PATOGENESIS, EPIDEMIOLOGIA Y TRATAMIENTO DE LOS TRASTORNOS OSEOS EN LA ENFERMEDAD CELIACA




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PATOGENESIS, EPIDEMIOLOGIA Y TRATAMIENTO DE LOS TRASTORNOS OSEOS EN LA ENFERMEDAD CELIACA

(especial para SIIC © Derechos reservados)
Las alteraciones óseas y la pérdida de masa ósea se observan con frecuencia en la enfermedad celíaca como consecuencia de la malabsorción intestinal y de la inflamación crónica.
Autor:
Maria Luisa Bianchi
Columnista Experta de SIIC

Institución:
Istituto Auxologico Italiano IRCCS


Artículos publicados por Maria Luisa Bianchi
Recepción del artículo
14 de Febrero, 2011
Aprobación
30 de Abril, 2011
Primera edición
31 de Mayo, 2011
Segunda edición, ampliada y corregida
7 de Junio, 2021

Resumen
El presente artículo tiene por objetivo presentar el compromiso óseo de la enfermedad celíaca en pacientes de cualquier edad: niños, adolescentes y adultos. Asimismo, se discuten en detalle los mecanismos patogénicos que se proponen en la actualidad (malabsorción e inflamación) y se resume la presentación clínica y el tratamiento de los trastornos óseos de esta entidad. También se presenta la información epidemiológica disponible sobre osteoporosis y fracturas por fragilidad en la enfermedad celíaca.

Palabras clave
enfermedad celíaca, hueso, fracturas, calcio, vitamina D


Artículo completo

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Extensión:  +/-13.31 páginas impresas en papel A4
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Abstract
The article is aimed at presenting the bone involvement in celiac disease (CD) in patients of any age: children, adolescents and adults. It is focused on the currently proposed pathogenetic mechanisms (malabsorption and inflammation). The clinical presentation and the treatment of bone problems in CD are summarized. The available data on the epidemiology of osteoporosis and fragility fractures in CD are also presented.

Key words
celiac disease, bone, fractures, calcium, vitamin D


Full text
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Clasificación en siicsalud
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Especialidades
Principal: Gastroenterología, Osteoporosis y Osteopatías Médicas
Relacionadas: Endocrinología y Metabolismo, Epidemiología, Inmunología, Medicina Familiar, Medicina Interna, Nutrición, Pediatría



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Enviar correspondencia a:
Maria Luisa Bianchi, Istituto Auxologico Italiano IRCCS Bone Metabolism Unit, 20145, via L. Ariosto, 13, Milán, Italia
Bibliografía del artículo
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1. Dube C, Rostom A, Sy R, et al. The prevalence of celiac disease in average-risk and at-risk Western European populations: a systematic review. Gastroenterology 128:S57-S67, 2005.
2. Holtmeier W, Caspary WF. Celiac disease. Orph J Rare Dis I:3. DOI 10.1186/1750-1172-1-3, 2006.
3. Rampertab SD, Pooran N, Brar P, Singh P, Green PH. Trends in the presentation of celiac disease. Am J Med 19:9-14, 2006.
4. Shah S, Leffler D. Celiac disease: an underappreciated issue in women's health. Women's Health (Lond Engl) 6:753-766, 2010.
5. Da Silva Kotze LM. Celiac disease in Brazilian patients: associations, complications and causes of death. Forty years of clinical experience. Arq Gastroenterol 46:261-269, 2009.
6. Ciclitira PJ. Molecular pathogenesis and clinical immunology of coeliac disease. In: YR. Mahida, editor. Immunological aspects of gastroenterology. Dordrecht. Kluwer Academic Publisher; p.177-240; 2001.
7. Mulder SJ, Mulder-Bos GC. Most probable origin of coeliac disease is low immune globulin A in the intestine caused by malfunction of Peyer's patches. Med Hypoth 66:757-762, 2006.
8. Alaedini A, Green PHR. Narrative review: celiac disease: understanding a complex autoimmune disorder. Ann Int Med 142:289-298, 2005.
9. Green PHR, Cellier C. Celiac disease. N Engl J Med 357:1731-1743, 2007.
10. Keaveny AP, Freaney R, McKenna MJ, Masterson J, O'Donoghue DP. Bone remodelling indices and secondary hyperparathyroidism in celiac disease. Am J Gastroenterol 91:1226-1231, 1996.
11. Duerksen DR, Leslie WD. Positive celiac disease serology and reduced bone mineral density in adult women. Can J Gastroenterol 24:103-107, 2010.
12. de Sèze S, Dreyfus P, Selmes J. Osseous demineralization and diseases of the alimentary tract in adults. Cah Coll Med Hop Paris 10:963-970, 1969.
13. Meyer D, Stavropolous S, Diamond B, Shane E, Green PH. Osteoporosis in a North American adult population with celiac disease. Am J Gastroenterol 96:112-119, 2001.
14. McFarlane XA, Bhalla AK, Reeves DE, Morgan LM, Robertson DA. Osteoporosis: a frequent finding in treated adult coeliac disease. Gut 33(Suppl 2):S48, 1992.
15. Valdimarsson T, Löfman O, Toss G, Ström M. Reversal of osteopenia with diet in adult coeliac disease. Gut 38:322-327, 1996.
16. Bardella MT, Fredella C, Prampolini L, Molteni N, Giunta AM, Bianchi PA. Body composition and dietary intakes in adult celiac disease patients consuming a strict gluten-free diet. Am J Clin Nutr 72:937-939, 2000.
17. Corazza GR, Di Stefano M, Mauriño E, Bai JC. Bones in coeliac disease: diagnosis and treatment. Best Pract Res Clin Gastrenterol 19:453-465, 2005.
18. Davie MW, Gaywood I, George E, et al. Excess non-spine fractures in women over 50 years with celiac disease: A cross-sectional, questionnaire-based study. Osteoporos Int 16:1150-1155, 2005.
19. Olmos M, Antelo M, Vazquez H, Smecuol E, Mauriño E, Bai JC. Systematic review and meta-analysis of observational studies on the prevalence of fractures in coeliac disease. Dig Liver Dis 40:46-53, 2008.
20. Ludvigsson JF, Michaelsson K, Ekbom A, Montgomery SM. Coeliac disease and the risk of fractures - a general population-based cohort study. Aliment Pharmacol Ther 25:273-285, 2007.
21. Walters JRF. The role of the intestine in bone homeostasis. Eur J Gastroenterol Hepatol 15:845-849, 2003.
22. Molteni N, Bardella MT, Vezzoli G, Pozzoli E, Bianchi P. Intestinal calcium absorption as shown by stable strontium test in celiac disease before and after gluten-free diet. Am J Gastroenterol 90:2025-2028, 1995.
23. Di Stefano M, Veneto G, Malservisi S, Corazza GR. Small intestine bacterial overgrowth and metabolic bone disease. Dig Dis Sci 46:1077-1082, 2001.
24. Khanal RC, Nemere I. Endocrine regulation of calcium transport in epithelia. Clin Exper Pharmac Phys 35:1277-1287, 2008.
25. Khanal RC, Nemere I. Regulation of intestinal calcium transport. Ann Rev Nutr 28:179-196, 2008.
26. Di Stefano M, Veneto G, Malservisi S, et al. Lactose malabsorption and intolerance and peak bone mass. Gastroenterology 122:1793-1799, 2002.
27. Bronner F. Mechanisms of intestinal calcium absorption. J Cell Biochem 88:387-393, 2003.
28. Norman DA, Fordtran JS, Brinkley LJ, et al. Jejunal and ileal adaptation to alterations in dietary calcium. J Clin Invest 67:1599-1603, 1981.
29. Lo CW, Paris PW, Clemens TL, Nolan J, Holick MF. Vitamin D absorption in healthy subjects and in patients with intestinal malabsorption syndromes. Am J Clin Nutr 42:644-649, 1985.
30. Arnaud SB, Goldsmith RS, Lambert P, Go VLW. 25-hydroxyvitamin D3: evidence of an enterohepatic circulation in man. Proc Soc Exp Biol Med 149:570-572, 1975.
31. Karbach U, Ewe K. Enteric protein loss in various gastrointestinal diseases determined by intestinal alpha 1-antitrypsin clearance. Z Gastroenterol 27:362-365, 1989.
32. Clements MR, Chalmers TM, Fraser DR. Enterohepatic circulation of vitamin D: a reappraisal of the hypothesis. Lancet 1:1376-1379, 1984.
33. Bhatnagar A, Kashyap R, Chauhan UP, Mishra P, Chopra MK, Khanna CM. Diagnosing protein losing enteropathy. A new approach using Tc-99m human immunoglobulin. Clin Nucl Med 20:969-972, 1995.
34. Haddad JG. Plasma vitamin D-binding protein (Gc-globulin): multiple tasks. J Steroid Biochem Mol Biol 53:579-582, 1995.
35. Gomme PT, Bertolini J. Therapeutic potential of vitamin D-binding protein. Trends Biotechnol 22:340-345, 2004.
36. Lerner A, Shapira Y, Agmon-Levin N, et. al. The clinical significance of 25OH-Vitamin D status in celiac disease. Clin Rev Allergy Immunol DOI: 10.1007/s12016-010-8237-8, 2011.
37. Brandtzaeg P, Bjerke K, Kett K, et al. Production and secretion of immunoglobulins in the gastrointestinal tract. Ann Allergy 59:21-39, 1987.
38 Baumgart DC, Metzke D, Schmitz J, et al. Patients with active inflammatory bowel disease lack immature peripheral blood plasmacytoid and myeloid dendritic cells. Gut 54:228-236, 2005.
39. Wei S, Kitaura H, Zhou P, Ross FP, Teitelbaum SL. IL-1 mediates TNF-induced osteoclastogenesis. J Clin Invest 115:282-290, 2005.
40. Shen F, Ruddy MJ, Plamondon P, Gaffen SL. Cytokines link osteoblasts and inflammation: microarray analysis of interleukin-17- and TNF-alpha-induced genes in bone cells. J Leukoc Biol 77:388-399, 2005.
41. Taranta A, Fortunati D, Longo M, et al. Imbalance of osteoclastogenesis-regulating factors in patients with celiac disease. J Bone Miner Res 19:1112-1121, 2004.
42. Moschen AR, Kaser A, Enrich B, et al. The RANKL/OPG system is activated in inflammatory bowel disease and relates to the state of bone loss. Gut 54:479-487, 2005.
43. Bardella MT, Bianchi ML, Teti A. Chronic inflammatory intestinal diseases and bone loss. Gut 54:1508, 2005.
44. Khosla S, Minireview: the OPG/RANKL/RANK system. Endocrinology 142:5050-5055, 2001.
45. Tsangari H, Findlay DM, Kuliwaba JS, Atkins GJ, Fazzalari NL. Increased expression of IL-6 and RANK mRNA in human trabecular bone from fragility fracture of the femoral neck. Bone 35:334-342, 2004.
46. Moreno ML, Crusius JBA, Cherñavsky A, et al. The IL-1 gene family and bone involvement in celiac disease. Immunogenetics 57:618-620, 2005.
47. Bai JC, Gonzalez D, Mautalen C, et al. Long-term effect of gluten restriction on bone mineral density in coeliac disease. Aliment Pharmacol Ther 11:157-164, 1997.
48. Sategna-Guidetti C, Grosso SB, Grosso S, et al. The effects of 1-year gluten withdrawal on bone mass, bone metabolism and nutritional status in newly-diagnosed adult coeliac disease patients. Aliment Pharmacol Ther 14:35-43, 2000.
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