Human Pathology
Volume 41, Issue 11 , Pages 1593-1600, November 2010

Gastric foveolar metaplasia and gastric heterotopia in the duodenum: no evidence of an etiologic role for Helicobacter pylori

  • Robert M. Genta, MD

      Affiliations

    • Caris Diagnostics, Gastrointestinal Pathology, Irving, TX 75039, USA
    • Dallas VAMC and University of Texas Southwestern medical Center, Dallas, TX 75016, USA
    • Corresponding Author InformationCorresponding author. Caris Diagnostics, Irving, TX 75039, USA.
  • ,
  • R. Shawn Kinsey, MD

      Affiliations

    • Caris Diagnostics, Gastrointestinal Pathology, Irving, TX 75039, USA
  • ,
  • Anuradha Singhal, MD

      Affiliations

    • Caris Diagnostics, Gastrointestinal Pathology, Irving, TX 75039, USA
  • ,
  • Smita Suterwala, MD

      Affiliations

    • Caris Diagnostics, Gastrointestinal Pathology, Irving, TX 75039, USA

Received 14 January 2010; received in revised form 10 April 2010; accepted 15 April 2010. published online 26 July 2010.

Summary 

Gastric-type epithelium and islands of oxyntic mucosa in duodenal biopsies are considered by some to be part of a spectrum of metaplastic change related to peptic disorders. This study was designed to assess prevalence and associations of metaplastic-heterotopic gastric mucosa in the duodenum. Demographic, clinical, and histopathologic data from patients who had duodenal biopsy specimens for a 12-month period were collected from a national database. The duodenal findings of patients with duodenitis, gastric metaplasia, and gastric heterotopia were correlated with gastric pathology, Helicobacter pylori status, and clinical information. Of 28 210 patients with duodenal biopsy specimens, 80.9% were healthy, 2.1% had active duodenitis, 2.2% gastric foveolar metaplasia without active inflammation (“peptic duodenopathy”), 4.8% gastric foveolar metaplasia with active inflammation (“peptic duodenitis”), and 1.9% gastric heterotopia. Helicobacter pylori was documented in 9.8% of patients with normal duodenum, 6.9% of those with gastric metaplasia without active inflammation, 15.8% of those with active duodenitis, and 29.1% of those with gastric foveolar metaplasia with active inflammation; 2.2% of 543 patients with gastric heterotopia had H pylori gastritis. Helicobacter pylori was detected in the metaplastic epithelium of 67.6% of patients with active inflammation and in 16.4% of those with metaplasia without inflammation. Gastric heterotopia was strongly associated with concurrent fundic gland polyps. In conclusion, active duodenitis was more common in patients with H pylori infection, but gastric metaplasia was not. We suggest that there is insufficient evidence to ascribe duodenitis with foveolar metaplasia to a “peptic” disorder, as “peptic duodenopathy” and “peptic duodenitis” seem to imply. Gastric heterotopia is likely a congenital lesion; its association with fundic gland polyps suggests that use of proton pump inhibitors may enhance its endoscopic detection.

Keywords: Duodenitis, Duodenopathy, Gastric heterotopia, Duodenal disease, Helicobacter pylori, Gastric metaplasia, Peptic disorders

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 This work was not supported by external funding; the authors are entirely responsible for the conception and execution of the study and for writing the article. None of the authors declares any conflict of interest regarding the contents of this article.

PII: S0046-8177(10)00142-5

doi:10.1016/j.humpath.2010.04.010

Human Pathology
Volume 41, Issue 11 , Pages 1593-1600, November 2010