Analysis of Gastroduodenitis and Oesophagitis in Relation to Dyspeptic/Reflux Symptoms

Abstract

Background/Aims: The pathogenesis of dyspeptic/reflux symptoms and the clinico-pathologic profile of affected patients are still poorly understood. To improve our knowledge in this field we carried out a systematic, comparative analysis of symptom profiles and histopathologic patterns of oesophagogastroduodenal mucosa in a series of 221 subjects, 140 with and 81 without endoscopic evidence of hiatal hernia. Of these, 190 showed reflux and/or dyspeptic symptoms. Methods: Before endoscopy, all the subjects were questioned about the presence and severity of 12 individual symptoms. Biopsies were taken from the distal oesophagus, cardia, corpus, angulus, antrum and duodenal bulb, and were scored in accordance with the Sydney system. Results: Patient groups with a distinct clinico-pathologic profile were better identified when symptoms of adequate severity were compared with histopathologic parameters. A correlation between gastroesophageal reflux disease (GORD) symptoms and histologic signs of oesophagitis was mostly restricted to patients endoscopically positive for oesophagitis. Retroxiphoid pyrosis correlated with cardial gastritis but not with oesophagitis, either endoscopic or histologic, while ulcer-like epigastric pain correlated with active duodenitis and distal gastritis. No definite histopathologic background was detected in patients with putative dysmotility-like symptoms, endoscopy-negative GORD and low score or mixed symptoms. Conclusion: A contribution of Helicobacter pylori gastroduodenitis to the pathogenesis of some dyspeptic symptoms seems likely. However, the identification of specific histologic changes causing individual symptoms remains rather elusive, with the exception of active antroduodenitis in patients with ulcer-like pain and of active proximal gastritis in patients with severe retroxiphoid pyrosis.

Altered intercellular glycoconjugates and dilated intercellular spaces of esophageal epithelium in reflux disease

“…Patients were considered pathologic when the percentage time with a pH of less than 4 was above 4.2% of the total time, above 6.3% of the time in upright position, or above 1.2% of the time in supine position. Reflux symptoms were evaluated according to severity and frequency with the help of a questionnaire, as previously reported [30]. Only cases with heartburn or acid regurgitation occurring regularly or interfering with the patient's ordinary life were considered significant for GERD.…”

“…The patients underwent esophagogastroduodenal endoscopy, during which esophagitis was assessed according to the Savary-Miller criteria, and two routine grasp biopsies were taken 2-3 cm above the Z-line. To test for site-related variability of histological findings [31], additional biopsies were taken at 6-7 cm in 30 cases negative for erosive esophagitis [30]. In erosive cases, biopsies were taken on the border of the erosion as well as from non-erosive mucosa.…”

“…Of the 86 subjects investigated, 12 endoscopy-negative cases were taken as controls. They complained of various reflux-unrelated dyspeptic symptoms (nausea, early satiety, post-prandial fullness or bloating of the upper abdomen, and food-relieved epigastric pain) while being free of reflux symptoms (heartburn, acid regurgitation, dysphagia, non-cardiac chest pain, respiratory or throat symptoms) and showing a pH less than 4 for less than 4.2% of total recording time, less than 6.3% of time in upright position, and less than 1.2% in supine position [5,24,30]. Among the remaining 74 symptomatic patients, 22 showed endoscopic evidence of erosive reflux esophagitis, while 44 had reflux symptoms as well as evidence of pathologic reflux during the 24-h pHmetry coupled with negative endoscopy (endoscopy-negative GERD).…”

“…Five-micron deparaffinized sections were stained with hematoxylin-eosin, Giemsa and alcian blue-PAS-hematoxylin methods or immunostained using the avidin-biotin procedure [13] using anti-CD15 (leu-M1) mouse monoclonal antibodies (clone MMA, Becton Dickinson, San Jose, Calif.; or clone Tii 9, Biotest, Dreieich, Germany) directed against the lacto-N-fuco-pentose III/3-fucosyl-N-acetyllactosamine oligosaccharide. Hematoxylin-eosin and Giemsa sections were evaluated for granulocyte infiltration (intraepithelial eosinophils and intraepithelial as well as lamina propria neutrophils) and microscopic erosion-necrosis as previously reported [2,26,30]. CD15-immunostained sections were used to investigate the "cement" material filling the intercellular spaces; they were also of help in detecting intraepithelial neutrophils [23].…”

“…The diagnostic value of these findings has been the subject of many investigations leading to conflicting results [4,25,30]. In general, histological lesions were well represented in the esophageal mucosa, showing erosive esophagitis at endoscopy.…”