title: Gluten sensitive enteropathy in patients with iron deficiency anemia of unknown origin.
abstract: OBJECTIVE
  To determine the prevalence of gluten sensitive enteropathy (GSE) in a large group of patients with iron deficiency anemia (IDA) of obscure origin.
  
  
  METHODS
  In this cross-sectional study, patients with IDA of obscure origin were screened for GSE. Anti-endomysial antibody (EMA) and tissue transglutaminase antibody (tTG) levels were evaluated and duodenal biopsies were taken and scored according to the Marsh classification. The diagnosis of GSE was based on a positive serological test and abnormal duodenal histology. Gluten free diet (GFD) was advised for all the GSE patients.
  
  
  RESULTS
  Of the 4120 IDA patients referred to our Hematology departments, 206 (95 male) patients were found to have IDA of obscure origin. Thirty out of 206 patients (14.6%) had GSE. The mean age of GSE patients was 34.6 +/- 17.03 (range 10-72 years). The female to male ratio was 1.3:1. Sixteen patients had Marsh 3, 12 had Marsh 2, and 2 had Marsh 1 lesions. The severity of anemia was in parallel with the severity of duodenal lesions. Twenty-two GSE patients (73.3%) had no gastrointestinal symptoms. Fourteen GSE patients who adhered to GFD without receiving iron supplementation agreed to undergo follow up visits. After 6 mo of GFD, their mean hemoglobin levels (Hb) increased from 9.9 +/- 1.6 to 12.8 +/- 1.0 g/dL (P < 0.01). Interestingly, in 6 out of 14 patients who had Marsh 1/2 lesions (e.g. no villous atrophy) on duodenal biopsy, mean Hb increased from 11.0 +/- 1.1 to 13.1 +/- 1.0 g/dL (P < 0.01) while they did not receive any iron supplementation.
  
  
  CONCLUSIONS
  There is a high prevalence (e.g. 14.6%) of GSE in patients with IDA of obscure origin. Gluten free diet can improve anemia in GSE patients who have mild duodenal lesions without villous atrophy.
authors.affiliation: Gastrointestinal and Liver Disease Research Center, Iran University of Medical Sciences, Tehran, Iran.
authors.forename: Farhad
authors.initials: F
authors.lastname: Zamani
authors.forename: Mehdi
authors.initials: M
authors.lastname: Mohamadnejad
authors.forename: Ramin
authors.initials: R
authors.lastname: Shakeri
authors.forename: Afsaneh
authors.initials: A
authors.lastname: Amiri
authors.forename: Safa
authors.initials: S
authors.lastname: Najafi
authors.forename: Seyed-Meysam
authors.initials: SM
authors.lastname: Alimohamadi
authors.forename: Seyed-Mohamad
authors.initials: SM
authors.lastname: Tavangar
authors.forename: Ardeshir
authors.initials: A
authors.lastname: Ghavamzadeh
authors.forename: Reza
authors.initials: R
authors.lastname: Malekzadeh
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D018798:Anemia, Iron-Deficiency / Q000150:complications* / Q000175:diagnosis / Q000453:epidemiology*; D000906:Antibodies / Q000097:blood; D001706:Biopsy; D002446:Celiac Disease / Q000150:complications* / Q000175:diagnosis / Q000453:epidemiology*; D002648:Child; D003430:Cross-Sectional Studies; D004386:Duodenum / Q000473:pathology; D005260:Female; D006801:Humans; D007070:Immunoglobulin A / Q000097:blood; D007492:Iran / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D011446:Prospective Studies; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D011503:Transglutaminases / Q000276:immunology; D055815:Young Adult
chemical_list: D000906:Antibodies; D007070:Immunoglobulin A; D011503:Transglutaminases