OBJECTIVES: Serum antiendomysial antibodies (EMAs), highly sensitive and specific serological markers of celiac disease (CD), are detectable in culture media of biopsy samples from CD patients. This finding can be considered an in vitro evidence that intestinal mucosa is a site of EMA production. To confirm this finding, we investigated the presence of EMAs and of anti-tissue transglutaminase (anti-tTG), recently identified as the autoantigen of the EMA, in fecal supernatants of CD patients. METHODS: Twenty-one newly diagnosed CD patients, 10 treated CD patients on a gluten-free diet, and 14 control disease patients on a gluten-containing diet were enrolled. Twenty-four-hour stool collections and fecal supernatants were obtained from all patients in the study. Biopsy cultures were also performed. IgA EMAs were detected in sera, culture media, and fecal supernatants. IgA, IgG, IgM, and IgE anti-gliadin antibodies (AGAs) and IgA anti-tTG antibodies were measured in fecal supernatants. The weights, water content, and pHs of the 24-h stool collections were also measured. RESULTS: In all untreated CD patients EMAs were detectable in sera, culture media, and fecal supernatants. In treated CD patients, EMAs were detected only in culture media after in vitro gliadin challenge. No EMAs were detected in controls. Anti-tTG levels were higher in untreated CD patients than in treated CD patients and controls. IgA AGA levels were higher in untreated CD patients than in treated CD and control patients, whereas IgM AGAs were higher in both untreated and treated CD patients than in controls. No statistically significant differences were observed for IgG and IgE AGAs among the above-mentioned populations. Fecal weights, water content, and pHs were higher in untreated CD than in control patients. CONCLUSIONS: The presence of EMAs in fecal supernatants represents the in vivo proof that intestinal mucosa is a site of EMA production. Furthermore, EMA detection in the stools could be a simple and useful additional tool to clarify diagnosis in the patchy conditions of CD.
OBJECTIVES: Serum antiendomysial antibodies (EMAs), highly sensitive and specific serological markers of celiac disease (CD), are detectable in culture media of biopsy samples from CDpatients. This finding can be considered an in vitro evidence that intestinal mucosa is a site of EMA production. To confirm this finding, we investigated the presence of EMAs and of anti-tissue transglutaminase (anti-tTG), recently identified as the autoantigen of the EMA, in fecal supernatants of CDpatients. METHODS: Twenty-one newly diagnosed CDpatients, 10 treated CDpatients on a gluten-free diet, and 14 control disease patients on a gluten-containing diet were enrolled. Twenty-four-hour stool collections and fecal supernatants were obtained from all patients in the study. Biopsy cultures were also performed. IgA EMAs were detected in sera, culture media, and fecal supernatants. IgA, IgG, IgM, and IgE anti-gliadin antibodies (AGAs) and IgA anti-tTG antibodies were measured in fecal supernatants. The weights, water content, and pHs of the 24-h stool collections were also measured. RESULTS: In all untreated CDpatients EMAs were detectable in sera, culture media, and fecal supernatants. In treated CDpatients, EMAs were detected only in culture media after in vitro gliadin challenge. No EMAs were detected in controls. Anti-tTG levels were higher in untreated CDpatients than in treated CDpatients and controls. IgA AGA levels were higher in untreated CDpatients than in treated CD and control patients, whereas IgM AGAs were higher in both untreated and treated CDpatients than in controls. No statistically significant differences were observed for IgG and IgE AGAs among the above-mentioned populations. Fecal weights, water content, and pHs were higher in untreated CD than in control patients. CONCLUSIONS: The presence of EMAs in fecal supernatants represents the in vivo proof that intestinal mucosa is a site of EMA production. Furthermore, EMA detection in the stools could be a simple and useful additional tool to clarify diagnosis in the patchy conditions of CD.
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: A Tosco; R Auricchio; R Aitoro; D Ponticelli; M Primario; E Miele; V Rotondi Aufiero; V Discepolo; L Greco; R Troncone; M Maglio Journal: Clin Exp Immunol Date: 2014-09 Impact factor: 4.330
Authors: Antonio Picarelli; Marco Di Tola; Raffaele Borghini; Claudia Isonne; Annarita Saponara; Mariacatia Marino; Rossella Casale; Antonio Tiberti; Roberta Pica; Giuseppe Donato; Giuseppe Frieri; Enrico Corazziari Journal: J Clin Immunol Date: 2013-07-06 Impact factor: 8.317