Buscar en
Revista Colombiana de Reumatología
Toda la web
Inicio Revista Colombiana de Reumatología Enfermedades metabólicas óseas: análisis clínico y radiológico en cinco cas...
Información de la revista
Vol. 17. Núm. 2.
Páginas 123-131 (Junio 2010)
Compartir
Compartir
Descargar PDF
Más opciones de artículo
Vol. 17. Núm. 2.
Páginas 123-131 (Junio 2010)
Acceso a texto completo
Enfermedades metabólicas óseas: análisis clínico y radiológico en cinco casos
Metabolic bone diseases: clinical and radiologic analysis in five cases
Visitas
19640
Carlos Darío Ochoa1, Carlos E. Toro1, Fabián Ramírez1, Jaime Mercado2, Orlando Olivares3, José Félix Restrepo1, Federico Rondón1, Antonio Iglesias-Gamarra1
1 Unidad de Reumatología, Escuela de Medicina. Universidad Nacional de Colombia
2 Nefrólogo, Fresenius. Barranquilla
3 Nefrólogo, Fresenius. Bogotá
Este artículo ha recibido
Información del artículo
Resumen
Bibliografía
Descargar PDF
Estadísticas
Resumen

El estudio de la enfermedad metabólica ósea es amplio y complejo. La enfermedad ósea más reconocida por médicos de todas las especialidades es la osteoporosis, probablemente debido a su elevada frecuencia. No obstante, es importante reconocer que existen numerosas entidades que afectan el metabolismo óseo de diferentes formas, llevando a fragilidad ósea, aumento del riesgo de fractura, osteoporosis u osteocondensación, de acuerdo a cada caso particular. Tanto el diagnóstico clínico como el reconocimiento de la alteración metabólica subyacente son importantes porque la identificación de la anormalidad específica se constituye en la base para el tratamiento. Se presentan 5 casos diferentes en los que un trastorno metabólico conlleva a una patología ósea específica; se discute la patogenia de las calcificaciones arteriales y se presenta una entidad mixta que nosotros llamamos osteoporomalacia.

Palabras clave:
enfermedad metabólica ósea
osteomalacia
osteoporomalacia
hiperparatiroidismo
osteodistrofia renal
calcificaciones arteriales
Summary

The study of metabolic bone disease is broad and complex. The most widely recognized bone disease by physicians of all specialties is osteoporosis, probably due to its high frequency. However, it is important to recognize that there are numerous entities that affect bone metabolism in different ways, leading to brittle bones, increased risk of fracture, osteoporosis or osteocondensation, according to each particular case. Both the clinical diagnosis and recognition of the underlying metabolic abnormality are important because they identify the specific abnormality that will be the base for treatment. There were 5 different cases in which a metabolic disorder leads to specific bone pathology, we discuss the pathogenesis of arterial calcifications and presents a mixed entity we call osteoporomalacia.

Key words:
metabolic bone disease
osteomalacia
osteoporomalacia
hyperparathyroidism
renal osteodystrophy
arterial calcification
bone tumor
El Texto completo está disponible en PDF
Referencias
[1.]
G. Firestein, R. Budd, et al.
Metabolic Bone Disease.
Eighth, (2008), pp. 1579-1599
[2.]
M.F. Holick, M. Garabedian, D. Vitamin.
Photobiology, metabolism, mechanism of action, and clinical applications.
Primer on Metabolic Bone Diseases and Disorders of Mineral Metabolism, (2006),
[3.]
Fauci, Braunwald, Kasper, et al.
Disorders of the Kidney and Urinary Tract.
Harrison's principles of internal medicine, 17th, (2008), pp. 1797-1806
[4.]
National Osteoporosis, Foundation.
Osteoporos Int, 4 (1998), pp. S7-S80
[5.]
B.L. Riggs, L.J. Melton.
The prevention and treatment of osteoporosis.
N Engl J Med, 327 (1992), pp. 620-627
[6.]
S.C. Manolagas, R.L. Jilka.
Bone Marrow, cytokines, and bone remodeling.
N Engl J Med, 332 (1995), pp. 305-311
[7.]
K. Hruska, S. Teittelbaum.
Renal Osteodystrophy.
N Engl J Med, (1995), pp. 166-174
[8.]
E. Slatopolsky, J.A. Delmez.
Pathogenesis of secondary hyperparathyroidism.
Am J Kidney Dis, 23 (1994), pp. 229-236
[9.]
M.J. Borrego, A.J. Felsenfeld, A. Martin-Malo, Y. Almaden, M.T. Concepción, P. Aljama, et al.
Evidence for adaptation of the entire PTH-calcium curve to sustained changes in the serum calcium in haemodialysis patients.
Nephrol Dial Transplant, 12 (1997), pp. 505-513
[10.]
D.J. Sherrard, G. Hercz, Y. Pei, N.A. Maloney, C. Greenwood, A. Manuel, C. Saiphoo, et al.
The spectrum of bone disease in end-stage renal failure: An evolving disorder.
Kidney Int, 43 (1993), pp. 436-442
[11.]
K.J. Martin, K. Olgaard, J.W. Coburn, G.M. Coen, M. Fukagawa, C. Langman, et al.
Diagnosis, assessment, and treatment of bone turnover abnormalities in renal osteodystrophy.
Am J Kidney Dis, 43 (2004), pp. 558-565
[12.]
S. Moe, T. Drueke, J. Cunningham, et al.
Definition, evaluation, and classification of renal osteodystrophy: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO).
Kidney Int, 69 (2006), pp. 1945-1953
[13.]
S. Roe, M.J. Cassidy.
Diagnosis and monitoring of renal osteodystrophy.
Curr Opin Nephrol Hypertens, 9 (2000), pp. 675-681
[14.]
D. Resnick, G. Niwayama.
Parathyroid disorders and renal osteodystrophy.
Diagnosis of bone and joint disorders, pp. 2012-2075
[15.]
M. Sundaram.
Renal osteodystrophy.
Skeletal Radiology, (1989), pp. 415-426
[16.]
C.M. Shanahan.
Mechanisms of vascular calcification in renal disease.
Clin Nephrol, 63 (2005), pp. 146-157
[17.]
G.M. Chertow, S.K. Burke, P. Raggi.
Sevelamer attenuates the progression of coronary and aortic calcification in hemodialysis patients.
Kidney, 62 (2002), pp. 245-252
[18.]
W.G. Goodman, J. Goldin, B.D. Kuizon, C. Yoon, B. Gales, D. Sider, Y. Wang, et al.
Coronary-artery calcification in young adults with end-stage renal disease who are undergoing dialysis.
N Engl J Med, 342 (2000), pp. 1478-1483
[19.]
G.M. London, C. Marty, S.J. Marchais, A.P. Guerin, F. Metivier, M.C. de Vernejoul.
Arterial calcifications and bone histomorphometry in end-stage renal disease.
J Am Soc Nephrol, 15 (2004), pp. 1943-1951
[20.]
K.J. Martin, Z. Al-Aly, E.A. Gonzales.
pp. 359-366
[21.]
G. London.
Cardiovascular disease in end-stage renal failure: Role of calcium-phosphate disturbances and hyperparathyroidism.
J Nephrol, 15 (2000), pp. 209-210
[22.]
G.M. London, C. Marty, S.J. Marchais, A.P. Guerin, F. Metivier, M.C. de Vernejoul.
Arterial calcifications and bone histomorphometry in end-stage renal disease.
Jam Soc Nephrol, 15 (2004), pp. 1943-1951
[23.]
K.A. Lomashvili, S. Cobbs, R.A. Hennigar, K.I. Hardcastle, W.C. O’ Neil.
Phosphate-induced vascular calcification Role of phyrophosphate and ostepontin.
J Am Soc Nephron, 15 (2004), pp. 1392-1401
[24.]
M. Ketteler.
Fetuin-A and extraosseous calcification in uremia.
Curr Opin Nephrol Hypertens, 14 (2005), pp. 337-342
[25.]
A. Farzaneh-Far, C.M. Shanahan.
Biology of vascular calcification in renal disease.
Nephron Exp Nephrol, 101 (2005), pp. 134-138
[26.]
C.M. Giachelli, S. Jono, A. Shioi, Y. Nishizawa, K. Mori, H. Morii.
Vascular calcification and inorganic phosphate.
Am J Kidney Dis, 38 (2001), pp. S34-S37
[27.]
S. Jono, M.D. Mckee, C.E. Murry, A. Shioi, Y. Nishizawa, K. Mori, et al.
Phospate regulation of vascular smooth muscle cell calcification.
Circ Res, 87 (2000), pp. E10-E17
Copyright © 2010. Asociación Colombiana de Reumatología
Opciones de artículo
Herramientas