Pascual V, Dieli-Crimi R, López-Palacios N, Bodas A, Medrano LM, Núñez C. Inflammatory bowel disease and celiac disease: Overlaps and differences. World J Gastroenterol 2014; 20(17): 4846-4856 [PMID: 24803796 DOI: 10.3748/wjg.v20.i17.4846]
Corresponding Author of This Article
Concepción Núñez, PhD, UGC de Inmunología, Hospital Clínico San Carlos, Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), C/ Profesor Martín Lagos s/n Madrid, 28040 Madrid, Spain. conchita.npardo@gmail.com
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Topic Highlight
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World J Gastroenterol. May 7, 2014; 20(17): 4846-4856 Published online May 7, 2014. doi: 10.3748/wjg.v20.i17.4846
Inflammatory bowel disease and celiac disease: Overlaps and differences
Virginia Pascual, Romina Dieli-Crimi, Natalia López-Palacios, Andrés Bodas, Luz María Medrano, Concepción Núñez
Virginia Pascual, Romina Dieli-Crimi, Luz María Medrano, Concepción Núñez, UGC de Inmunología, Hospital Clínico San Carlos, Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), 28040 Madrid, Spain
Natalia López-Palacios, Servicio de Digestivo, Hospital Clínico San Carlos, Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), 28040 Madrid, Spain
Andrés Bodas, Servicio de Pediatría, Hospital Clínico San Carlos, Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), 28040 Madrid, Spain
Author contributions: Pascual V contributed to the extensive literature search and preparation of the first manuscript draft; Dieli-Crimi R contributed to the literature search and preparation of the first manuscript draft; López-Palacios N contributed to the literature search and preparation of the first manuscript draft; Bodas A contributed to the literature search and preparation of the first manuscript draft; Medrano LM contributed to the literature search and preparation of the first manuscript draft; Núñez C contributed to the study idea, literature search, manuscript writing and final revision of the article; all authors approved the manuscript.
Supported by Grants from “Fondo de Investigaciones Sanitarias”, PI11/00614; and “Fundación Eugenio Rodríguez Pascual”
Correspondence to: Concepción Núñez, PhD, UGC de Inmunología, Hospital Clínico San Carlos, Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), C/ Profesor Martín Lagos s/n Madrid, 28040 Madrid, Spain. conchita.npardo@gmail.com
Telephone: +34-913-302499 Fax: +34-913-303344
Received: September 27, 2013 Revised: November 20, 2013 Accepted: January 14, 2014 Published online: May 7, 2014 Processing time: 221 Days and 10.3 Hours
Abstract
Recent findings demonstrate the common genetic basis for many immune-mediated diseases, and consequently, the partially shared pathogenesis. We collected these findings and reviewed the extension of these overlaps to other disease characteristics. Two autoimmune diseases were selected that also share the specific target organ, the bowel. The etiology and immunopathogenesis of both conditions characterized by chronic intestinal inflammation, inflammatory bowel disease (IBD) and celiac disease (CeD), are not completely understood. Both are complex diseases with genetics and environment contributing to dysregulation of innate and adaptive immune responses, leading to chronic inflammation and disease. CeD constitutes a particular disease because the main environmental and genetic triggers are largely known. IBD comprises two main clinical forms, Crohn’s disease and ulcerative colitis, which most likely involve a complex interplay between some components of the commensal microbiota and other environmental factors in their origin. These multifactorial diseases encompass a broad spectrum of clinical phenotypes and ages of onset, although the clinical presentation often differs depending on childhood or adult onset, with greater heterogeneity commonly observed in adults.
Core tip: Inflammatory bowel disease and celiac disease are two immune-mediated diseases characterized by chronic intestinal inflammation. Recent findings demonstrate shared genetics and functional pathways. We reviewed the extension of these overlaps to other disease features and suggest future research approaches.