IBS is the most common intestinal disorder in our society, and is characterized by abdominal pain and altered bowel habit in the absence of an underlying structural abnormality. IBS is often diagnosed by the costly exclusion of other diseases, which may include celiac disease” a chronic enteropathy triggered by gluten in persons with genetic predisposition. Despite an estimated worldwide prevalence of 1 percent, and the availability of specific diagnostic serological and pathological algorithms, celiac disease remains significantly underdiagnosed. When screening is actively undertaken by specific serology and biopsy, 4 percent of patients labeled as having IBS have underlying celiac disease, but this often goes undetected.1 Moreover, the burden and morbidity caused to those who suffer from the disease is underestimated. Since IBS is a symptomatic complex, in the absence of any discernible organic cause, a diagnosis of celiac disease should exclude IBS.
Once a clear diagnosis of celiac disease is established, the only current available treatment is a gluten-free diet for life, which is usually effective in improving symptoms and inducing mucosal recovery. However, the gluten-free diet is hardly an optimal therapy, and a substantial proportion of patients remain symptomatic despite efforts to adhere to the diet. This often relates to inadvertent or voluntary dietary transgressions in a substantial proportion of patients. One of the most common causes of persistent symptoms relates to continuous gluten exposure. Indeed, this has been reported in approximately 70 percent of celiac disease patients on a gluten-free diet.1,2 Until a pharmacological therapy that targets this patient population is approved and available, the best we can offer is medical follow up to rule out complications of celiac disease and true refractory cases, and professional dietary advice.
Although there are many possible causes for persistent symptoms in celiac patients who are on a gluten-free diet, an overlap with IBS has been proposed once other potential causes are ruled out. Such overlap should fall within the definition of IBS, and requires the exclusion of significant persistent mucosal inflammation or any other organic disease, food allergy or intolerance that could justify the symptoms. One of the proposed underlying pathways for symptom generation in IBS is low-grade inflammation, which could be induced by multiple stimuli including sensitivity to dietary components or infectious gastroenteritis. The same concept may apply to mucosal recovery after initiation of the gluten-free diet in celiac disease, and thus the residual low-grade inflammation might be associated with persistent symptomatology in some patients. This post-celiac IBS condition could eventually resolve or be perpetuated by other stimuli.
The question of whether there is true overlap between celiac disease in resolution and IBS onset cannot be clearly answered thus far.
The question of whether there is true overlap between celiac disease in resolution and IBS onset cannot be clearly answered thus far, but it is reminiscent of the association between IBS in patients with inflammatory bowel disease.3 There is ample basic research evidence that inflammation impairs intestinal motor and sensory systems, altering gut function that can lead to symptom generation. Microscopic and functional rewiring of the neuromotor system of the upper gut after years of gluten exposure and inflammation in a celiac patient could explain some persistent symptomatology despite the gluten-free diet.
Finally, although basic research and emerging clinical reports suggest there could be a true overlap of IBS and celiac disease, the management of symptomatic celiac patients on a gluten-free diet should include more than a potential diagnosis of IBS. We must bear in mind that an IBS diagnosis is based on exclusion of organic causes, and therefore potential gluten exposure or contamination, true refractory cases and other overlapping diseases need to be ruled out first.
Dr. Verdu has received grant support from Nestle. She is a member of the Rome Foundation, the Canadian Association of Gastroenterology, and serves on the research committee and is the president elect of the North American Society for the Study of Celiac Disease.
1. Ford AC, Chey WD, Talley NJ, Malhotra A, Spiegel BM, Moayyedi P. Yield of diagnostic tests for celiac disease in individuals with symptoms suggestive of irritable bowel syndrome: systematic review and meta-analysis. Arch Intern Med. 2009. Apr 13;169(7):651-8.
2. N.J.Hall,G.P.Rubin,A.Charnock.Intentionaland inadvertentnon-adherenceinadultcoeliacdisease.A cross-sectional survey. Appetite, 68 (2013), pp. 56″62.
3. Halpin SJ, Ford AC. Prevalence of symptoms meeting criteria for irritable bowel syndrome in in ammatory bowel disease: systematic review and meta-analysis. Am J Gastroenterol. 2012 Oct;107(10):1474-82. doi: 10.1038/ajg.2012.260.