Study ofHelicobacter pylori colonization of patches of heterotopic gastric mucosa (HGM) at the upper esophagus

Abstract

Helicobacter pylori (HP), known to cause active chronic gastritis, has primarily been found in gastric-type mucosa. Even in the duodenum, the organism was detected in islands of metaplastic gastric mucosa. HP has also been found in gastric metaplasia of Barrett's esophagus in 15-50%. The aim of our study was to determine: (1) the frequency with which HP is found on histopathological sections of heterotopic gastric mucosa (HGM) patch(es) at the upper esophagus, as compared to that of the stomach proper, and (2) the histopathological significance of infection in the HGM patches. From 63 patients with HGM patches at the upper esophagus, 48 patients were found to have concurrent adequate specimen from the stomach for modified Steiner's stain. In 22 patients (45.8%), pair sections from HGM and stomach were negative for HP. Of 26 patients (54.1%) HP-positive on sections from the antrum and/or body (both in 21 cases) nine patients (18.7%) demonstrated HP in the HGM patches. Whereas focal acute inflammatory changes on the H&E section of HGM was present in six patients, HP was detected in HGM only in one. Chronic inflammatory cell infiltration was detected in all nine HP-positive HGM patches and in 37 of 39 HP-negative patches. A mixed acute and chronic inflammatory cell infiltration was found in five of these 37 patients. Our data demonstrate that HP infection of HGM patches at the upper esophagus is part of the HP gastritis and an independent colonization of HGM patches without gastric infection does not occur.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma of the upper esophagus arising in heterotopic gastric mucosa: common pathogenesis with Barrett's adenocarcinoma?

“…Intestinal metaplasia is rarer in HGM, its incidence ranging from 0% to 12% [5,25,37,40,41]. In contrast to intestinal metaplasia of the gastric antrum, intestinal metaplasia in HGM does not seem to be correlated with H. pylori colonization of the inlet patch [6,25]. In our case the submucosa and muscularis mucosae located beneath intestinal metaplasia show the musculofibrous anomaly usually observed in Barrett's mucosa [35].…”

Structures of the normal esophagus and Barrett?s esophagus

“…This esophagitis has also been associated with stenosis, ulcers [11], and fistulae [12]. Helicobacter pylori infection, with associated gastritis, has been reported in islets of ectopic gastric mucosa [13]. In the present authors' series [10] goblet cells were observed in 1 of the 246 subjects but no Paneth cells were found.…”

Helicobacter pylori: recent advances in the study of its pathogenicity and prevention

“…18 The World Health Organization classifies this bacterium as a Type 1 carcinogen. 19 Although H. pylori infection is minimally invasive, metaplastic gastric tissue may also spread to other parts of the alimentary tract such as the duodenum, 20 the proximal esophagus, 21 the distal esophagus, 22 Meckel's diverticulum, 23 and the rectum. 24 In addition, it has been proposed that although H. pylori infection is circumscribed to the gastric mucosa, it could conceivably produce lesions remote to the primary site of infection, by altering levels of systemic inflammatory mediators.…”