Inflammatory bowel diseases: Current problems and future tasks

Abstract

Current knowledge on inflammatory bowel disease (IBD) is mainly endorsed by controlled trials and epidemiologic studies. Yet, we seldom look at the messages from real-world practice. Among a patient population followed since 2008, we looked at an unselected sample of 64 IBD patients [26 Crohn’s disease (CD) and 38 ulcerative colitis (UC)] who had been seen as out-patients in the last year. Inducing remission, mesalamines (86% for UC/69% for CD/33%-16% as MMX formulation) prevailed as prescriptions; steroids (55%/19% for UC/CD) ranked second. Prescription of third-party drugs (antibiotics, NSAIDs, biologics) and adherence, were issues in the maintenance. 34% of CD, and 23% of UC patients showed accompanying immunologic diseases: CD-associated familiar psoriasis (4:9) ranked first. Main Message. The association between IBD (CD mainly) and psoriasis, now found in our practice, matches current basic science gathering IBD together with psoriasis (and perhaps chronic respiratory disease) under the comprehensive term “barrier organ disease” wherein an epithelial surface with sensor systems rules contacts between outer antigens and a reactive underneath tissue, with the balance between inflammation and quiescence kept at any time by mucosal permeability. IBD is thus viewed as a polyfactorial/polygenic/syndromic disorder, embedded into a galaxy of immune conditions offering multiple points of attack. This mindset of splitting the IBDs into pathogenic categories may allow overcoming the uniformly targeting of a single cytokine by biological drugs, in favor of demarcating the boundaries between different disease-subtype-specific indications, and paving the way to future personalized strategies.

Keywords: Inflammatory bowel disease; Immunopharmacology; Barrier organs; Future trends in inflammatory bowel disease; Microbiome

Core tip: Long after their description, ulcerative colitis and Crohn’s disease (IBD) are still treated but not cured. This somber spell has now begun to be broken by genetic discoveries and by the study of the human microbiome. The former have uncovered hundreds of genetic variants lending support to the clinical hint that IBD is a syndrome encompassing discrete polymorphisms of the immune response pathways, each requiring a personalized approach. The latter has shown the microbiome to be a cell universe which, if disrupted, can provoke IBD together with a myriad of disturbances apparently unrelated with the gut. A frame of mind seeing the IBDS as embedded into a plethora of genetically linked immune disturbances must fuel IBD research from now on.