title: [Latent celiac disease in subjects with serum anti-endomysial antibodies and normal intestinal biopsy].
abstract: OBJECTIVE
  Data on the follow-up of a group of subjects with serum antiendomysial antibodies (EMA) and normal mucosal architecture at the intestinal biopsy are reported. Clinical problems concerning possible evolution of potential celiac disease (CD) towards gluten-induced histological damage are discussed.
  
  
  METHODS
  Eleven patients belonging to high-risk groups for CD (5 with type-1 diabetes, 2 with familiarity for CD and 4 with symptoms suggesting CD) who had a normal intestinal biopsy, despite positive antiendomysial test, were followed-up. Antigliadin and antitransglutaminase antibodies (anti-tTG) and HLA genotyping were also assessed. According to clinical and serological data a second biopsy was performed in six of them.
  
  
  RESULTS
  At the time of the first normal biopsy, all patients were positive for EMA and 5/8 for anti-tTG. Five of 6 subjects genotyped were HLA-DQ2+ or DQ8+. Six patients were rebiopsed after 1 to 4 years. Three had mucosal atrophy, 1 had mild increase of intraepithelial lymphocytes and 2 were morphologically normal.
  
  
  CONCLUSIONS
  Subjects with antiendomysial antibodies and normal intestinal biopsy deserve clinical and serological follow-up to reduce the time of possible latency of CD. Although good predictors of progression of the disease are not still available, antiendomysial antibodies assessment and HLA genotyping may help to suggest individuals at higher risk to develop gluten-induced enteropathy. This study confirms that subjects with persistent signs of gluten sensitivity and normal biopsy should be re-examined.
authors.affiliation: Dipartimento Materno-Infantile e di Biologia e Genetica, Sezione di Pediatria, Università di Verona, Verona, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Piccoli
authors.forename: P
authors.initials: P
authors.lastname: Capelli
authors.forename: A
authors.initials: A
authors.lastname: Castagnini
authors.forename: M
authors.initials: M
authors.lastname: Cipolli
authors.forename: G
authors.initials: G
authors.lastname: Contreas
authors.forename: D
authors.initials: D
authors.lastname: Ulmi
authors.forename: G
authors.initials: G
authors.lastname: Zanoni
authors.forename: E
authors.initials: E
authors.lastname: Valletta
mesh_terms: D000293:Adolescent; D000328:Adult; D000906:Antibodies / Q000097:blood / Q000276:immunology*; D001323:Autoantibodies / Q000097:blood / Q000276:immunology*; D001706:Biopsy; D002446:Celiac Disease / Q000097:blood* / Q000201:enzymology / Q000276:immunology*; D002648:Child; D002675:Child, Preschool; D005260:Female; D005903:Gliadin / Q000276:immunology; D005983:Glutens / Q000276:immunology; D006683:HLA-DQ Antigens / Q000235:genetics / Q000276:immunology; D006801:Humans; D007070:Immunoglobulin A / Q000276:immunology; D007422:Intestines / Q000473:pathology*; D008297:Male; D018485:Muscle Fibers, Skeletal / Q000276:immunology; D012680:Sensitivity and Specificity; D011503:Transglutaminases / Q000276:immunology / Q000378:metabolism
chemical_list: D000906:Antibodies; D001323:Autoantibodies; D006683:HLA-DQ Antigens; C053186:HLA-DQ2 antigen; D007070:Immunoglobulin A; D005983:Glutens; D005903:Gliadin; D011503:Transglutaminases