Prevalence of Plasma Cells and Lymphoid Follicles in Sleeve Gastresctomy Specimens: Redefining Normal Stomach Histology
Maya Saroufim, Ghassan Shamseddine, Bassem Safadi, Fouad Boulos. American University of Beirut Medical Center, Beirut, Lebanon
Background: The finding of lymphoid follicles/aggregates in gastric biopsies has been traditionally linked to H. pylori gastritis, and less commonly to other inflammatory and neoplastic conditions. The frequency of such aggregates in normal stomachs has yet to be adequately evaluated. This is especially relevant when it comes to diagnosing non-specific chronic gastritis in biopsy specimens with chronic inflammation but no evidence of H. Pylori infection. Sleeve gastrectomies represent an opportunity to study adequately preserved gastric mucosa in patients who are likely to be asymptomatic and to lack a history of gastric disease.
Design: 68 bariatric sleeve gastrectomies were examined for multiple histologic features including type, quantity, and distribution of chronic inflammation and lymphoid follicles/aggregates. Presence of H. pylori was documented by H&E and IHC. Clinical information including age, sex, medication intake, history of prior endoscopy and/or H. pylori infection was recorded.
Results: 263 fundic sections (range 2-9, mean 4) from 68 patients (32 males, 36 females) were examined. Among 55 H. pylori IHC-negative (versus 13 IHC-positive) patients, the maximum number of superficial i.e. foveolar, and deep i.e. fundic inter-glandular plasma cells ranged from 0 to 7 (vs. 2 to 8) and 0 to 6 (vs. 0 to 4) respectively (mean: 2, <1 vs. 5, 1); similarly, the number of lymphoid aggregates/follicles per section ranged from 0 to 14 (vs. 1 to 10), (mean: 3 vs. 5) with 10% (vs. 20%) showing germinal center formation. The follicles ranged from 0.2 to 1.5 mm in greatest dimension (mean: 0.58). Focal acute inflammation was seen in 3 (vs. 4) patients. Clinical information revealed that 11 of the H. Pylori-negative cases had EGD, all of which showed endoscopic mild non-erosive to diffuse gastritis. The remaining had no documentation of symptoms or medication intake, including NSAIDs and PPI.
Conclusions: Although cases with H. Pylori infection show a qualitative and occasionally significant increase in inflammatory changes (e.g. germinal centers), there appears to be significant overlap and no pathognomonic features in the histology of stomachs with or without documented gastric symptoms and/or disease. Hence, the spectrum of acceptable “normal” chronic inflammatory changes in the stomach is possibly wider than currently believed. A high threshold for diagnosing chronic gastritis in patients without H. Pylori or other well-established causes of gastritis is therefore advised.
Wednesday, March 6, 2013 1:00 PM
Poster Session VI # 77, Wednesday Afternoon