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Helicobacter pylori Infection in the Pathogenesis of Gastro-oesophageal Reflux Disease
There was no significant change in reflux symptoms score and total al. studied the autonomic response to feeding in H. pylori-positive
time pH <4 in eradicated versus infected patients. Similarly, Manifold GORD patients and they found blunted sympathetic reactivity and
et al., studying 25 patients with H. pylori gastritis before and after exacerbated vagal response to feeding.
41
An interesting explanation
H. pylori eradication, did not find differences in acid alkaline reflux or was proposed by Shahabi et al.
42
They believe that a
bilirubin exposure between the groups.
33
Wu et al. studied patients neuroimmunological mechanism is responsible for the protective
with RO and healthy controls.
34
There was no difference in the severity effect of H. pylori on GORD. H. pylori infection of the gastric mucosa
of oesophagitis or acid exposure between H. pylori-positive and induces a T-helper1-like immune response and production of pro-
inflammatory cytokines. These cytokines can inhibit local
sympathetic tone, whereas they increase systemic sympathetic
tone. Increased sympathetic tone can induce an anti-inflammatory
Acid secretion in H. pylori-infected
milieu, which in turn can inhibit inflammation in the oesophagus and
patients depends not only on mechanisms
LOS. Furthermore, H. pylori infection may stimulate the cholinergic
anti-inflammatory pathway. Reduction of oesophageal inflammation
leading to hypergastrinaemia, but also on
by increased systemic sympathetic tone and vagal activity may lead
the pattern of gastritis.
to a decrease in reflux-induced oesophageal injury and LOS
dysfunction in GORD. This phenomenon may underlie one of the
mechanisms by which Helicobacter exerts a preventative rather
than pathogenic role in GORD development.
-negative groups. However, infected subjects had lower basal LOS
pressure and decreased amplitude of distal oesophageal contractions Summary
than controls. Moreover, oesophageal dysmotility and subsequent low H. pylori infection influences the pathogenesis of GORD in multiple
acid clearance was more prevalent in H. pylori-positive patients. In ways: it causes modification of reflux content by increasing or
another study, Wu et al. studied oesophageal acid exposure in decreasing gastric acid production and affects oesophageal and
patients with GORD before and after H. pylori eradication.
35
They found gastric motility as well as OGJ function. The net effect triggered by
no difference in the percentage of time oesophageal pH was <4, but activation of all or some of these mechanisms may be very different in
the percentage of time when oesophageal pH was <2 was separate patients. Some of them may present with various types of
significantly increased in patients with successful H. pylori GORD, while others may have duodenal ulcers, gastric ulcers,
eradication. All these data strongly suggest that chronic H. pylori dyspeptic symptoms or no complaints at all. Also, the effect of
infection is associated with oesophageal dysmotility. The question eradication is fairly unpredictable. A few years ago we developed a
arises of why GORD seems to be more prevalent post-eradication hypothesis that explains possible scenarios.
43
In patients with
treatment. The most obvious mechanism is that the motility antral-predominant gastritis and duodenal ulcer, H. pylori eradication
disturbances are counterbalanced by low acidity of reflux contents. may result in complete recovery or GORD symptom development. This
latter phenomenon occurs in patients who might already have reflux
From epidemiological studies it is known that in some oesophagitis or non-erosive reflux disease, the symptoms of which
H. pylori-positive GORD patients eradication results in symptom were masked by or accounted for by duodenal ulcer. The
improvement but in others it causes symptom worsening or even de predominance of symptoms due to antral gastritis is probably
novo development when not occurring previously. As the studies dependent on mechanical factors, leading to duodenal ulcer
cited above have shown a strong effect of H. pylori eradication on in patients with rapid gastric emptying and competent OGJ and, in
distal oesophageal motility and LOS but little effect on distal contrast, to RO in patients with delayed emptying and incompetent
oesophageal acid exposure, the pathways responsible must involve OGJ. The same hypothetical factors are responsible for the diversity
more mechanisms than H. pylori-related OGJ dysfunction and acid among patients who had H. pylori eradicated: some of them may
production disturbances. These mechanisms may be associated present with improvement of symptoms and in others the healing of
with impaired control of the autonomic nervous system. Lee et al.
investigated the association of intra-oesophageal pH with the
autonomic functional changes in GORD patients.
36
Oesophageal acid
In patients with antral-predominant
exposure was generally associated with decreases in autonomic
tonus. Diurnal characteristics of autonomic regulation indicated
gastritis and duodenal ulcer, H. pylori
predominant parasympathetic fluctuation during sleeping and a
eradication may result in complete
superimposed sympathetic interaction during waking. In a different
study performed by Lee et al., autonomic tonus in patients with
recovery or gastro-oesophageal
endoscopically confirmed oesophagitis (even without symptoms)
symptom development.
was lower in comparison with NERD subjects.
37
Chen et al. found
that patients with RO and NERD display a similar degree of symptom
severity, but the pattern of autonomic function was different as LF an ulcer may unmask GORD that was formerly present but not
band power (%) and LF/HF ratio were significantly lower in the NERD dominant, resulting in a new diagnosis of RO or NERD. As was shown
patients.
38
A study focusing on heart rate variability (HRV)-based previously, low vagal activity may play a pivotal role in reflux
analysis showed more precisely that parasympathetic activity development in this setting.
impairment in particular contributes to reflux development.
39
In
another study, positive correlation between H. pylori infection and In patients with corpus-predominant gastritis, acid secretion,
parameters reflecting vagal tone was reported.
40
Moreover, Lugon et plasma ghrelin levels and probably vagal activity dramatically
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