Fasano Alessio
Center for Celiac Research and Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.
Curr Opin Gastroenterol. 2006 Nov;22(6):674-9. doi: 10.1097/01.mog.0000245543.72537.9e.
Celiac disease is an immune-mediated disorder clinically characterized by a multitude of symptoms and complications. The comorbidity between celiac disease and other autoimmune disorders has been clearly established.
Two main theories have been postulated to explain this comorbidity: (1) linkage disequilibrium between the genes responsible for celiac disease and those responsible for the coexpressed autoimmune diseases or (2) untreated celiac disease leading to the onset of other autoimmune diseases. This article reviews the current literature supporting either theory and places the current knowledge in the field within the context of the most recent data on the pathogenesis of celiac disease.
The current literature did not clearly establish which of the two theories explain the comorbidity between celiac disease and other autoimmune disorders. There is, however, growing evidence that the loss of the intestinal barrier function typical of celiac disease could be responsible of the onset of other autoimmune disease. This concept implies that the autoimmune response can be theoretically stopped and perhaps reversed if the interplay between autoimmune predisposing genes and trigger(s) is prevented or eliminated by a prompt diagnosis and treatment.
乳糜泻是一种免疫介导的疾病，临床特征为多种症状和并发症。乳糜泻与其他自身免疫性疾病之间的共病关系已得到明确证实。
为解释这种共病关系提出了两种主要理论：（1）乳糜泻相关基因与共表达的自身免疫性疾病相关基因之间的连锁不平衡，或（2）未经治疗的乳糜泻导致其他自身免疫性疾病的发生。本文综述了支持这两种理论的当前文献，并将该领域的现有知识置于乳糜泻发病机制最新数据的背景下。
当前文献并未明确哪种理论能解释乳糜泻与其他自身免疫性疾病之间的共病关系。然而，越来越多的证据表明，乳糜泻典型的肠道屏障功能丧失可能是其他自身免疫性疾病发病的原因。这一概念意味着，如果通过及时诊断和治疗预防或消除自身免疫易感基因与触发因素之间的相互作用，理论上自身免疫反应可以停止甚至逆转。
