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Study Shows that Celiac-associated Intestinal Degradation May Take Years to Show Up after Reintroducing Gluten into the Diet
Jefferson Adams is a freelance writer living in San Francisco. His poems, essays and photographs have appeared in Antioch Review, Blue Mesa Review, CALIBAN, Hayden's Ferry Review, Huffington Post, the Mississippi Review, and Slate among others.
He is a member of both the National Writers Union, the International Federation of Journalists, and covers San Francisco Health News for Examiner.com.View all articles by Jefferson Adams
Celiac.com 10/30/2007 - Many studies over the years have supported the idea that celiac disease is a permanent condition, and that those who strayed from the strict gluten-free diet that forms the core of celiac treatment risked relapsing and suffering the telltale intestinal damage associated with celiac disease. However, it was generally assumed that symptoms of celiac disease and associated intestinal degradation occurred within two years of reintroducing gluten back into the diet.
The medical journal GUT recently published a paper by Matysiak-Budnik et al. concerning the natural history of celiac disease, which indicates that classic celiac damage to the intestinal lining may take years or decades to develop in some cases. A team of researchers looked at 61 adults who had been diagnosed with celiac disease as children, and who felt themselves to be asymptomatic for anywhere from 3 to 21 years, with a group average of 11 years. An exam revealed that 48 of the 61 test subjects indeed showed villous atrophy with crypt hypoplasia. The 13 other patients showed no celiac-associated intestinal damage.
Strangely, 2 of the 13 patients with no signs of damage had showed such damage a short time after gluten was reintroduced into their diets, only to return to normal as they continued to consume gluten. From this, the researchers concluded that some people might actually become truly latent and tolerate gluten with no adverse effects. It’s also possible that such people actually still have celiac disease and that the intestinal damage has yet to recur, as villous atrophy occurs only at the tail end of celiac disease.
In fact, delayed relapse of celiac disease after gluten reintroduction supports the notion that people with normal mucosa may in fact have celiac disease. Still, it is highly uncommon for patients with celiac disease to show no clinical symptoms on a long-term gluten-inclusive diet. The level of CD+ intraepithelial lymphocytes has proven to be more useful than mucosal Marsh Type 1 lymphocytes in revealing early developing celiac disease in such cases and in general.
Reliable diagnosis of celiac disease is important, as untreated celiac disease carries a broad range of associated risks including markedly higher rates of certain cancers. A recent study also suggests celiac disease may also adversely impact both the peripheral the central nervous systems.
However, regarding the 13 asymptomatic patients, the original diagnosis of celiac would seem to be accurate in each case, as each had celiac-type HLA, either HLA DQ2 or DQ8, and their follow-up exam results showed that 5 of those patients had positive serum antibody results and higher densities of small bowel mucosa CD+ and CD3+ intraepithelial lymphocytes than did the non-celiac control groups. Two of the 13 patients developed symptoms of a relapse during the follow-up.
The study team concluded that the “2 year rule” for reintroducing gluten is invalid and supports the view that celiac disease exists beyond villous atrophy. As villous atrophy of the small intestine is only one manifestation of genetic gluten intolerance, and that the present diagnostic guidelines based on mucosal damage and ignoring early developing celiac disease and dermatitis herpetiformis is only one incarnation of celiac disease.
GUT 2007; 56:1339-1340
Katri Kaukinen, Pekka Collin, Medical School, University of Tampere and Department of Gastroenterology and Alimentary Tract Surgery, Tampere University Hospital, Tampere, Finland Markku Ma¨ki, Medical School, University of Tampere and Department of Paediatrics, Tampere University Hospital, Tampere, Finland
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