Everyone who carries H pylori
in their stomach develops a cellular infiltrate in their gastric mucosa, termed chronic gastritis. In most people this causes no symptoms, but H pylori
carriers do have an increased risk of developing peptic ulcer disease (about threefold to 10-fold) and adenocarcinoma of the antrum and body of the stomach (twofold to 10-fold). Elimination of H pylori
with antimicrobial treatment heals the ulceration and substantially reduces the risk of recurrence.8
Peptic ulcer disease and gastric cancer involving the antrum and body have been declining in the 20th century in precisely those parts of the world in which the prevalence of H pylori
colonisation has declined, and much evidence suggests the events are related. Carriage of H pylori
also increases the risk (about sixfold) of developing primary non-Hodgkin’s lymphomas of the stomach (MALTomas).9
Elimination of H pylori
markedly attenuates the course of low grade MALTomas.10
Non-ulcer dyspepsia occurs roughly as often in H pylori carriers as in non-carriers. Non-ulcer dyspepsia is a heterogeneous group of disorders, and if H pylori plays any role in this it affects only a minority of patients.
While ulcer disease and distal gastric adenocarcinomas have become less common as H pylori
is disappearing, a new group of diseases has been increasing rapidly in Western countries—gastro-oesophageal reflux disease and its sequelae, Barrett’s oesophagus, and adenocarcinoma of the (distal) oesophagus. The incidences of adenocarcinoma of the oesophagus and gastric cardia are increasing rapidly in several Western countries,11
and in white American men now exceed the prevalences of squamous cell oesophageal cancers and distal gastric adenocarcinomas respectively. Their rapid rise indicates a strong environmental cause, and there is no evidence that the epidemic is abating.
A key question, therefore, is whether the advent of these diseases is related to the simultaneous fall in carriage of H pylori
(fig ). Evidence links the lack of H pylori
with gastro-oesophageal reflux disease, Barrett’s oesophagus, and the risk of adenocarcinoma of the oesophagus and gastric cardia.12–14
In particular, it seems that cag+
strains exert a protective effect whereas cag−
strains have essentially no effect.14,15
These preliminary observations need confirmation but, if correct, suggest that clinicians should not eliminate H pylori
from everyone, as they will be trading a decreased risk for certain diseases (peptic ulcers, adenocarcinomas of gastric antrum or body) with increased risk for others.
Figure 2 Changing incidence of acquisition of H pylori and gastric cancers in Western countries. Colonisation with H pylori seems to have been nearly universal among adults before 1800 and then began to diminish until the present, when <20% of (more ...)