Celiac disease and its relation to bone metabolism
Authors:
I. Žofková
Authors place of work:
Endokrinologický ústav, Praha
Published in the journal:
Čas. Lék. čes. 2009; 148: 246-248
Category:
Review Article
Summary
Celiac disease (nontropical sprue) is autoimmune disorder of the intestinal mucose, which usually develops in humans hypersensitive to gluten. The disease can occur at any age, with the greatest occurrence in early adulthood. Besides intestinal symptomatology – abdominal pain, diarrhoea and weight loss - celiac disease is often accompanied by extra-intestinal complications including osteopenia or osteoporosis and osteomalacia. Overproduction of cytokines IL-1 alpha, IL-1 beta and TNF-alpha increases bone resorption, which is further accelerated by hyperparathyroidism connected with malabsorption of calcium and vitamin D. Interaction of both these mechanisms activated bone loss.
Similarly as the classic (symptomatic) celiac disease, the occult form, commonly seen in the elderly, may be associated with a risk of osteoporosis or osteomalacia related fractures. Diagnosis is based on positivity of IgA and IgG antigliadin and endomysial antibodies and characteristic endoscopic detection of inflammation and atrophy of duodenal mucose. Areal screening of celiac disease in osteoporotic patients is very dubious. However, a methodical examination should be performed in all patients with unexplainable hyperparathyroidism or in those with various autoimmune diseases (type 1 diabetes, thyroiditis chronica), or in premenopausal women and men, who did not reach the appropriate peak bone mass. On the other hand, detailed analysis of calcium metabolism, including markers of bone remodlling and X-ray densitometry (DXA), are recommended in all patients with verified celiac disease. The effectiveness of a gluten-free diet and substitution with vitamin D and calcium, or treatment with bisphosphonates are discussed. The promising therapy appears to be new molecules with reparative effect on intestinal mucose such as AT-1001.
Key words:
celiac disease, genetics, inflammation, malabsorption, hyperparathyroidism, osteoporosis.
Zdroje
1. Briani C, Samaroo D, Alaedini A. Celiac disease: from gluten to autoimmunity. Autoimmune Rev 2008; 7: 644–650.
2. Akobeng AK, Thomas AG. Systematic review: tolerable amount of gluten for people with coeliac disease. Aliment Pharmacol Ther 2008; 27: 1044–1052.
3. Barker JM, Liu E. Celiac disease: pathophysiology, clinical manifestations, and associated autoimmune conditions. Adv Pediatr 2008; 55: 349–365.
4. Hopman EG, von Biomberg ME, Batstra MR, et al. Gluten tolerance in adult patients with celiac disease 20 years after diagnosis. Eur J Gatroenterol Hepatol 2008; 20: 423–429.
5. Hovhannisyan Z, Weiss A, Martin A, et al. The role of HLA-DQ8 beta57 polymorphism in the anti-gluten T-cell response in celiac disease. Nature 2008; 456: 534–538.
6. Nenna R, Mora B, Megiorni MC, et al. HLA-DQB1*02 dose on RIA anti-tissue transglutaminase antibody levels and clinicopathological expresivity of celiac disease. J Pediatr Gastroenterol Nutr 2008; 47: 288–292.
7. Dezsofi A, Szebeni B, Hermann CS, et al. Frequencies of genetic polymorphisms of TLR4 and CD14 and of HLA-DQ genotypes in children with celiac disease, type 1 diabetes mellitus, or both. J Pediatr Gastroenterol Nutr 2008; 47: 283–287.
8. Smyth DJ, Plagnol V, Walker NM, et al. Shared and distinct genetic variants in type 1 diabetes and celiac disease. The N Engl J Med 2008; 359: 2767–2777.
9. Lettre G, Rioux JD. Autoimmune diseases: insight from genome-wide association studies. Hum Mol Genet 2008; 17: R116–R121.
10. McGovern DP, Tailor KD, Landers C, et al. MAG12 genetic variation and inflamatory bowel disease. Inflamm Bowel Dis 2009; 15: 75–83.
11. Hernandez L, Green PH. Extraintestinal manifestations of celiac disease. Curr Gastroenterol Rep 2006; 8: 383–389.
12. Johnson MW, Ellis HJ, Asante MA, Ciclitria PJ. Celiac disease in the elderly. Nat Clin Pract Gastroenterol Hepatol 2008; 5: 697–706.
13. Holt PR. Intestinal malabsorption in the elderly. Dig Dis 2007; 25: 144–150.
14. Bardella MT, Elli L, De Matteis S, et al. Autoimmune disorders in patiens affected by celiac sprue and inflammatory bowel disease. Ann Med 2008; 41: 139–143.
15. Neuhausen SL, Steele L, Ryan S, et al. Co-occurence of celiac disease and other autoimmune diseases in celiacs and their first-degree relatives. J Autoimmun 2008; 31: 160–165.
16. Nóvoa Medina Y, López-Capapé M, Lara Orejas E, et al. Impact of diagnosis of celiac disease on metabolic control of type 1 diabetes. An Pediatr (Barc) 2008; 68: 13–17.
17. Ch’ng CL, Jones MK, Kingham JG. Celiac disease and autoimmune thyroid disease. Clin Med Res 2007; 5: 184–192.
18. Bergamaschi G, Markopoulos K, Albertini R, et al. Anemia of chronic disease and defective erythropoietin production in patients with celiac disease. Haematologica 2008; 93: 1785–1791.
19. Krzesiek E, Iwańczak B. Assessment of bone mineral density in children with celiac disease. Pol Merkur Lekarski 2008; 24: 219–226.
20. Bianchi ML, Bardella MT. Bone in celiac disease. Osteoporosis Int 2008; 19: 1705–1716.
21. Stazi AV, Trecca A, Trinti B. Osteoporosis in celiac disease and in endocrine and reproductive disorders. World J Gastroenterol 2008; 14: 498–505.
22. Moreno ML, Crusius JB, Cherńavsky A, et al. Immunogenetics 2005; 57: 618–620.
23. Cashman KD. Altered bone metabolism in inflammatory disease: role of nutrition. Proc Nutr Soc 2008; 67: 196–205.
24. Kavuncu V, Sundar U, Ciftci, et al. Is there any requirement for celiac disease screening routinely in postmenopausal women with osteoporosis? Rheumatol Int 2008; 29: 841–845.
25. Presutti RJ, Cangemi JR, Cassidy HD, Hill DA. Celiac disease. Am Fam Physician 2007; 76: 1795–1802.
26. Kubincová L, Payer J, Killinger Z, et al. Celiac disease – a frequent cause of „idiopathic osteoporosis“ in premenopausal and early postmenopausal women. Vnitř Lék 2007; 53: 1296–1302.
27. Palička V. Celiakie a osteoporóza – je vazba natolik těsná, že vyžaduje akci? – editorial. Vnitř Lék 2007; 53: 1243–1244.
28. Efe C, Ozaslan E, Yazici C, et al. Celiac disease presenting with vertebral fracture in an elderly man. J Am Geriatr Soc 2008; 56: 1978–1980.
29. Zanchi C, Di Leo G, Ronfani L, et al. Bone metabolism in celiac disease. J Pediatr 2008; 153: 262–265.
30. McFarlane XA, Bhalla AK, Reeves DE, et al. Osteoporosis in treated adult coeliac disease. Gut 1995; 36: 710–714.
31. Matysiak-Budnik T, Malamut G, de Serre NP, et al. Long-term follow-up of 61 coeliac patients diagnosed in childhood: evolution toward latency is possible on a normal diet. Gut 2007; 56: 1379–1386.
32. Stenman SM, Venalainen JI, Lindfors K, et al. Enzymatic detoxification of gluten by germinating wheat proteases: Implication for new treatment of celiac disease. Ann Med 2009; 41: 390–400.
33. Senger S, Luongo D, Maurano F, et al. Intranasal administration of a recombinant alpha-gliadin down-regulates the immune response to wheat Iliadin in DQ8 transgenic mice. Immunol Lett 2003; 88: 127–134.
34. Tilg H, Moschen AR, Kaser A, et al. Gut, inflammation and osteoporosis: basic and clinical concepts. Gut 2008; 57: 684–694.
Štítky
Addictology Allergology and clinical immunology Angiology Audiology Clinical biochemistry Dermatology & STDs Paediatric gastroenterology Paediatric surgery Paediatric cardiology Paediatric neurology Paediatric ENT Paediatric psychiatry Paediatric rheumatology Diabetology Pharmacy Vascular surgery Pain management Dental HygienistČlánok vyšiel v časopise
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