Article Text

Download PDFPDF
TGFα-associated MUC2 and MUC3 expression of the gastric epithelium in Ménétrier's disease during remission of ulcerative colitis
  1. Klaus-Peter Zimmer1,
  2. Martin Heine2,
  3. Gabriele Weissen-Plenz3,
  4. Kristine Anna Scholand1,
  5. Hermann Herbst4,
  6. Hassan Y Naim2
  1. 1Department of Pediatrics and Neonatology, Justus-Liebig-University of Giessen, Giessen, Germany
  2. 2Department of Physiological Chemistry, University of Veterinary Medicine Hannover, Hannover, Germany
  3. 3Leibniz Institute for Arteriosclerosis Research, University of Münster, Münster, Germany
  4. 4Fachbereich Pathologie, Vivantes Klinikum Am Urban, Berlin, Germany
  1. Correspondence to Professor Hassan Y Naim, Department of Physiological Chemistry, University of Veterinary Medicine Hannover, Hannover D-30559, Germany; hassan.naim{at}

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

The broad clinical heterogeneity of Ménétrier's disease (MD) has been recently described by Rich et al.1 There are few reports on MD patients with a history of ulcerative colitis (UC). Overexpression of the transforming growth factor α (TGFα) leads to gastric epithelium abnormalities similar to those of MD.2 A significant increase in TGFα levels has been observed in inactive UC compared with healthy controls. TGFα could be the link between both inactive UC and the development of MD.

TGFα stimulates gastric cell proliferation as well as mucin biosynthesis. Normal gastric mucosa expresses MUC1 and MUC5Ac in foveolar epithelium and MUC6 in the glands, while MUC2 and MUC3 are predominantly expressed in goblet cells and enterocytes, respectively, of the small intestine.

We investigated mucin expression in …

View Full Text


  • Disclosure of funding: All authors disclosed no financial relationships relevant to this publication.

  • Funding German Research Council.

  • Competing interests None.

  • Patient consent Obtained.

  • Ethics approval This study was conducted with the approval of the University of Münster.

  • Provenance and peer review Not commissioned; not externally peer reviewed.