title: Lymphocytic duodenosis: aetiology and long-term response to specific treatment.
abstract: BACKGROUND
  The clinical significance of lymphocytic duodenosis remains unclear.
  
  
  OBJECTIVE
  To prospectively assess the aetiology of lymphocytic duodenosis and the patterns of clinical presentation.
  
  
  METHODS
  Ninety consecutive patients with lymphocytic duodenosis and clinical symptoms of the coeliac disease spectrum were prospectively included. All subjects underwent serological testing and HLA genotyping for coeliac disease, assessment of Helicobacter pylori infection, and parasite stool examination. Intake of non-steroidal anti-inflammatory drugs was also recorded. The final aetiology of lymphocytic duodenosis was evaluated on the basis of the long-term response to specific therapy.
  
  
  RESULTS
  More than one initial potential aetiology was observed in 44% of patients. The final diagnosis was gluten-sensitive enteropathy alone or associated with Helicobacter pylori infection in 43.3%, Helicobacter pylori infection (without gluten-sensitive enteropathy) in 24.4%, non-steroidal anti-inflammatory drugs intake in 5.5%, autoimmune disease in 3.3%, and parasitic infection in 2.2%. Among first degree relatives and patients with chronic diarrhoea, the most common final diagnosis was gluten-sensitive enteropathy. In contrast, in the group presenting with chronic dyspepsia the most common diagnosis was Helicobacter pylori infection ('Diarrhoea' vs 'Dyspepsia' groups, p=0.008).
  
  
  CONCLUSIONS
  Lymphocytic duodenosis is often associated with more than one potential initial aetiology. Clinical presentation may be useful to decide the initial therapeutic approach with these patients.
authors.affiliation: Department of Gastroenterology, Hospital Universitari Mutua Terrassa, University of Barcelona, Plaza Dr. Robert 5, Terrassa, Catalonia, Spain.
authors.forename: Mercé
authors.initials: M
authors.lastname: Rosinach
authors.forename: Maria
authors.initials: M
authors.lastname: Esteve
authors.forename: Clarisa
authors.initials: C
authors.lastname: González
authors.forename: Rocio
authors.initials: R
authors.lastname: Temiño
authors.forename: Meritxell
authors.initials: M
authors.lastname: Mariné
authors.forename: Helena
authors.initials: H
authors.lastname: Monzón
authors.forename: Empar
authors.initials: E
authors.lastname: Sainz
authors.forename: Carme
authors.initials: C
authors.lastname: Loras
authors.forename: Jorge C
authors.initials: JC
authors.lastname: Espinós
authors.forename: Montse
authors.initials: M
authors.lastname: Forné
authors.forename: Josep M
authors.initials: JM
authors.lastname: Viver
authors.forename: Antonio
authors.initials: A
authors.lastname: Salas
authors.forename: Fernando
authors.initials: F
authors.lastname: Fernández-Bañares
mesh_terms: D000328:Adult; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects; D001327:Autoimmune Diseases / Q000150:complications; D016776:Blastocystis Infections / Q000150:complications; D017252:CD3 Complex / Q000378:metabolism; D002446:Celiac Disease / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D004378:Duodenal Diseases / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D005260:Female; D019204:GTP-Binding Proteins; D005838:Genotype; D006683:HLA-DQ Antigens / Q000235:genetics; D016481:Helicobacter Infections / Q000150:complications*; D016480:Helicobacter pylori; D006801:Humans; D018655:Lymphocyte Count; D008214:Lymphocytes / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D000091345:Protein Glutamine gamma Glutamyltransferase 2; D011503:Transglutaminases / Q000276:immunology
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D017252:CD3 Complex; D006683:HLA-DQ Antigens; C053186:HLA-DQ2 antigen; C109756:HLA-DQ8 antigen; D000091345:Protein Glutamine gamma Glutamyltransferase 2; D011503:Transglutaminases; D019204:GTP-Binding Proteins