title: Coeliac disease hidden by cryptogenic hypertransaminasaemia.
abstract: BACKGROUND
  Hypertransaminasaemia of unknown, cryptogenic, origin occasionally has been found to be the only sign of coeliac disease. Raised concentrations of transaminases, or aminotransferases, have been retrospectively observed in about a half of patients with coeliac disease who are on a gluten-containing diet. We aimed to establish the overall prevalence of coeliac disease among patients with cryptogenic hypertransaminasaemia.
  
  
  METHODS
  Of the 600 consecutive patients referred to our outpatient clinic for liver disease due to raised serum transaminases from September, 1995, to June, 1997, 55 were classified as having cryptogenic hypertransaminasaemia after the exclusion of every known cause of liver disease. These patients were tested by indirect immunofluorescence for IgA to endomysium and for IgA and IgG to gliadin.
  
  
  RESULTS
  Five patients were positive for both IgA to endomysium and IgG to gliadin, whereas IgA to gliadin was only found in four patients. IgG to gliadin was also present in another patient who was not positive for antibodies to endomysium. The six antibody-positive patients had duodenal biopsy that showed a subtotal villous atrophy consistent with coeliac disease in the five patients with antibodies to endomysium. The patient with only IgG to gliadin had a normal small-intestine mucosa. None of the five patients with coeliac disease had gastrointestinal symptoms. Liver biopsy samples were taken from three of the five patients with flat mucosa and showed a histological picture of nonspecific reactive hepatitis. Transaminase concentrations reverted to normal within 6 months in four patients with coeliac disease who followed a strict gluten-free diet.
  
  
  CONCLUSIONS
  Our results show that about 9% of patients with cryptogenic hypertransaminasaemia are affected by symptom-free coeliac disease. Gluten-sensitive enteropathy and antibody screening for coeliac disease by means of antibodies to endomysium and gliadin should be considered in these patients.
authors.affiliation: Department of Internal Medicine Cardioangiology, Hepatology, University of Bologna, Policlinic S Orsola-Malpighi, Italy.
authors.forename: U
authors.initials: U
authors.lastname: Volta
authors.forename: L
authors.initials: L
authors.lastname: De Franceschi
authors.forename: F
authors.initials: F
authors.lastname: Lari
authors.forename: N
authors.initials: N
authors.lastname: Molinaro
authors.forename: M
authors.initials: M
authors.lastname: Zoli
authors.forename: F B
authors.initials: FB
authors.lastname: Bianchi
mesh_terms: D000328:Adult; D002446:Celiac Disease / Q000201:enzymology*; D005260:Female; D019084:Fluorescent Antibody Technique, Indirect; D005903:Gliadin / Q000276:immunology; D006801:Humans; D007070:Immunoglobulin A / Q000032:analysis; D007074:Immunoglobulin G / Q000032:analysis; D008297:Male; D018485:Muscle Fibers, Skeletal / Q000276:immunology; D012189:Retrospective Studies; D000637:Transaminases / Q000097:blood*
chemical_list: D007070:Immunoglobulin A; D007074:Immunoglobulin G; D005903:Gliadin; D000637:Transaminases