TY - JOUR
T1 - Gluten-sensitive disease with mild enteropathy
AU - Picarelli, A.
AU - Maiuri, L.
AU - Mazzilli, M. C.
AU - Coletta, S.
AU - Ferrante, P.
AU - Di Giovambattista, F.
AU - Greco, M.
AU - Torsoli, A.
AU - Auricchio, S.
PY - 1996
Y1 - 1996
N2 - Background and Aims: Celiac disease is a permanent gluten intolerance strongly associated with HLA class II antigens and possibly showing milder changes of mucosal architecture. Ten patients with symptoms suggesting celiac disease and serum antiendomysium antibodies with normal mucosal architecture were studied. Methods: Immunohistochemical detection of mucosal immune activation and HLA typings were performed. Results: Mucosal immune activation, with normal mucosal architecture and normal τ/δ+ intraepithelial lymphocytes counts, was found on a gluten-containing diet. In 3 of 6 patients, multiple biopsy specimens showed one sample with severe villous atrophy. Clinical and immunomorphologic features were strictly gluten dependent. The mucosal immune activation was elicited in vitro by gliadin. Only 4 patients had the typical HLA typing of celiac disease. Conclusions: Gluten-sensitive celiac-like symptoms may occur in patients with serum antiendomysium antibodies, apparently normal intestinal mucosa, and HLA typing not commonly associated with celiac disease. These patients should undergo multiple biopsies, and signs of immunologic activation should be sought accurately; in the presence of mucosal immune activation, a trial with a gluten-free diet should be encouraged to detect gluten dependency. In vitro immunologic response of small intestinal mucosa to gliadin may support the diagnosis of gluten-sensitive enteropathy.
AB - Background and Aims: Celiac disease is a permanent gluten intolerance strongly associated with HLA class II antigens and possibly showing milder changes of mucosal architecture. Ten patients with symptoms suggesting celiac disease and serum antiendomysium antibodies with normal mucosal architecture were studied. Methods: Immunohistochemical detection of mucosal immune activation and HLA typings were performed. Results: Mucosal immune activation, with normal mucosal architecture and normal τ/δ+ intraepithelial lymphocytes counts, was found on a gluten-containing diet. In 3 of 6 patients, multiple biopsy specimens showed one sample with severe villous atrophy. Clinical and immunomorphologic features were strictly gluten dependent. The mucosal immune activation was elicited in vitro by gliadin. Only 4 patients had the typical HLA typing of celiac disease. Conclusions: Gluten-sensitive celiac-like symptoms may occur in patients with serum antiendomysium antibodies, apparently normal intestinal mucosa, and HLA typing not commonly associated with celiac disease. These patients should undergo multiple biopsies, and signs of immunologic activation should be sought accurately; in the presence of mucosal immune activation, a trial with a gluten-free diet should be encouraged to detect gluten dependency. In vitro immunologic response of small intestinal mucosa to gliadin may support the diagnosis of gluten-sensitive enteropathy.
UR - http://www.scopus.com/inward/record.url?scp=0029831409&partnerID=8YFLogxK
U2 - 10.1053/gast.1996.v111.pm8780564
DO - 10.1053/gast.1996.v111.pm8780564
M3 - Article
SN - 0016-5085
VL - 111
SP - 608
EP - 616
JO - Gastroenterology
JF - Gastroenterology
IS - 3
ER -