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Vol. 17. Núm. 4.
Páginas 249-256 (diciembre 2010)
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Vol. 17. Núm. 4.
Páginas 249-256 (diciembre 2010)
Acceso a texto completo
Osteomalacia inducida por tumor
Tumor-induced osteomalacia
Visitas
3527
Mario Andrés Quintana Duque1, Adriana Varela Nariño2, Federico Rondón3, José Félix Restrepo4, Antonio Iglesias Gamarra4,
Autor para correspondencia
1 Residente tercer año Medicina Interna. Facultad de Medicina. Universidad Nacional de Colombia
2 Médico Interno. Universidad Nacional de Colombia
3 Reumatólogo. Profesor Asociado de Medicina Interna y Reumatología. Universidad Nacional de Colombia
4 Reumatólogo. Profesor Titular de Medicina Interna y Reumatología. Universidad Nacional de Colombia
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Resumen

La osteomalacia inducida por tumor es un síndrome paraneoplásico secundario en la mayoría de los casos a tumores de origen mesenquimal. Se caracteriza por pérdida aumentada de fosfato a nivel urinario por el efecto inhibidor que ejerce el factor de crecimiento fibroblástico 23 sobre el transporte de fósforo en el túbulo renal proximal. Debe sospecharse en un paciente con debilidad y dolor osteomuscular generalizado que se presente con hipofosfatemia, normocalcemia, fosfatasa alcalina elevada y niveles de 25 hidroxivitamina D y PTH normales. El tratamiento definitivo de la enfermedad es la resección quirúrgica del tumor. Cuando se desconozca la neoplasia primaria o no sea posible el tratamiento quirúrgico debe iniciarse reposición de fósforo y calcitriol. En este artículo se presenta el primer caso de una paciente con osteomalacia inducida por tumor asociada a un carcinoma lobulillar infiltrante de seno.

Palabras clave:
osteomalacia
hipofosfatemia
25-hidroxivitamina D
parathormona (PTH)
Summary

The tumor-induced osteomalacia is a paraneoplastic syndrome secondary in most cases to tumors of mesenchymal origin. It is characterized by increased lost of urinary phosphate by the inhibitory effect exerted by the fibroblast growth factor 23 on phosphorus transport in the proximal renal tubule. Should be suspected in a patient with weakness and generalized muscle in addition to hypophosphatemia, normocalcemia, elevated alkaline phosphatase and normal serum 25-hydroxyvitamin D and PTH. The definitive treatment of the disease is surgical resection of the tumor. When the primary tumor is unknown or is not possible the surgical treatment should be initiated replacement of phosphorus and calcitriol. This paper presents the first case of a patient with tumor-induced osteomalacia associated with lobular breast cancer.

Key words:
osteomalacia
hypophosphatemia
25-hydroxyvitamin D
parathormone (PTH)
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Referencias
[1.]
R.A. McCance.
Osteomalacia with Looser's nodes due to a raised resistance to vitamin D acquired about the age of 15 years.
Q J Med, 16 (1947), pp. 33-46
[2.]
V. Prader, R. Illig, E. Vehlinger, G. Stalder.
Rachitis, infolge, knochen tumors.
Helv Paediatr Acta, 14 (1959), pp. 554-565
[3.]
M.K. Drezner.
Tumor-induced osteomalacia.
Primer on the metabolic bone diseases and disorders of mineral metabolism,, 4th, pp. 331-337
[4.]
M.K. Drezner.
Tumor-induced osteomalacia.
Rev Endocr Metab Disord, 2 (2001), pp. 175-186
[5.]
R. Kumar.
Tumor-induced osteomalacia and the regulation of phosphate homeostasis.
Bone, 27 (2000), pp. 333-338
[6.]
S.M. Jan De Beur.
Tumor-induced osteomalacia.
Primer on the metabolic bone diseases and disorders of mineral metabolism,, 6th, pp. 345-350
[7.]
Weiss D, Bar RS, Weidner N. Oncogenic osteomalacia. Ann Intern Med 198;102:557.
[8.]
J.C. Reubi, B. Waser, J.A. Laissue, J.O. Gebbers.
Somatostatin and vasoactive intestinal peptide receptors in human mesenchymal tumors: in vitro identification.
Cancer Res, 56 (1996), pp. 1922-1931
[9.]
C. Garcia, R. Spencer.
Bone and In-111 octreotide imaging in oncogenic osteomalacia: a case report.
Clin Nucl Med, 27 (2002), pp. 582-583
[10.]
N.A. Avila, M. Skarulis, D.M. Rubino, J.L. Doppman.
Oncogenic osteomalacia: lesion detection by MR skeletal survey.
Am J Roentgenol, 167 (1996), pp. 343-345
[11.]
J.L. Dupond, H. Mahammedi, D. Prié.
Oncogenic osteomalacia: diagnostic importance of fibroblast growth factor 23 and F-18 fluorodeoxyglucose PET/CT scan for the diagnosis and follow-up in one case.
[12.]
S.M. Jan de Beur.
Tumor-induced osteomalacia.
JAMA, 294 (2005), pp. 1260-1267
[13.]
T. Shimada, S. Mizutani, T. Muto, T. Yoneya, R. Hino, S. Takeda, et al.
Cloning and characterization of FGF23 as a causative factor of tumor-induced osteomalacia.
Proc Natl Acad Sci USA, 98 (2001), pp. 6500-6505
[14.]
T. Yamashita, M. Konsishi, A. Miayke.
Fibroblast growth factor (FGF)-23 inhibits renal phosphate reabsorption by activation of themitogen-activated protein kinase pathway.
J Biol Chem, 277 (2002), pp. 28265-28270
[15.]
Shimada T, Muto T, Urakawa I, Yoneya T, Yamazaki Y, Okawa K, et al. Mutant FGF-23 responsible for autosomal dominant hypophosphatemic rickets is resistant to proteolytic cleavage and causes hypophosphatemia in vivo. Endocrinology 143:3179-3182.
[16.]
M. Riminucci, M.T. Collins, N.S. Fedarko, N. Cherman, A. Corsi, K.E. White, et al.
FGF-23 in fibrous dysplasia of bone and its relationship to renal phosphate wasting.
J Clin Invest, 112 (2003), pp. 683-692
[17.]
A.E. Nelson, R.C. Bligh, M. Mirams, A. Gill, A. Au, A. Clarkson, et al.
Fibroblast growth factor 23: a new clinical marker for oncogenic osteomalacia.
J Clin Endocrinol Metab, 88 (2003), pp. 4088-4094
[18.]
T. Larsson, U. Nisbeth, O. Ljunggren, H. Juppner, K.B. Jonsson.
Circulating concentration of FGF-23 increases as renal function declines in patients with chronic kidney disease, but does not change in response to variation in phosphate intake in healthy volunteers.
Kidney Int, 64 (2003), pp. 2272-2279
[19.]
Y. Imanishi, M. Inaba, K. Nakatsuka, K. Nagasue, S. Okuno, A. Yoshihara, et al.
FGF-23 in patients with end-stage renal disease on hemodialysis.
Kidney Int, 65 (2004), pp. 943-946
[20.]
Y. Takeuchi, H. Suzuki, S. Ogura, R. Imai, Y. Yamazaki, T. Yamashita, et al.
Venous sampling for fibroblast growth factor-23 confirms preoperative diagnosis of tumorinduced osteomalacia.
J Clin Endocrinol Metab, 89 (2004), pp. 3979-3982
[21.]
E.A. Imel, M. Peacock, P. Pitukcheewanont, H.J. Heller, L.M. Ward, D. Shulman, et al.
Sensitivity of fibroblast growth factor 23 measurements in tumor-induced osteomalacia.
J Clin Endocrinol Metab, 91 (2006), pp. 2055-2061
[22.]
S.M. Jan De Beur, R.B. Finnegan, J. Vassiliadis, B. Cook, D. Barberio, S. Estes, et al.
Tumors associated with oncogenic osteomalacia express genes important in bone and mineral metabolism.
J Bone Miner Res, 17 (2002), pp. 1102-1110
[23.]
T. Berndt, T.A. Craig, A.E. Bowe, J. Vassiliadis, D. Reczek, R. Finnegan, et al.
Secreted frizzled-related protein 4 is a potent tumor-derived phosphaturic agent.
J Clin Invest, 112 (2003), pp. 785-794
[24.]
T.O. Carpenter, B.K. Ellis, K.L. Insogna, W.M. Philbrick, J. Sterpka, R. Shimkets.
FGF7, an inhibitor of phosphate transport derived from oncogenic osteomalacia- causing tumors.
J Clin Endocrinol Metab, 90 (2005), pp. 1012-1020
[25.]
P.S. Rowe, P.A. de Zoysa, R. Dong, H.R. Wang, K.E. White, M.J. Econs, et al.
MEPE, a new gene expressed in bone marrow and tumors causing osteomalacia.
Genomics, 67 (2000), pp. 54-68
[26.]
C.E. Dent, T.C.B. Stamp.
Vitamin D rickets and osteomalacia.
pp. 237
[27.]
M.P. Whyte, M.N. Podgornik, V.A. Wollberg, M.C. Eddy, W.H. McAlister.
Pseudo-(tumor-induced) rickets.
J Bone Miner Res, 16 (2001), pp. 1564-1571
[28.]
N. Weidner, D.S. Cruz.
Phosphaturic mesenchymal tumors: a polymorphous group causing osteomalacia or rickets.
Cancer, 59 (1987), pp. 1442-1454
[29.]
A.L. Folpe, J.C. Fanburg-Smith, S.D. Billings, M. Bisceglia, F. Bertoni, J.Y. Cho, et al.
Most osteomalaciaassociated mesenchymal tumors are a single histopathologic entity: an analysis of 32 cases and a comprehensive review of the literature.
Am J Surg Pathol, 28 (2004), pp. 1-30
[30.]
J. Seufert, K. Ebert, J. Müller, J. Eulert, C. Hendrich, Werner, et al.
Octreotide therapy for tumor-induced osteomalacia.
N Engl J Med, 345 (2001), pp. 1883-1888
Copyright © 2010. Asociación Colombiana de Reumatología
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