45 In line with the latter fi ndings the detection of antigliadin antibodies in

45 in line with the latter fi ndings the detection of

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45 In line with the latter fi ndings, the detection of antigliadin antibodies in >50% of patients with NCGS provides further support to adaptive immunity in NCGS pathogenesis. 46 Second, discordant data exist on epithelial barrier dysfunction. Initial studies showed a reduced intestinal permeability in NCGS, thus sug- gesting an increased intestinal barrier function. This fi nding has been also supported by a signi fi cantly higher expression of claudin-4 mRNA, a marker of reduced permeability, in duodenal De Giorgio R, et al . Gut 2016; 65 :169 178. doi:10.1136/gutjnl-2015-309757 171 Recent advances in clinical practice group.bmj.com on March 9, 2016 - Published by Downloaded from
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biopsies of patients with NCGS. 44 However, more recently, some evidence for increased intestinal permeability in a sub- group of patients with IBS-D carrying the human leucocyte antigen (HLA)-DQ2+/DQ8+ was reported when consuming a gluten-containing diet compared with a GFD. 47 Further studies are needed. Third, changes of gut microbiota, as detected in CD, 48 might also occur in patients with NCGS. Finally, a further aspect potentially linking NCGS with IBS is that HLA-DQ8 transgenic mice sensitised by gliadin displayed an increased secretion of acetylcholine from the myenteric plexus, enhancing muscle contractility and epithelial hypersecretion. Gluten withdrawal reversed both abnormalities. 49 Evidence from double-blind placebo-controlled trials Consistent evidence indicates the existence of an overlap between IBS and gluten-related disorders. In fact, about 5% of patients with IBS tests positive for CD and, conversely, CD may present with typical IBS-like symptoms. 50 51 Moreover, IBS-like symptoms occur in the majority of patients with NCGS, 40 while about one-third of patients with IBS may have NCWPS. 37 Although wheat is now established to be linked to IBS, the com- ponent(s) that actually trigger(s) symptoms remain unknown. In this line, the only way to con fi rm the possible role of gluten or wheat as causative factors of NCGS/NCWPS is a DBPC strat- egy. 27 This is an expensive and time-consuming procedure and, therefore, it is not yet of routine use being con fi ned to research setting. 37 39 43 52 53 So far, few DBPC trials have been per- formed. Their design and results are shown in table 1 . The fi nd- ings are discordant with a variation from approximately 30% of 920 patients with IBS in a routine clinical setting being sensitive to wheat protein, of whom the majority has NCWPS associated with multiple food hypersensitivity, 37 to greater symptoms induction overall with gluten or wheat protein, 38 39 53 to gluten-speci fi c responses for current feelings of depression but not for abdominal symptoms. 38 53 Reasons for apparent heterogeneity of results require dissec- tion. First, subject selection might be a factor. For example, con- tamination of the cohort with CD can unduly skew results. This is why the exclusion of CD by combined histological and sero- logical assessment while consuming adequate gluten is so important. In this respect, a critical point is to decide whether
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