Abstract and Introduction
Abstract
Objectives: Recent studies using histology alone in select patients have suggested that Helicobacter pylori-negative gastritis may be common. The objective of this study was to investigate the prevalence of H. pylori among individuals with histologic gastritis.
Methods: Subjects between 40 and 80 years underwent elective esophagogastroduodenoscopy at a VA Medical Center. Gastric biopsies were mapped from seven prespecified sites (two antrum, four corpus, and one cardia) and graded by two gastrointestinal pathologists, using the Updated Sydney System. H. pylori-negative required four criteria: negative triple staining at all seven gastric sites, negative H. pylori culture, negative IgG H. pylori serology, and no previous treatment for H. pylori. Data regarding tobacco smoking, alcohol drinking, nonsteroidal anti-inflammatory drug, and proton pump inhibitor (PPI) use were obtained by questionnaire.
Results: Of the 491 individuals enrolled, 40.7% (200) had gastritis of at least grade 2 in at least one biopsy site or grade 1 in at least two sites. Forty-one (20.5%) had H. pylori-negative gastritis; most (30 or 73.2%) had chronic gastritis, five (12.2%) had active gastritis, and six (14.6%) had both. H. pylori-negative gastritis was approximately equally distributed in the antrum, corpus, and both antrum and corpus. Past and current PPI use was more frequent in H. pylori-negative vs. H. pylori-positive gastritis (68.2% and 53.8%; P=0.06).
Conclusions: We used multiple methods to define non-H. pylori gastritis and found it in 21% of patients with histologic gastritis. While PPI use is a potential risk factor, the cause or implications of this entity are not known.
Introduction
Gastritis is typically defined based on histologic examination of gastric mucosal biopsies. The discovery that Helicobacter pylori (H. pylori) infection was etiologically associated with peptic ulcer and gastric cancer has resulted in the frequent performance of gastric mucosal biopsies. The evaluating pathologist is expected to comment on whether gastritis was present and, if so, to provide additional details, especially in relation to H. pylori infection, to assist the clinician in patient management.
Worldwide the most common cause of gastritis is H. pylori infection. Treatment of an H. pylori infection results in the rapid disappearance of polymorphonuclear infiltration, followed by a reduction in the chronic inflammatory infiltrate, with gradual normalization of the mucosa. However, mucosal atrophy and metaplastic changes resolve slowly if at all. Of interest, a recent study of patients in clinical trials with erosive esophagitis reported that between 75 and 90% of H. pylori-negative subjects had gastritis. Similarly, 56–69% of H. pylori-negative subjects enrolled in clinical trials with functional dyspepsia or nonerosive gastroesophageal reflux were reported to have gastritis. In those studies, two biopsy specimens were taken from the gastric antrum and body (i.e., four biopsy samples per subject), and Warthin-Starry silver staining was used to examine for H. pylori infection. Gastric-body biopsies were obtained from the middle of the greater curvature of the gastric body, whereas antral biopsies were obtained from the lesser curvature. The unexpected results of these studies led us to question whether the concept that most stomachs could be characterized as either normal or H. pylori-infected (active or past infection) might be too simple. However, those two studies were relatively limited by their biopsy protocols, the reliance of histology alone (i.e., the lack of adjustment for previous H. pylori treatment or potential confounders such as smoking, alcohol, nonsteroidal anti-inflammatory drug (NSAID), or proton pump inhibitor (PPI) use). To investigate the prevalence and risk factors associated with H. pylori-negative gastritis, we performed gastric mapping to identify gastritis in a large number of patients undergoing endoscopy. We also used histology, culture, serology, and past treatment history to identify H. pylori.