Héctor Jairo Correa Cardona

Helicobacter pylori and Hetertopic Gastric Mucosa in the Upper Esophagus (the Inlet Patch)

OBJECTIVES:Helicobacter pylori (H. pylori) may colonize gastric mucosa wherever it is found in the GI tract. Heterotopic gastric mucosa in the upper esophagus (inlet patch) is a potential site for H. pylori infection and may provide a reservoir for oral-oral transmission or a niche where antibiotics might have difficulty reaching. The aim of this study was to analyze the intensity and distribution of H. pylori in the inlet patch.METHODS:Whenever a cervical inlet patch was observed, mucosal biopsy samples were taken to confirm the endoscopic diagnosis and to search for H. pylori and active inflammation. In addition, mucosal biopsy samples were also taken from the gastric mucosa. Formalin-fixed biopsy specimens were cut and stained with a new dual stain developed in our laboratory. The stain is a combination of periodic acid-Schiff and a silver stain that allows simultaneous visualization of H. pylori and gastric type epithelium. The density of H. pylori was scored using a visual analog scale of 0 to 5. The type of mucosa in the inlet patch was also recorded.RESULTS:The study included 48 patients; 37 had H. pylori gastritis and 27 of these (73%) had H. pylori identified on their heterotopic gastric mucosa. A higher density of H. pylori in the stomach was associated with a higher prevalence in the inlets. Active inflammation correlated with active infection in the inlet patch and the presence of antral type mucosa.CONCLUSION:H. pylori colonization of heterotopic gastric mucosa in the upper esophagus is common and is closely related to the H. pylori density in the stomach. The fact that H. pylori was not found in all cases suggests that another event such as reflux may be required for H. pylori to colonize heterotopic mucosa.

7217 The importance of an enlarged gastric fold in a hiatal hernia.

Background: In the pathogenesis of GERD the presence of a sliding hiatal hernia (HH) does not predict the presence of reflux, but it is a pejorative factor in those in whom reflux is present. The role of an enlarged gastric fold in a HH in GERD is unknown. AIM To investigate the endoscopic and histological findings of patients with an enlarged fold in the HH. Methods: The investigated group consisted of patients who underwent EGD for any reason. In those with an HH and enlarged gastric fold, biopsies were obtained from the distal esophagus and cardial fold as well as from the antrum and corpus (Group I). The histological findings were compared to those observed in an age and sex matched group of patients with HH without a enlarged gastric fold (Group II) and a group of 211 patients without HH or enlarged gastric fold. Each group contained 32 patients. Results: The 31 patients with HH and enlarged gastric fold consisted of 18 M and F, mean age 47.7 +/-14 yr. The enlarged gastric fold was found in the right side of the cardias in 27/31 case and in 5 cases there was an polypoid aspect in the fold. HH with enlarged gastric fold was associated with erosive esophagitis in 84% compared to 54.8% of those with HH alone, and in16% of those with neither. The presence of erosive esophagitis was 4 and 27 fold greater with HH and with HH with enlarged gastric fold, respectively, than in those with neither. Conclusion: The presence of an enlarged fold which is typically a continuation of the lesser curvature gastric folds to the Z-line is associated with a high prevalence of erosive esophagitis. It is possible that the enlarged gastric fold acts as a mechanical hindrance to effective barrier to gastro-esophageal reflux and deserves further studies about its role in the pathogenesis of GERD