. 2013;10(3):180–2.

Elder CJ, Bishop NJ. Rickets. Lancet (London, England). 2014;383(9929):1665–76. https://doi.org/10.1016/s0140-6736(13)61650-5.CrossRef

Tiosano D, Hochberg Z. Hypophosphatemia: the common denominator of all rickets. J Bone Miner Metab. 2009;27(4):392–401. https://doi.org/10.1007/s00774-009-0079-1.CrossRefPubMed

Basha B, Rao DS, Han ZH, Parfitt AM. Osteomalacia due to vitamin D depletion: a neglected consequence of intestinal malabsorption. Am J Med. 2000;108(4):296–300.CrossRef

Colares Neto GP, Pereira RM, Alvarenga JC, Takayama L, Funari MF, Martin RM. Evaluation of bone mineral density and microarchitectural parameters by DXA and HR-pQCT in 37 children and adults with X-linked hypophosphatemic rickets. Osteoporos Int. 2017;28(5):1685–92. https://doi.org/10.1007/s00198-017-3949-8.CrossRefPubMed

10.

Rosenthall L. DEXA bone densitometry measurements in adults with X-linked hypophosphatemia. Clin Nucl Med. 1993;18(7):564–6.CrossRef

11.

Bhan A, Qiu S, Rao SD. Bone histomorphometry in the evaluation of osteomalacia. Bone Rep. 2018;8:125–34. https://doi.org/10.1016/j.bonr.2018.03.005.CrossRefPubMedPubMedCentral

12.

Carpenter TO, Imel EA, Holm IA, Jan de Beur SM, Insogna KL. A clinician’s guide to X-linked hypophosphatemia. J Bone Miner Res. 2011;26(7):1381–8. https://doi.org/10.1002/jbmr.340.CrossRefPubMedPubMedCentral

13.

Munns CF, Shaw N, Kiely M, Specker BL, Thacher TD, Ozono K, et al. Global consensus recommendations on prevention and management of nutritional rickets. J Clin Endocrinol Metab. 2016;101(2):394–415. https://doi.org/10.1210/jc.2015-2175.CrossRefPubMedPubMedCentral

14.

Christov M, Juppner H. Phosphate homeostasis disorders. Best Pract Res Clin Endocrinol Metab. 2018;32(5):685–706. https://doi.org/10.1016/j.beem.2018.06.004.CrossRefPubMed

15.

Riminucci M, Collins MT, Fedarko NS, Cherman N, Corsi A, White KE, et al. FGF-23 in fibrous dysplasia of bone and its relationship to renal phosphate wasting. J Clin Invest. 2003;112(5):683–92. https://doi.org/10.1172/jci18399.CrossRefPubMedPubMedCentral

16.

Toro L, Barrientos V, Leon P, Rojas M, Gonzalez M, Gonzalez-Ibanez A, et al. Erythropoietin induces bone marrow and plasma fibroblast growth factor 23 during acute kidney injury. Kidney Int. 2018;93(5):1131–41. https://doi.org/10.1016/j.kint.2017.11.018.CrossRefPubMed

17.

Florenzano P, Gafni RI, Collins MT. Tumor-induced osteomalacia. Bone Rep. 2017;7:90–7. https://doi.org/10.1016/j.bonr.2017.09.002.CrossRefPubMedPubMedCentral

18.

El-Maouche D, Sadowski SM, Papadakis GZ, Guthrie L, Cottle-Delisle C, Merkel R, et al. (68)Ga-DOTATATE for tumor localization in tumor-induced osteomalacia. J Clin Endocrinol Metab. 2016;101(10):3575–81. https://doi.org/10.1210/jc.2016-2052.CrossRefPubMedPubMedCentral

19.

Agrawal K, Bhadada S, Mittal BR, Shukla J, Sood A, Bhattacharya A, et al. Comparison of 18F-FDG and 68Ga DOTATATE PET/CT in localization of tumor causing oncogenic osteomalacia. Clin Nucl Med. 2015;40(1):e6–e10. https://doi.org/10.1097/rlu.0000000000000460.CrossRefPubMed

20.

Cagnoli M, Richter R, Bohm P, Knye K, Empting S, Mohnike K. Spontaneous growth and effect of early therapy with calcitriol and phosphate in X-linked hypophosphatemic rickets. Pediatr Endocrinol Rev. 2017;15(Suppl 1):119–22. https://doi.org/10.17458/per.vol15.2017.crb.spontaneousgrowtheffect.CrossRefPubMed

21.

A gene (PEX) with homologies to endopeptidases is mutated in patients with X-linked hypophosphatemic rickets. The HYP Consortium. Nat Genet. 1995;11(2):130–6. https://doi.org/10.1038/ng1095-130.CrossRef

22.

Autosomal dominant hypophosphataemic rickets is associated with mutations in FGF23. Nat Genet. 2000;26(3):345–8. doi:https://doi.org/10.1038/81664.CrossRef

23.

Imel EA, Peacock M, Gray AK, Padgett LR, Hui SL, Econs MJ. Iron modifies plasma FGF23 differently in autosomal dominant hypophosphatemic rickets and healthy humans. J Clin Endocrinol Metab. 2011;96(11):3541–9. https://doi.org/10.1210/jc.2011-1239.CrossRefPubMedPubMedCentral

24.

Clinkenbeard EL, Hanudel MR, Stayrook KR, Appaiah HN, Farrow EG, Cass TA, et al. Erythropoietin stimulates murine and human fibroblast growth factor-23, revealing novel roles for bone and bone marrow. Haematologica. 2017;102(11):e427–e30. https://doi.org/10.3324/haematol.2017.167882.CrossRefPubMedPubMedCentral

25.

Levy-Litan V, Hershkovitz E, Avizov L, Leventhal N, Bercovich D, Chalifa-Caspi V, et al. Autosomal-recessive hypophosphatemic rickets is associated with an inactivation mutation in the ENPP1 gene. Am J Hum Genet. 2010;86(2):273–8. https://doi.org/10.1016/j.ajhg.2010.01.010.CrossRefPubMedPubMedCentral

26.

Marcucci G, Masi L, Ferrari S, Haffner D, Javaid MK, Kamenicky P, et al. Phosphate wasting disorders in adults. Osteoporos Int. 2018;29(11):2369–87. https://doi.org/10.1007/s00198-018-4618-2.CrossRefPubMed

27.

Lorenz-Depiereux B, Schnabel D, Tiosano D, Hausler G, Strom TM. Loss-of-function ENPP1 mutations cause both generalized arterial calcification of infancy and autosomal-recessive hypophosphatemic rickets. Am J Hum Genet. 2010;86(2):267–72. https://doi.org/10.1016/j.ajhg.2010.01.006.CrossRefPubMedPubMedCentral

28.

Carpenter TO. The expanding family of hypophosphatemic syndromes. J Bone Miner Metab. 2012;30(1):1–9. https://doi.org/10.1007/s00774-011-0340-2.CrossRefPubMed

29.

Collins MT, Chebli C, Jones J, Kushner H, Consugar M, Rinaldo P, et al. Renal phosphate wasting in fibrous dysplasia of bone is part of a generalized renal tubular dysfunction similar to that seen in tumor-induced osteomalacia. J Bone Miner Res. 2001;16(5):806–13. https://doi.org/10.1359/jbmr.2001.16.5.806.CrossRefPubMed

30.

Bhattacharyya N, Wiench M, Dumitrescu C, Connolly BM, Bugge TH, Patel HV, et al. Mechanism of FGF23 processing in fibrous dysplasia. J Bone Miner Res. 2012;27(5):1132–41. https://doi.org/10.1002/jbmr.1546.CrossRefPubMed

31.

Boyce AM, Bhattacharyya N, Collins MT. Fibrous dysplasia and fibroblast growth factor-23 regulation. Curr Osteoporos Rep. 2013;11(2):65–71. https://doi.org/10.1007/s11914-013-0144-5.CrossRefPubMedPubMedCentral

32.

Lim YH, Ovejero D, Sugarman JS, Deklotz CM, Maruri A, Eichenfield LF, et al. Multilineage somatic activating mutations in HRAS and NRAS cause mosaic cutaneous and skeletal lesions, elevated FGF23 and hypophosphatemia. Hum Mol Genet. 2014;23(2):397–407. https://doi.org/10.1093/hmg/ddt429.CrossRefPubMed

33.

Lim YH, Ovejero D, Derrick KM, Collins MT, Choate KA. Cutaneous skeletal hypophosphatemia syndrome (CSHS) is a multilineage somatic mosaic RASopathy. J Am Acad Dermatol. 2016;75(2):420–7. https://doi.org/10.1016/j.jaad.2015.11.012.CrossRefPubMedPubMedCentral

34.

Ovejero D, Lim YH, Boyce AM, Gafni RI, McCarthy E, Nguyen TA, et al. Cutaneous skeletal hypophosphatemia syndrome: clinical spectrum, natural history, and treatment. Osteoporos Int. 2016;27(12):3615–26. https://doi.org/10.1007/s00198-016-3702-8.CrossRefPubMed

35.

White KE, Cabral JM, Davis SI, Fishburn T, Evans WE, Ichikawa S, et al. Mutations that cause osteoglophonic dysplasia define novel roles for FGFR1 in bone elongation. Am J Hum Genet. 2005;76(2):361–7. https://doi.org/10.1086/427956.CrossRefPubMed

36.

Brownstein CA, Adler F, Nelson-Williams C, Iijima J, Li P, Imura A, et al. A translocation causing increased alpha-klotho level results in hypophosphatemic rickets and hyperparathyroidism. Proc Natl Acad Sci U S A. 2008;105(9):3455–60. https://doi.org/10.1073/pnas.0712361105.CrossRefPubMedPubMedCentral

37.

Schouten BJ, Hunt PJ, Livesey JH, Frampton CM, Soule SG. FGF23 elevation and hypophosphatemia after intravenous iron polymaltose: a prospective study. J Clin Endocrinol Metab. 2009;94(7):2332–7. https://doi.org/10.1210/jc.2008-2396.CrossRefPubMed

38.

Lorenz-Depiereux B, Benet-Pages A, Eckstein G, Tenenbaum-Rakover Y, Wagenstaller J, Tiosano D, et al. Hereditary hypophosphatemic rickets with hypercalciuria is caused by mutations in the sodium-phosphate cotransporter gene SLC34A3. Am J Hum Genet. 2006;78(2):193–201. https://doi.org/10.1086/499410.CrossRefPubMed

39.

Bergwitz C, Roslin NM, Tieder M, Loredo-Osti JC, Bastepe M, Abu-Zahra H, et al. SLC34A3 mutations in patients with hereditary hypophosphatemic rickets with hypercalciuria predict a key role for the sodium-phosphate cotransporter NaPi-IIc in maintaining phosphate homeostasis. Am J Hum Genet. 2006;78(2):179–92. https://doi.org/10.1086/499409.CrossRefPubMed

40.

Foreman JW. Fanconi syndrome. Pediatr Clin N Am. 2019;66(1):159–67. https://doi.org/10.1016/j.pcl.2018.09.002.CrossRef

41.

Clarke BL, Wynne AG, Wilson DM, Fitzpatrick LA. Osteomalacia associated with adult Fanconi's syndrome: clinical and diagnostic features. Clin Endocrinol. 1995;43(4):479–90.CrossRef

42.

Forlino A, Marini JC. Osteogenesis imperfecta. Lancet (London, England). 2016;387(10028):1657–71. https://doi.org/10.1016/s0140-6736(15)00728-x.CrossRef

43.

Marini JC, Forlino A, Bachinger HP, Bishop NJ, Byers PH, Paepe A, et al. Osteogenesis imperfecta. Nat Rev Dis Primers. 2017;3:17052. https://doi.org/10.1038/nrdp.2017.52.CrossRefPubMed

44.

Arundel P. Osteogenesis imperfecta. Paediatr Child Health (United Kingdom). 2015;25(12):574–9. https://doi.org/10.1016/j.paed.2015.07.007.CrossRef

45.

Bishop NJ, Walsh JS. Osteogenesis imperfecta in adults. J Clin Invest. 2014;124(2):476–7. https://doi.org/10.1172/JCI74230.CrossRefPubMedPubMedCentral

46.

Davie MW, Haddaway MJ. Bone mineral content and density in healthy subjects and in osteogenesis imperfecta. Arch Dis Child. 1994;70(4):331–4. https://doi.org/adc.70.4.331%J/adc.70.4.331%J.

47.

Eller-Vainicher C, Bassotti A, Imeraj A, Cairoli E, Ulivieri FM, Cortini F, et al. Bone involvement in adult patients affected with Ehlers-Danlos syndrome. Osteoporos Int. 2016;27(8):2525–31. https://doi.org/10.1007/s00198-016-3562-2.CrossRefPubMed

48.

Pepin M, Schwarze U, Superti-Furga A, Byers PH. Clinical and genetic features of Ehlers-Danlos syndrome type IV, the vascular type. N Engl J Med. 2000;342(10):673–80. https://doi.org/10.1056/NEJM200003093421001.CrossRefPubMed

49.

Moura B, Tubach F, Sulpice M, Boileau C, Jondeau G, Muti C, et al. Bone mineral density in Marfan syndrome. A large case-control study. Joint Bone Spine. 2006;73(6):733–5. https://doi.org/10.1016/j.jbspin.2006.01.026.CrossRefPubMed

50.

Haine E, Salles JP, Khau Van Kien P, Conte-Auriol F, Gennero I, Plancke A, et al. Muscle and bone impairment in children with Marfan syndrome: correlation with age and FBN1 genotype. J Bone Miner Res. 2015;30(8):1369–76. https://doi.org/10.1002/jbmr.2471.CrossRefPubMed

51.

Moe S, Drueke T, Cunningham J, Goodman W, Martin K, Olgaard K, et al. Definition, evaluation, and classification of renal osteodystrophy: a position statement from kidney disease: improving global outcomes (KDIGO). Kidney Int. 2006;69(11):1945–53. https://doi.org/10.1038/sj.ki.5000414.CrossRef

52.

Coco M, Rush H. Increased incidence of hip fractures in dialysis patients with low serum parathyroid hormone. Am J Kidney Dis. 2000;36(6):1115–21. https://doi.org/10.1053/ajkd.2000.19812.CrossRefPubMed

53.

Kim SM, Long J, Montez-Rath M, Leonard M, Chertow GM. Hip fracture in patients with non-dialysis-requiring chronic kidney disease. J Bone Miner Res. 2016;31(10):1803–9. https://doi.org/10.1002/jbmr.2862.CrossRefPubMed

54.

Ketteler M, Block GA, Evenepoel P, Fukagawa M, Herzog CA, McCann L, et al. Executive summary of the 2017 KDIGO chronic kidney disease-mineral and bone disorder (CKD-MBD) guideline update: what’s changed and why it matters. Kidney Int. 2017;92(1):26–36. https://doi.org/10.1016/j.kint.2017.04.006.CrossRefPubMed

55.

Malluche HH, Mawad HW, Monier-Faugere MC. Renal osteodystrophy in the first decade of the new millennium: analysis of 630 bone biopsies in black and white patients. J Bone Miner Res. 2011;26(6):1368–76. https://doi.org/10.1002/jbmr.309.CrossRefPubMed

56.

Wilson LM, Rebholz CM, Jirru E, Liu MC, Zhang A, Gayleard J, et al. Benefits and harms of osteoporosis medications in patients with chronic kidney disease: a systematic review and meta-analysis. Ann Intern Med. 2017;166(9):649–58. https://doi.org/10.7326/M16-2752.CrossRefPubMed

57.

Lammert M, Kappler M, Mautner VF, Lammert K, Storkel S, Friedman JM, et al. Decreased bone mineral density in patients with neurofibromatosis 1. Osteoporos Int. 2005;16(9):1161–6. https://doi.org/10.1007/s00198-005-1940-2.CrossRefPubMed

58.

Friedman JM. Neurofibromatosis 1: clinical manifestations and diagnostic criteria. J Child Neurol. 2002;17(8):548–54; discussion 71–2, 646–51. https://doi.org/10.1177/088307380201700802.CrossRefPubMed

59.

Stevenson DA, Moyer-Mileur LJ, Murray M, Slater H, Sheng X, Carey JC, et al. Bone mineral density in children and adolescents with neurofibromatosis type 1. J Pediatr. 2007;150(1):83–8. https://doi.org/10.1016/j.jpeds.2006.10.048.CrossRefPubMedPubMedCentral

60.

Tucker T, Schnabel C, Hartmann M, Friedrich RE, Frieling I, Kruse HP, et al. Bone health and fracture rate in individuals with neurofibromatosis 1 (NF1). J Med Genet. 2009;46(4):259–65. https://doi.org/10.1136/jmg.2008.061895.CrossRefPubMed

61.

Kamiya N, Yamaguchi R, Aruwajoye O, Kim AJ, Kuroyanagi G, Phipps M, et al. Targeted disruption of NF1 in osteocytes increases FGF23 and osteoid with osteomalacia-like bone phenotype. J Bone Miner Res. 2017;32(8):1716–26. https://doi.org/10.1002/jbmr.3155.CrossRefPubMed

62.

Choudhry KS, Grover M, Tran AA, O'Brian Smith E, Ellis KJ, Lee BH. Decreased bone mineralization in children with Noonan syndrome: another consequence of dysregulated RAS MAPKinase pathway? Mol Genet Metab. 2012;106(2):237–40. https://doi.org/10.1016/j.ymgme.2012.04.003.CrossRefPubMedPubMedCentral

63.

Leoni C, Stevenson DA, Martini L, De Sanctis R, Mascolo G, Pantaleoni F et al. Decreased bone mineral density in Costello syndrome. Mol Genet Metab 2014;111(1):41–45. doi:https://doi.org/10.1016/j.ymgme.2013.08.007.CrossRef

64.

Whyte MP. Hypophosphatasia: an overview for 2017. Bone. 2017;102:15–25. https://doi.org/10.1016/j.bone.2017.02.011.CrossRefPubMed

65.

Henthorn PS, Raducha M, Fedde KN, Lafferty MA, Whyte MP. Different missense mutations at the tissue-nonspecific alkaline phosphatase gene locus in autosomal recessively inherited forms of mild and severe hypophosphatasia. Proc Natl Acad Sci U S A. 1992;89(20):9924–8.CrossRef

66.

Whyte MP, Greenberg CR, Salman NJ, Bober MB, McAlister WH, Wenkert D, et al. Enzyme-replacement therapy in life-threatening hypophosphatasia. N Engl J Med. 2012;366(10):904–13. https://doi.org/10.1056/NEJMoa1106173.CrossRefPubMed

67.

Loeys BL, Dietz HC. Loeys-Dietz syndrome. In: Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJH, Stephens K et al., editors. GeneReviews((R)). Seattle (WA): University of Washington, Seattle University of Washington, Seattle. GeneReviews is a registered trademark of the University of Washington, Seattle. All rights reserved; 1993.

68.

Tan EW, Offoha RU, Oswald GL, Skolasky RL, Dewan AK, Zhen G, et al. Increased fracture risk and low bone mineral density in patients with loeys-dietz syndrome. Am J Med Genet A. 2013;161a(8):1910–4. https://doi.org/10.1002/ajmg.a.36029.CrossRefPubMed

69.

Ratjen F, Doring G. Cystic fibrosis. Lancet. 2003;361(9358):681–9. https://doi.org/10.1016/S0140-6736(03)12567-6.CrossRefPubMed

70.

Siwamogsatham O, Alvarez J, Tangpricha V. Diagnosis and treatment of endocrine co-morbidities in ptaients with cystic fibrosis. Current opinion in endocrinology, diabetes, and obesity. 2015. https://doi.org/10.1097/MED.

71.

Sheikh S, Gemma S, Patel A. Factors associated with low bone mineral density in patients with cystic fibrosis. J Bone Miner Metab. 2015;33(2):180–5. https://doi.org/10.1007/s00774-014-0572-z.CrossRefPubMed

72.

Paccou J, Zeboulon N, Combescure C, Gossec L, Cortet B. The prevalence of osteoporosis, osteopenia, and fractures among adults with cystic fibrosis: a systematic literature review with meta-analysis. Calcif Tissue Int. 2010;86(1):1–7. https://doi.org/10.1007/s00223-009-9316-9.CrossRefPubMed

73.

Siwamogsatham O, Stephens K, Tangpricha V. Evaluation of teriparatide for treatment of osteoporosis in four patients with cystic fibrosis: a case series. Case Rep Endocrinol. 2014;2014:893589–4. https://doi.org/10.1155/2014/893589.CrossRefPubMedPubMedCentral

74.

Almeida A, Roberts I. Bone involvement in sickle cell disease. Br J Haematol. 2005;129(4):482–90. https://doi.org/10.1111/j.1365-2141.2005.05476.x.CrossRefPubMed

75.

Meeuwes M, Souza de Carvalho TF, Cipolotti R, Gurgel RQ, Ferrao TO, Peters M, et al. Bone mineral density, growth, pubertal development and other parameters in Brazilian children and young adults with sickle cell anaemia. Tropical Med Int Health. 2013;18(12):1539–46. https://doi.org/10.1111/tmi.12211.CrossRef

76.

Sarrai M, Duroseau H, D'Augustine J, Moktan S, Bellevue R. Bone mass density in adults with sickle cell disease. Br J Haematol. 2007;136(4):666–72. https://doi.org/10.1111/j.1365-2141.2006.06487.x.CrossRefPubMed

77.

Garadah TS, Hassan AB, Jaradat AA, Diab DE, Kalafalla HO, Kalifa AK, et al. Predictors of abnormal bone mass density in adult patients with homozygous sickle-cell disease. Clin Med Insights Endocrinol Diabetes. 2015;8:35–40. https://doi.org/10.4137/CMED.S24501.CrossRefPubMedPubMedCentral

78.

Schundeln MM, Goretzki SC, Hauffa PK, Wieland R, Bauer J, Baeder L, et al. Impairment of bone health in pediatric patients with hemolytic anemia. PLoS One. 2014;9(10):e108400. https://doi.org/10.1371/journal.pone.0108400.CrossRefPubMedPubMedCentral

79.

Steer K, Stavnichuk M, Morris M, Komarova SV. Bone health in patients with hematopoietic disorders of bone marrow origin: systematic review and meta-analysis. J Bone Miner Res. 2017;32(4):731–42. https://doi.org/10.1002/jbmr.3026.CrossRefPubMed

80.

Scheuerman O, Hoffer V, Cohen AH, Woellner C, Grimbacher B, Garty BZ. Reduced bone density in patients with autosomal dominant hyper-IgE syndrome. J Clin Immunol. 2013;33(5):903–8. https://doi.org/10.1007/s10875-013-9895-0.CrossRefPubMed

81.

Sowerwine KJ, Shaw PA, Gu W, Ling JC, Collins MT, Darnell DN, et al. Bone density and fractures in autosomal dominant hyper IgE syndrome. J Clin Immunol. 2014;34(2):260–4. https://doi.org/10.1007/s10875-013-9982-2.CrossRefPubMedPubMedCentral

82.

Leung DY, Key L, Steinberg JJ, Young MC, Von Deck M, Wilkinson R, et al. Increased in vitro bone resorption by monocytes in the hyper-immunoglobulin E syndrome. J Immunol. 1988;140(1):84–8.PubMed

83.

Staines Boone AT, Alcantara-Montiel JC, Sanchez-Sanchez LM, Arce-Cano M, Garcia-Campos J, Lugo Reyes SO. Zoledronate as effective treatment for minimal trauma fractures in a child with STAT3 deficiency and osteonecrosis of the hip. Pediatr Blood Cancer. 2016;63(11):2054–7. https://doi.org/10.1002/pbc.26119.CrossRefPubMed

84.

Weber DR, Coughlin C, Brodsky JL, Lindstrom K, Ficicioglu C, Kaplan P, et al. Low bone mineral density is a common finding in patients with homocystinuria. Mol Genet Metab. 2016;117(3):351–4. https://doi.org/10.1016/j.ymgme.2015.12.003.CrossRefPubMed

85.

Lim JS, Lee DH. Changes in bone mineral density and body composition of children with well-controlled homocystinuria caused by CBS deficiency. Osteoporos Int. 2013;24(9):2535–8. https://doi.org/10.1007/s00198-013-2351-4.CrossRefPubMed

86.

Demirci U, Cizmecioglu A, Aydogdu I. Actual reason for bone fractures in the case of a patient followed-up with the osteogenesis imperfecta: Gaucher’s disease. Clin Cases Miner Bone Metab. 2017;14(3):336–9. https://doi.org/10.11138/ccmbm/2017.14.3.336.CrossRefPubMedPubMedCentral

Titel: When Low Bone Mineral Density and Fractures Is Not Osteoporosis
verfasst von: Smita Jha
Marquis Chapman
Kelly Roszko
Publikationsdatum: 29.08.2019
Verlag: Springer US
Erschienen in: Current Osteoporosis Reports / Ausgabe 5/2019
Print ISSN: 1544-1873
Elektronische ISSN: 1544-2241
DOI: https://doi.org/10.1007/s11914-019-00529-7

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