Coeliac disease

Abstract

Coeliac disease occurs in about 1% of people in most populations. Diagnosis rates are increasing, and this seems to be due to a true rise in incidence rather than increased awareness and detection. Coeliac disease develops in genetically susceptible individuals who, in response to unknown environmental factors, develop an immune response that is subsequently triggered by the ingestion of gluten. The disease has many clinical manifestations, ranging from severe malabsorption to minimally symptomatic or non-symptomatic presentations. Diagnosis requires the presence of duodenal villous atrophy, and most patients have circulating antibodies against tissue transglutaminase; in children, European guidelines allow a diagnosis without a duodenal biopsy provided that strict symptomatic and serological criteria are met. Although a gluten-free diet is an effective treatment in most individuals, a substantial minority develop persistent or recurrent symptoms. Difficulties adhering to a gluten-free diet have led to the development of non-dietary therapies, several of which are undergoing trials in human beings.

Impact of Cereal Seed Sprouting on Its Nutritional and Technological Properties: A Critical Review

“…Celiac disease is an inflammatory disease of the upper small intestine in genetically susceptible individuals (approximately 1% of the population worldwide) triggered by the storage proteins of wheat, rye, or barley (Catassi, Gatti, & Lionetti, ; Lebwohl, Sanders, & Green, ; P. Singh et al., ). Gluten proteins, including α‐gliadins, γ‐gliadins, and low‐molecular‐weight (LMW) glutenins, are not completely hydrolyzed by human gastrointestinal enzymes resulting in peptides that stimulate T‐cells in the intestinal mucosa of people suffering from celiac disease (Kerpes, Knorr, Procopio, Koehler, & Becker, ; Schwalb et al., ).…”

Masked bolus gluten challenge low in FODMAPs implicates nausea and vomiting as key symptoms associated with immune activation in treated coeliac disease

“…Persistent intestinal mucosal injury appears to be explained by recurrent, inadvertent gluten exposure . Indeed, patients and clinicians may not be able to accurately recognise episodes of gluten ingestion if reported symptoms are attributed to irritable bowel syndrome (IBS) . The symptoms of IBS may be triggered by poorly absorbed, fermentable, short‐chain carbohydrates (FODMAPs) present in many gluten‐free foods as well as being enriched in wheat flour, the commonest source of gluten in Western diets .…”

“…Although the immune mechanisms are debated and supportive blood biomarkers are lacking, onset of digestive symptoms is about 2 hours after food exposure in non‐IgE immune‐mediated food hypersensitivities . In contrast, clinical descriptions of coeliac disease, a T cell‐mediated condition, emphasise chronic symptoms similar to IBS . There are, however, reports of acute reactions to gluten in patients with coeliac disease on gluten‐free diet, but until recently there appeared to be no mechanistic explanation, and well‐controlled gluten food challenge studies addressing this issue are absent.…”

Editorial: a non‐dietary treatment for coeliac disease—two steps forward, one step back?

“…Truitt et al present a phase 1 study of Nexvax2, a vaccine designed to desensitise HLA‐DQ2.5‐positive individuals to gluten. In affected individuals, deamidation of gliadin peptides derived from gluten by tissue transglutaminase leads to binding to HLA‐DQ2 and/or HLA‐DQ8 on antigen‐presenting cells, activating an adaptive immune response . Nexvax2 comprises an equimolar mixture of three 15‐16 amino‐acid residue gluten‐derived peptides—NPL001, NPL002 and NPL003—obtained from 16 838 unique oligopeptides following interferon‐γ ELISpot assays in T‐cell clones and peripheral blood mononuclear cells from patients with coeliac disease .…”