CELIAC DISEASE: FROM PATHOGENESIS TO TREATMENT
https://doi.org/10.15690/vsp.v12i3.676
Abstract
Celiac disease is characterized by intolerance to gluten, which is a protein composite of grain species. The prevalence of this condition in Europe and USA is 1:100–1:500. Gluten can indirectly initiate immune response through the molecules of major histocompatibility complex I and II. Changes in gluten tolerance are likely to be a key factor of celiac disease development, with increase of epithelial barrier permeability having the primary role in gluten intrusion into the mucous membrane and immune response initiation. Treatment of celiac disease at present is based on strict lifelong gluten free diet with exception of grain species containing gluten (wheat, rye, barley) and certain products of their processing. Safe threshold of gluten contain in food is considered to be 20 ppm (parts per million). The optimal management decision is intake of manufactured gluten free products, which are totally safe, variously represented and have good organoleptic characteristics. Appropriate diet in combination with correction of secondary metabolic disturbances and treatment of associated disorders can provide high life quality in patients with celiac disease.
About the Authors
S. V. Bel'merRussian Federation
T. V. Gasilina
Russian Federation
References
1. Filatov N. F. Semiotika i diagnostika detskikh boleznei. Ruko vodstvo dlya vrachei [Semiotics and diagnosis of child diseases]. 1905. 681 p.
2. Wieser H., Seilmleier W. Prolamins. Getreide Mehl. Brot. 1991; 45: 35–38.
3. Sapone A., Bai J. C., Ciacci C., Dolinsek J., Green P. H. R., Hadjivassiliou M., Kaukinen K., Rostami K., Sanders D. S., Schumann M., Ullrich R., Villalta D., Volta U., Catassi C., Fasano A. Spectrum of gluten-related disorders: consensus on new nomenclature and classification. BMC Medicine. 2012; 10: 13.
4. Fasano A. European and North American populations should be screened for coeliac disease. Gut. 2003; 52: 168–169.
5. Corrao G., Corazza G. R., Bagnardi V., Brusco G., Ciacci C., Cottone M., Sategna Guidetti C., Usai P., Cesari P,. Pelli M. A., Loperfido S., Volta U., Calabro A., Certo M. Club del Tenue Study Group. Mortality in patients with coeliac disease and their relatives: a cohort study. Lancet. 2001; 358 (9279): 356–361.
6. Ivarsson A., Hernell O., Stenlund H., Persson L. A. Breastfeeding protects against celiac disease. Am. J. Clin. Nutr. 2002; 75: 914–921.
7. Troncone R., Scarcella A., Donatiello A. et al. Passage of gliadin into human breast milk. Acta. Paediatr. Scand. 1987; 76: 453–456.
8. Chirdo F. G., Rumbo M., Anon M. C. et al. Presence of high levels of non-degraded gliadin in breast milk from healthy mothers. Scand. J. Gastroenterol. 1998; 33: 1186–1192.
9. Hogen Esch C. E., Rosen A., Auricchio R. et al. PreventCD Study Group. The PreventCD Study design: towards new strategies for the prevention of coeliac disease. Eur. J. Gastroenterol. Hepatol. 2010; 22: 1424–1430.
10. ESPGHAN Committee on Nutrition. Breast feeding. A position paper by the ESPGHAN Committee on Nutrition. J. Pediatr. Gastroenterol. Nutr. 2009; 49: 112–125.
11. Szajewska H., Chmielewska A., Piescik-Lech M., Ivarsson A., Kolacek S., Koletzko S., Mearin M. L., Shamir R., Auricchio R., Troncone R. PREVENTCD Study Group. Systematic review: early infant feeding and the prevention of coeliac disease. Aliment. Pharmacol. Ther. 2012; 36: 607–518.
12. Spaenij-Dekking L., Kooy-Winkelaar Y., van Veelen P., Drijfhout J. W., Jonker H. et al. Natural variation in toxicity of wheat: potential for selection of nontoxic varieties for celiac disease patients. Gastroenterology. 2005; 129: 797–806.
13. Gass J., Bethune M. T., Siegel M., Spencer A., Khosla C. Combi nation enzyme therapy for gastric digestion of dietary gluten in patients with celiac sprue. Gastroenterology. 2007; 133: 472–480.
14. Cornell H. J., Macrae F. A., Melny J., Pizzey C. J., Cook F. et al. Enzyme therapy for management of coeliac disease. Scand. J. Gastroenterol. 2005; 40: 1304–1312.
15. Paterson B. M., Lammers K. M., Arrieta M. C., Fasano A., Meddings J. B. The safety, tolerance, pharmacokinetic and pharmacodynamic effects of single doses of AT-1001 in coeliac disease subjects: a proof of concept study. Aliment. Pharmacol. Ther. 2007; 26: 757–766.
16. Siegel M., Khosla C. Transglutaminase 2 inhibitors and their thera peutic role in disease states. Pharmacol. Ther. 2007; 115: 232–245.
17. Bethune M. T., Khosla C. Parallels between pathogens and gluten peptides in celiac sprue. PLoS Pathogens. 2008; 4 (2–34): 1–16.
18. Collin P., Thorell L., Kaukinen K., Maki M. The safe threshold for gluten contamination in gluten-free products. Can trace amounts be accepted in the treatment of coeliac disease? Aliment. Pharmacol. Ther. 2004; 19: 1277–1283.
19. Dewar D. H., Ciclitira P. J. Clinical studies on thresholds for gluten sensitivity in coeliac disease: Introduction. Proceedings of the 18th Meeting of Working Group on Prolamin Analysis and Toxity. Stockholm. 2003. P. 155–160.
Review
For citations:
Bel'mer S.V., Gasilina T.V. CELIAC DISEASE: FROM PATHOGENESIS TO TREATMENT. Current Pediatrics. 2013;12(3):12-17. (In Russ.) https://doi.org/10.15690/vsp.v12i3.676