Medical Chronicle November/December 2013 | Page 41

GASTROENTEROLOGY FORUM
BY DR JOHN WRIGHT

Why persecute the H pylori ?

To answer this question...
because it has been common cause
since its discovery in duodenal ulcer
(DU) patients by Brian Marshall in
1982. Initially, it was shown that
90% of DUs are associated with
Helicobacter pylori (HP) infection.
Furthermore, subtypes were identified that were associated with DUs
and other subtypes with gastric
cancer. The jury was in and the onslaught justified. The development
of simple blood tests, in addition
to stool and saliva tests simplified the decision making so that all
patients with dyspepsia were tested
and if found positive treated with
clarithromycin and amoxicillin. This
is a regimen that will clear 80%90% of infections but resistance
is growing.
The use of antibiotics also avoided
the need for expensive proton pump
inhibitors (PPIs). Recently, however,
these have fallen faster than the
cost of the antibiotics, so that a
month’s course of PPIs is now less
than seven days of clarithromycin.
The first fallacy in this protocol
was the confusion between sensitivity and specificity. Whereas originally
90% of DUs were associated with HP
infection, this rate has been falling
progressively in the Western world
and is now closer to 50%.
More important, however, is the
specificity. At best, only 15% of
patients with HP have ulcer disease
and only 40% of patients with
dyspepsia have a duodenal ulcer. The
latter has also been falling, as the
incidence of oesophageal reflux has
been increasing. Furthermore, other
conditions that require confirmatory biopsy such as gastric ulcers
and gastric cancer will be missed
or the diagnosis delayed during the
pointless eradication of HP. In fact,
almost half the patients with a positive HP test have no gastro-duodenal
pathology at all.
Some HP strains appear to
protect against peptic ulcer disease
but methods to differentiate the
good from the bad are not widely
available. In this context, the side
effects of clarithromycin need to be
remembered. Gastrointestinal symptoms occur in up to 7% of patients.
More important is the very rare but
potentially fatal liver failure. Drug
interactions are assured by its inhibition of the CYP3A4 pathway.
The incidence of oesophageal
disease such as Barrett’s metaplasia and upper oesophageal cancer
is associated with the absence of
gastric HP. The presence of HP could
protect against the development

of these GORD complications. As in Crohn’s disease, it
might be that a change in the
natural flaura and fauna of
the gastrointestinal tract has
unintended consequences on
gastro-duodenal and intestinal
mucosal defences.
So where do we stand in the
HP/DU debate.

On the plus side:
• HP is present in “most” patients who
have a DU (if not due to NSAIDs)
• HP infection precedes the
development if DUs
• HP eradication prevents DU
recurrence.

On the negative side
• ‘Most’ patients with HP infection do

not have peptic ulcers
• The treatment of HP has cost and
safety questions
• The ‘blind’ treatment of HP infection
without a diagnosis is ‘unscientific’
• As antibiotic pollution engulfs our
environment, a short trial of a PPI is
safer
• As always in evidence-based medicine a
diagnosis is essential before therapy.

MEDICAL CHRONICLE NOVEMBER/DECEMBER 2013 41