Coeliac disease is an autoimmune-mediated enteropathy triggered in genetically susceptible persons by the ingestion of a single dietary factor – wheat, rye and barley-derived gluten. The permanency of gluten intolerance was suggested in early studies, which showed that symptoms and intestinal lesions recurred usually within 2 years when gluten was reintroduced to the diet.^1,2 Later it was recognised that the process of gluten-induced mucosal deterioration may take years or even decades in some individual cases.^3,4

The paper by Matysiak-Budnik et al⁵ in the present issue of Gut brings new aspects into the natural history of coeliac disease (see page 1379). They studied 61 adult patients who had had the diagnosis of coeliac disase in childhood, and who had regarded themselves as asymptomatic despite remaining on a gluten-containing diet for 11 years (median, range 3–21 years). In the follow-up examination, 48 out of these 61 patients had, as expected, developed small bowel mucosal villous atrophy with crypt hyperplasia; 70% of them were also suffering from osteopenia or osteoporosis, which may well have been due to untreated coeliac disease. However, the remaining 13 patients showed normal small bowel mucosal morphology. Surprisingly, two out of the 13 patients evinced mucosal atrophy shortly after the beginning of the gluten challenge, but their mucosa eventually normalised when the gluten ingestion continued. The authors concluded that there might be some patients with coeliac disease who may develop true latency and tolerance against dietary gluten.

The current diagnostic criteria of coeliac disease require the presence of small intestinal mucosal villous atrophy …