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

Department of Medicine, Veterans Affairs Medical Center and Baylor College of Medicine, Houston, Texas, USA.
The American Journal of Gastroenterology (Impact Factor: 10.76). 07/2003; 98(6):1266-70. DOI: 10.1111/j.1572-0241.2003.07488.x
Source: PubMed


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.
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.
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.
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.

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    • "However, there are case reports showing that this lesion may play a role in the development of web, stricture, ulcer, perforation, or esophagotracheal fistula related to its capability of hydrochloric acid secretion [1–5]. These complications may be exacerbated by Helicobacter pylori, which colonizes 73% of “inlet patches” [6, 7]. Furthermore, HGMUE may be the origin of malignant progression to cervical esophageal carcinoma [8, 9]. "
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    ABSTRACT: The prevalence of heterotopic gastric mucosa (HGM) in the cervical esophagus is frequently underestimated. Tiny microscopic foci have to be distinguished from a macroscopically visible patch, also called "inlet patch." Symptoms as well as morphologic changes associated with HGM are regarded as a result of the damaging effect of acid, produced by parietal cells in the mostly fundic type of HGM. We herein review the literature and propose a new clinicopathologic classification of esophageal HGM: Most of the carriers of esophageal HGM are asymptomatic (HGM I). Some individuals with HGM in the esophagus complain of dysphagia, odynophagia, or "extraesophageal manifestations" (hoarseness and coughing), without further morphologic findings (HGM II). Still fewer patients are symptomatic due to morphologic changes, i.e., esophageal strictures, webs, or esophagotracheal fistula (HGM III). Malignant transformation via dysplasia (intraepithelial neoplasia, HGM IV) to cervical esophageal adenocarcinoma (HGM V) is exceedingly rare (only 24 reported cases). In contrast to Barrett's esophagus, HGM should not be regarded as a precancerous lesion. Symptoms are more likely to occur in patients with inlet patch, whereas malignant transformation and adenocarcinogenesis can also occur in microscopic HGM foci. Asymptomatic HGM requires neither specific therapy nor endoscopic surveillance. Only in symptomatic cases treatment, i.e., dilatation for (benign) strictures or acid suppression for reflux symptoms, can be recommended. Patients with low-grade dysplasia in HGM might be candidates for surveillance strategies, whereas in cases of high-grade dysplasia and invasive adenocarcinoma oncological treatment strategies must be employed.
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