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Industry: Email Alert RSS FeedHelicobacter pylori and chronic antral gastritis in elderly patients
Age and Ageing, July, 1994 by I.A. Gillanders, P.J.W. Scott, G.D. Smith
Summary
Fifty-five elderly patients with chronic antral gastritis (CAG) were studied to assess the relationship between Helicobacter pylori (H. pylori) status and CAG subtypes as specified in the Sydney System for Gastritis Classification. Twenty-eight patients (51%) were H. Pylori positive and 27 (49%) H. pylori negative. H. pylori-positive patients had a significantly greater association with features of severe active CAG (chronic inflammation and polymorph activity) than H. Pylori-negative patients. No association was apparent between H. pylori and more advanced stages of CAG (atrophy and intestinal metaplasia) thought to carry pre-malignant potential.
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The recognized association between dyspeptic symptoms in elderly people and an H. pylori-positive gastritis was confirmed. Use of NSAIDs correlated with a predominantly H. pylori-negative gastritis which was relatively asymptomatic.
Introduction
The prevalence of Helicobacter pylori infection increases with age and may be present in around 75% of patients above 65 years of age (1). H. pylori is known to be the commonest cause of antral gastritis (2) and is associated with duodenal ulcer relapse (3). H. pylori infection in elderly people is receiving increased attention, and studies have confirmed H. pylori gastritis to have a high prevalence in older dyspeptic individuals (4)(5). The age-related increase in gastric antral H. pylori carriage has been shown to parallel the age-related increase in the prevalence of chronic antral gastritis (CAG) (6)(7).
It has been proposed that severe chronic antral gastritis may eventually progress to an atrophic stage, which combined with the development of intestinal metaplasia predisposes to gastric dysplasia and malignancy (8). The role of H. pylori in the histological progression of CAG, however, is unclear. We undertook this study in order to examine the relationship betweeen H. pylori status and the different histological stages of CAG in elderly patients.
Patients and Methods
Fifty-five elderly patients with isolated CAG taken from a previously-reported series of 112 patients undergoing upper gastro-intestinal endoscopy (9) were studied. We reviewed the case records of all 55 patients in terms of their principal presenting symptoms and NSAID use at the time of endoscopy.
Histology: Paired antral biopsies were taken from all 55 patients. One biopsy was stained with H & E for histological examination and the other with a modified Giemsa stain for identification of H. pylori. The histological features of CAG were then classified according to the Sydney System for Gastritis Classification (10), namely chronic inflammation (Chr. Inf), polymorph activity (Poly. Act), atrophy (Atr) and intestinal metaplasia (IM). Each feature was graded in severity on a four-point scale reanging from 0 to 3, where 0 represented 'feature not present', 1 'mild', 2 'moderate', and 3 'severe'.
Statistical analysis: Two-sample t tests were used to compare mean total scores for each histological feature in patients positive and negative for H. pylori.
Results
Of the 55 patients studied, 28 (51%) were H. pylori positive and 27 (49%) were H. pylori negative. The majority of patients were women (40/55, 72%) and the mean age of the group was 79.3 years (range 72-89).
Table I shows the relationship between presenting symptoms, NSAID use and H. pylori status in the 55 patients with CAG. The commonest symptom was 'dyspepsia' and the majority of these subjects had an H. pylori-positive gastritis. NSAID use was associated with a predominantly H. pylori-negative gastritis, although fewer patients in this group complained of dyspepsia compared with NSAID-users with an H. pylori-positive gastritis.
Table I. Presenting symptoms, NSAID use and H. pylori status
Number of patients
H. pylori status
Total ve -ve
Symptoms
'Dyspepsia' 23 17 6
Nausea/vomiting 7 4 3
Anorexia/weight loss 11 3 8
Haematemesis/melaena 6 1 5
Anaemia 8 3 5
NSAID use 30 9 21
Dyspepsia and NSAID use 11 7 4
Table II shows the histological scores obtained in the 28 H. pylori-positive patients and the 27 H. pylori-negative individuals. H. pylori-positive patients had significantly higher mean scores than H. pylori-negative patients for both Chr. Inf (2.61 vs. 1.81, df = 45, p < 0.0001) and Poly. Act (2.43 vs. 1.26, df = 38, p < 0.0001). H. pylori-negative patients had higher mean scores than H. pylori-positive patients for both Atr (0.59 vs. 0.32) and IM (0.63 vs. 0.21), but the differences were not statistically significant (p = 0.25 and p = 0.11).
[TABULAR DATA OMITTED]
Discussion
This study confirms previous work suggesting a positive link between H. pylori infection and histological changes of severe chronic antral gastritis in older people (5)(9). Our findings differ from those of Safe et al. (5) in suggesting a negative relationship between H. pylori and atrophy and intestinal metaplasia, but we were unable to show this to a statistically significant degree. Our results are in keeping with those of previous reports showing a lower H. pylori prevalence in patients with atrophic gastritis and intestinal metaplasia compared with those with severe active chronic antral gastritis (11)(12). Farinati and colleagues (11) found progressively fewer H. pylori organisms present as histological changes advanced from chronic superficial and deep antral gastritis to atrophic gastritis, intestinal metaplasia and epithelial dysplasia. No patient with carcinoma had histological evidence of H. pylori. We believe that statements in the recent literature claiming a direct relationship between H. pylori infection and gastric antral malignancy are premature (13)(14). Some workers have demonstrated on histopathological grounds that H. pylori is commoner in patients with gastric cancer than in patients with no pathological lesions (15)(16). We have previously shown that around 67% of elderly patients with gastric antral carcinoma had an H. pylori-positive gastritis in the surrounding mucosa (9). The significance of these findings remains uncertain, but having now examined histological stages of CAG in more depth we suggest caution in linking H. pylori to gastric malignancy in elderly people. Even in the presence of pre-malignant rather than frankly malignant histological changes, H. pylori infection was uncommon. In theory, H. pylori could be the 'trigger' for a complex series of histological events culminating in a 'premalignant gastropathy', but as has already been suggested (8) the progression of gastritis is multifactorial in aetiology and includes not only H. pylori but also genetic and environmental factors as relevant in the elderly as they are in the young.
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