Intest Res.  2020 Jul;18(3):249-264. 10.5217/ir.2019.00128.

Pathogenesis and clinical perspectives of extraintestinal manifestations in inflammatory bowel diseases

• Kim JM
• Cheon JH

• KMID: 2504580
• DOI: http://doi.org/10.5217/ir.2019.00128

Abstract

A considerable number of patients with inflammatory bowel disease (IBD) experience extraintestinal manifestations (EIMs), which can present either before or after IBD diagnosis. Unraveling the pathogenic pathways of EIMs in IBD is challenging because of the lack of reliable criteria for diagnosis and difficulty in distinguishing EIMs from external pathologies caused by drugs or other etiologies. Optimizing treatment can also be difficult. Early diagnosis and management of EIM revolve around multidisciplinary teams, and they should have the resources necessary to make and implement appropriate decisions. In addition, specialists of the affected organs should be trained in IBD treatment. Furthermore, patient awareness regarding the extraintestinal symptoms of IBD is of paramount importance for improving patient understanding of disease and health outcomes. Herein, we review the pathogenesis and clinical perspectives of EIMs in IBD.

Keyword

Inflammatory bowel diseases; Neuromuscular manifestations; Skin manifestations; Eye manifestations

Figure

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  Fig. 1. Mechanisms of extraintestinal manifestations (EIMs). (a) Activation and expansion of effector memory T cells can lead to induction of mucosal vascular addressin cell adhesion molecule 1 and C-C motif chemokine ligand 25 (CCL25) expression in the liver. (b) Intercellular adhesion molecule-1, vascular adhesion protein-1, and vascular cell adhesion molecule 1 are associated with T cell trafficking. (c) Microbial antigens and materials translocate to extraintestinal sites and drive EIMs. (d) Circulating antibodies can provoke an autoimmune response and peptide(s) expressing common epitopes shared by colon and extra-colonic organs. (e) Neutrophil priming and alteration of circulating monocytes and macrophages can induce intestinal inflammation and are associated with innate immune responses. (f) Gut dysbiosis drives non-intestinal inflammation and increases mucosal permeability and lipopolysaccharides.

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