Celiac disease: Is the atypical really typical? Summary of the recent National Institutes of Health Consensus Conference and latest advances

被引：6

作者：

Gadewar S. ^{[1
]}

Fasano A. ^{[1
]}

机构：

[1] Department of Pediatrics, Mucosal Biology Research Center, University of Maryland School of Medicine, Baltimore, MD 21201

来源：

Current Gastroenterology Reports | 2005年 / 7卷 / 6期

关键词：

Celiac Disease; Coeliac Disease; Capsule Endoscopy; Villous Atrophy; Celiac Disease Patient;

D O I：

10.1007/s11894-005-0076-z

中图分类号：

学科分类号：

摘要：

Celiac disease (CD) is an immune-mediated enteropathy triggered by the ingestion of gluten in genetically susceptible individuals. Gluten is a protein component in wheat and other cereals, such as rye and barley. At present, the only available treatment is a strict gluten-free diet. Recent advances have increased our understanding of the molecular basis for this disorder. The past decade has seen new scientific developments in this disease and led to the formulation of new concepts of pathophysiology and clinical manifestations. There are several targets for new treatments. This article briefly summarizes the National Institutes of Health Consensus Statement and gives an overview of new findings in recent years and of future therapeutic options for CD. Copyright © 2005 by Current Science Inc.

引用

页码：455 / 461

页数：6

共 43 条

[21]

Marzari R., Sblattero D., Florian F., Et al., Molecular dissection of the tissue transglutaminase autoantibody response in celiac disease, J Immunol, 166, pp. 4170-4176, (2001)

[22]

Korponay-Szabo I.R., Halttunen T., Szalai Z., Et al., In vivo targeting of intestinal and extraintestinal transglutaminase 2 by coeliac autoantibodies, Gut, 53, pp. 641-648, (2004)

[23]

Kaukinen K., Peraaho M., Collin P., Et al., Small-bowel mucosal transglutaminase 2-specific IgA deposits in coeliac disease without villous atrophy: A prospective and randomized clinical study, Scand J Gastroenterol, 40, pp. 564-572, (2005)

[24]

Clemente M.G., Musu M.P., Frau F., Et al., Immune reaction against the cytoskeleton in coeliac disease, Gut, 47, pp. 520-526, (2000)

[25]

Clemente M.G., Musu M.P., Troncone R., Et al., Enterocyte actin autoantibody detection: A new diagnostic tool in celiac disease diagnosis: Results of a multicenter study, Am J Gastroenterol, 99, pp. 1551-1556, (2004)

[26]

Arentz-Hansen H., Fleckenstein B., Molberg O., Et al., The molecular basis for oat intolerance in patients with celiac disease, PLoS Med, 1, (2004)

[27]

Peraaho M., Collin P., Kaukinen K., Et al., Oats can diversify a gluten-free diet in celiac disease and dermatitis herpetiformis, J Am Diet Assoc, 104, pp. 1148-1150, (2004)

[28]

Thompson T., Gluten contamination of commercial oat products in the United States, N Engl J Med, 351, pp. 2021-2022, (2004)

[29]

Collin P., Thorell L., Kaukinen K., Et al., The safe threshold for gluten contamination in gluten-free products. Can trace amounts be accepted in the treatment of coeliac disease?, Aliment Pharmacol Ther, 19, pp. 1277-1283, (2004)

[30]

Peraaho M., Kaukinen K., Paasikivi K., Et al., Wheat-starch-based gluten-free products in the treatment of newly detected coeliac disease: Prospective and randomized study, Aliment Pharmacol Ther, 17, pp. 587-594, (2003)

← 1 2 3 4 5 →