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Helicobacter pylori and chronic antral gastritis in elderly patients.

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.

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.

Our study has confirmed work by others showing that elderly people who are H. pylori positive are more likely to be sufferers from symptomatic 'dyspepsia' than those who are H. pylori negative (5). The significance of this finding, however, is uncertain as it has also been shown that an H. pylori-positive gastritis is common in asymptomatic elderly individuals (17). None of our other four principal presenting symptoms could be definitively related to H. pylori status. Symptoms should not be a major factor when considering performing endoscopic biopsy in elderly patients to determine gastritis severity or H. pylori status.

A significant proportion of our patients on NSAID therapy (70%) had an H. pylori-negative gastritis. This also confirms a previous study (4). Patients on NSAID therapy who are H. pylori positive tend to be more symptomatic in terms of dyspepsia than those on NSAIDs without evidence of H. pylori infection (5). Our results support this observation.

We were surprised by the fact that only 51% of our elderly patients with CAG were H. pylori positive. This figure is significantly lower than those quoted by others (78% (4) and 81% (5)). We are unable to provide an explanation for our result: the elderly patient group we studied presented prospectively for endoscopy over a 9-month period without further selection. Over half (54%) of our patients were taking NSAIDs in whom an H. pylori-negative gastritis would be expected, but this figure is not significantly greater than that for NSAID use observed by others (50%) (5). One pathologist assessed both the classification of gastritis and H. pylori status of all our patients: slides were reviewed again for evidence of H. pylori and the figure of 51% was confirmed.

In conclusion, this study has shown that H. pylori is strongly associated with the histological changes of severe chronic antral gastritis in elderly patients but not with the more advanced stages of CAG which carry premalignant potential. Gastric antral dysplasia or malignancy arising from severe CAG in elderly patients is likely to be multifactorial in origin, and H. pylori probably does not have a role in this process.

References

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(2.)Rauws EA, Langenberg W, Houthoff HJ, Zanen HC, Tytgat GN. Campylobacter pyloridis-associated chronic active antral gastritis: a prospective study of its prevalence and the effects of antibacterial and antiulcer treatment. Gastroenterology 1988;94:33-40.

(3.)Borody TJ, Cole P, Noonan S, et al. Recurrence of duodenal ulcer and Campylobacter pylori infection after eradication. Med J Aust 1989;151:431-5.

(4.)O'Riordan TG, Tobin A, O'Morain C. Helicobacter pylori infection in elderly dyspeptic patients. Age Ageing 1991; 20:189-92.

(5.)Safe AF, Warren B, Corfield A, et al. Helicobacter pylori infection in elderly people: correlation between histology and serology. Age Ageing 1993;22:215-20.

(6.)Siurala M, Sipponen P, Kekki M. Chronic gastritis: dynamic and clinical aspects. Scand J Gastroenterol 1985; 20 (suppl 109):69-76.

(7.)Graham DY, Klein PD, Opekun AR, Boutton TW. Effect of age on the frequency of active Campylobacter pylori infection diagnosed by the [13C] urea breath test in normal subjects and patients with peptic ulcer disease. J Infect Dis 1988;157:777-80.

(8.)Correa P. A human model of gastric carcinogenesis. Cancer Res 1988;48:3554-65.

(9.)Gillanders IA, Scott PJW, Smith GD. Helicobacter pylori: what relevance to upper gastrointestinal disease in the elderly? J Clin Exp Gerontol 1992;14:235-50.

(10.)Misiewicz JJ, Tytgat CNJ, Goodwin CS, et al. Working party report of the World Congress of Gastroenterology. Oxford: Blackwell Scientific Publications, 1990;1-10.

(11.)Farinati F, Valiante F, Germana B, et al. Prevalence of Helicobacter pylori infection in patients with precancerous changes and gastric cancer [Abstract]. Gut 1992;33 (suppl 1):S40 (T160).

(12.)Craanen ME, Blok P, Dekker W, Ferwerda J, Tytgat GN. Subtypes of intestinal metaplasia and Helicobacter pylori. Gut 1992;33:597-600.

(13.)Talley NJ, Zinsmeister AR, Weaver A, et al. Gastric adenocarcinoma and Helicobacter pylori infection. J Natl Cancer Inst 1991;83:1734-9.

(14.)Forman D, Newell DG, Fullerton F, et al. Association between infection with Helicobacter pylori and risk of gastric cancer: evidence from a prospective investigation. Br Med J 1991;302:1302-5.

(15.)Feng Y, Wang Y. Campylobacter pylori in patients with gastritis, peptic ulcer and carcinoma of the stomach in Lanzhou, China. Lancet 1988;i:1055-6.

(16.)Robey-Cafferty SS, Ro JY, Cleary KR. The prevalence of Campylobacter pylori in gastric biopsies from cancer patients. Mod Pathol 1989;2:473-6.

(17.)Dooley CP, Cohen H, Fitzgibbons PL, Bayer M, Appleman MD, Perez-Perez GI. Prevalence of Helicobacter pylori infection and histologic gastritis in asymptomatic persons. N Engl J Med 1989;321:1562-6.

Authors' addresses I. A. Gillanders Geriatric Medicine Unit, City Hospital, Greenbank Drive, Edinburgh EH10 5SB P. J. W. Scott[dagger], G. D. Smith[double dagger] Departments of Geriatric Medicine[dagger] and Pathology[double dagger], Stobhill General Hospital, 133 Balornock Road, Glasgow G21 3UW

Received 3 October 1993
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Author:Gillanders, I.A.; Scott, P.J.W.; Smith, G.D.
Publication:Age and Ageing
Date:Jul 1, 1994
Words:1863
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