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

Abstract

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.