OBJECTIVE: Endomysial antibodies (EMAs) had been found recently after in vitro gluten challenge of duodenal mucosa from treated celiac patients. This was a promising result for diagnosis of potential/latent celiac disease. Therefore, we tested the usefulness of the production of EMAs of in vitro-challenged mucosa for diagnosis of celiac disease and determined the location of EMA production. METHODS: We investigated EMAs in the serum, in the supernatants of in vitro gliadin-challenged duodenal mucosa specimens in 68 patients, and in homogenized native duodenal and gastric specimens in seven patients. Twenty-one of the 68 patients served as nonceliac controls, 11 as candidates for potential celiac disease, 23 celiac patients were on glutenfree diet, and 13 were newly diagnosed. RESULTS: EMAs were just found in the supernatants of duodenal biopsies of those celiac patients who had demonstrable EMAs in serum, independent of gliadin challenge. In these patients EMAs were also found in homogenized native duodenal biopsies, but not in gastric biopsies. CONCLUSIONS: EMAs seem to be produced in the small bowel mucosa of celiac patients, but not in other tissues such as gastric mucosa. The production of EMAs could not be initiated under standard in vitro conditions and therefore, such as in vitro challenge cannot be used for diagnostic purposes.
OBJECTIVE: Endomysial antibodies (EMAs) had been found recently after in vitro gluten challenge of duodenal mucosa from treated celiac patients. This was a promising result for diagnosis of potential/latent celiac disease. Therefore, we tested the usefulness of the production of EMAs of in vitro-challenged mucosa for diagnosis of celiac disease and determined the location of EMA production. METHODS: We investigated EMAs in the serum, in the supernatants of in vitro gliadin-challenged duodenal mucosa specimens in 68 patients, and in homogenized native duodenal and gastric specimens in seven patients. Twenty-one of the 68 patients served as nonceliac controls, 11 as candidates for potential celiac disease, 23 celiac patients were on glutenfree diet, and 13 were newly diagnosed. RESULTS: EMAs were just found in the supernatants of duodenal biopsies of those celiac patients who had demonstrable EMAs in serum, independent of gliadin challenge. In these patients EMAs were also found in homogenized native duodenal biopsies, but not in gastric biopsies. CONCLUSIONS: EMAs seem to be produced in the small bowel mucosa of celiac patients, but not in other tissues such as gastric mucosa. The production of EMAs could not be initiated under standard in vitro conditions and therefore, such as in vitro challenge cannot be used for diagnostic purposes.
Authors: A Tosco; R Aitoro; R Auricchio; D Ponticelli; E Miele; F Paparo; L Greco; R Troncone; M Maglio Journal: Clin Exp Immunol Date: 2013-01 Impact factor: 4.330
Authors: L Maiuri; C Ciacci; V Raia; L Vacca; I Ricciardelli; F Raimondi; S Auricchio; S Quaratino; M Londei Journal: Gut Date: 2001-03 Impact factor: 23.059
Authors: Satumarja M Stenman; Katri Lindfors; Ilma R Korponay-Szabo; Olli Lohi; Päivi Saavalainen; Jukka Partanen; Katri Haimila; Herbert Wieser; Markku Mäki; Katri Kaukinen Journal: BMC Immunol Date: 2008-02-29 Impact factor: 3.615