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Re-evaluation of "Peptic" duodenitis: A review of 622 consecutive duodenal biopsies
Mohamed E Mostafa1, Christopher P Hartley2, Catherine E Hagen2
1Department of Pathology, Banner University Medical Center, Phoenix, AZ, 85006, USA.
Abstract:
"Peptic" duodenitis, classically attributed to peptic injury including Helicobacter pylori infection, comprises foveolar (gastric) metaplasia of the surface duodenal epithelium and Brunner gland hyperplasia. Despite a declining prevalence of H. pylori, duodenal foveolar metaplasia (FM) remains a common biopsy finding and may be encountered in endoscopically normal mucosa from asymptomatic patients. To determine its prevalence, clinicopathologic associations, and likely etiology, we reviewed 622 consecutive duodenal biopsies obtained over a 5-month period. Slides were reviewed by two gastrointestinal pathologists for FM, Brunner gland hyperplasia (BGH), gastric heterotopia, acute inflammation, lamina propria expansion, increased intraepithelial lymphocytes, and villous blunting; clinical data and corresponding gastric biopsies were also reviewed. Of 622 patients (M: F 1: 2; median age 54 years), 174 (28.0%) had duodenal FM. FM was more common in male patients (39.4% vs. 22.2%, p < 0.0001) and was associated with an abnormal endoscopic appearance, gastric heterotopia, acute inflammation, BGH, lamina propria expansion, and villous blunting (all p ≤ 0.005). FM was not associated with H. pylori on gastric biopsy (6.8% vs. 5.2%, p = 0.51), with any gastritis (p = 0.76), or with positive H. pylori serology (p > 0.99), and was inversely associated with PPI use (48.9% vs. 63.6%, p = 0.003). These associations persisted after exclusion of gastric heterotopia cases (n = 601), and a site-restricted sub-analysis showed FM was more prevalent in duodenal bulb biopsies (65.9%) than in second-portion or post-bulbar biopsies (37.5%, p = 0.026). Taken together, these findings support FM as a reparative/adaptive response to varied duodenal injury rather than a specific H. pylori-related disease entity, with gastric acid exposure as one contributing factor.
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