Helicobacter pylori

and Ian A. D. Bouchier²

(1)

Bishop Auckland, UK

(2)

Edinburgh, Midlothian, UK

1.1 Introduction

The discovery of the presence of this organism in many human stomachs and its association with disease revolutionized our approach to peptic ulcer. Detection of H. pylori infection of the gastric mucosa and proof of its absence after eradication therapy have become pivotal in patient management.

1.2 Epidemiology

H. pylori infection is strongly associated with age and cigarette smoking, and inversely with wealth. There appears to be an enhanced risk of infection in childhood and a lower rate in adult life. In British provincial patients in whom gastroscopy is normal, the overall infection rate is 16%, probably reflecting prior anti-microbial therapy in dyspepsia in H. pylori positive patients in the twenty first Century. Rates in the past were much higher.

Infection is much more frequent, and occurs earlier in life, in underdeveloped countries: 75% of residents of orphanages in Thailand are infected. Lower social class is associated with higher infection rates, possibly because of overcrowded conditions in childhood or the higher prevalence of cigarette smoking. There is no sex difference.

H. pylori infection is associated with endoscopic duodenal ulcer disease (32%) in patients not taking as aspirin or non-steroidal anti-inflammatory drugs. A similar but weaker association is documented for benign gastric ulcer (28%).

There is no lymphoid tissue in normal stomach, and the presence of this, particularly if it has progressed to a mucosa-associated lymphoid tumour, is strong evidence of H. pylori infection.

H. pylori infection is normally global in the stomach, but histological changes are mainly located in the gastric antrum where glandular destruction, polymorph and lymphocyte infiltration deeper than the epithelium; intestinal metaplasia; and gastric erosions are all common. Unfortunately the macroscopic recognition of gastritis caused by H. pylori infection is completely unreliable and histological proof is always required (Table 1.1).

Table 1.1

Positive direct urease test at endoscopy

	Twentieth century (%)	Twenty-first century (%)
Normal	45	16
Duodenal ulcer	95	32
Gastric ulcer	75	28

Infections are chronic and persistent unless effective treatment is given. Important epidemiological evidence exists to link H. pylori with the aetiology of gastric carcinoma and ischaemic heart disease, but these observations are not of significance to individual patients.

There is debate about whether all H. pylori infections develop in early life and thereafter persist, or whether there is an appreciable incidence of new infections up to the age of 70. It is known that after successful eradication re-infection is uncommon, occurring at a rate of approximately 1% per year.

1.3 Diagnostic Tests

1.3.1 Presence of Active Duodenal Ulcer

In patients who can be proved to have current active duodenal ulcer disease, and who are not taking ulcerogenic drugs, it may be assumed that H. pylori is more likely to be present. Benign gastric ulcer, antral gastritis and gastric mucosa-associated lymphoid tumour (MALToma) are also linked with H. pylori, but it is necessary to seek supporting evidence of active infection.

1.3.2 Direct Urease Test

At the time of gastroscopy a biopsy can be taken and examined for urease activity. H. pylori is almost unique among gastric pathogens in its possession of a very potent urease: demonstration of urease activity in a gastric antral biopsy is one of the best indicators of current infection.

Commercially available slides containing urea gel and an indicator are available, (CLOtest & HpFast). The antral biopsy is embedded in the gel and the end point is indicator colour change to magenta, showing that pH has risen with the generation of ammonia. Most positive results become available within minutes, but 5–10% of true-positive results only become available in hours and it is best to read slides the next morning before discarding them. Although intrinsically very sensitive, this test may give false-negative results if patients have recently been taking antibiotics, proton pump inhibitors or bismuth. In addition, specific anti-H pylori therapy may cause differential clearing of the organism from the gastric antrum, and in treated patients a biopsy should be taken from the fundus or body of the stomach as well as the gastric antrum, though they may be tested on the same slide.

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