Download April 2007 Research Review

Research Review: Helicobacter pylori
Sheu, B-S., Cheng, H-S., Kao, A-W. et al. (2006) Pretreatment with Lactobacillusand Bifidobacterium-containing yoghurt can improve the efficacy of quadruple
therapy in eradicating residual Helicobacter pylori infection after failed triple therapy.
American Journal of Clinical Nutrition 83: 864-869.
---------------------------------This study shows a lactic acid probiotic improving the eradication of Helicobacter
pylori infection, by using it in conjunction with standard drug treatment.
H. pylori is a bacterium that causes gastritis, which is an inflammation of the mucosa
(lining) of the stomach. Such infection is very common, with about a half of the
world’s human population infected. Individuals who acquire H. pylori tend to have
chronic, long-term infection unless they are treated with antibiotics. The great
majority of people with H. pylori infection remain symptomless (with less than 15%
having symptoms). The symptoms of gastritis are abdominal pain, nausea and
vomiting. Such disease also occurs in the duodenum (the first part of the small
intestine). [Symptomless gastritis is sometimes referred to as ‘chronic gastritis’ and
the symptomatic version as ‘acute gastritis’.]
If acute gastritis is left untreated, the lining of the stomach and duodenum may
become so damaged that ulcers are formed, which can be very painful.
Furthermore, there is a statistical association between H. pylori infection and cancer
of the stomach. In other words, it seems likely that heavy infection of the stomach by
H. pylori increases the risk of stomach cancer. Eradication of H. pylori from the
stomach and duodenum is therefore an important goal.
The standard treatment for eradicating H. pylori is the use of three drugs
simultaneously (‘triple therapy’). The need for three drugs indicates how difficult it is
to eliminate H. pylori infection. Triple therapy, consisting of two antibiotics and
another type of drug (proton pump inhibitor), is usually very successful in eliminating
the pathogen, but it fails in about 15% of cases. Several studies have indicated that
while probiotics are not able to eradicate H. pylori by themselves, they can be used to
improve the eradication rate (Kamiya, S. et al, 2006). Furthermore, adverse sideeffects of the ‘triple therapy’ drugs (such as diarrhoea, vomiting, nausea, and taste
disturbance) are reduced by probiotics.
In the Sheu (2006) study, a probiotics yoghurt containing Lactobacillus acidophilus
La5 and Bifidobacterium lactis Bb12 was taken by patients who had failed triple
therapy and were about to try ‘quadruple therapy’, in which a fourth drug is added to
the treatment.
Research Review – Helicobacter pylori
Probiotics International Ltd., Matts Lane, Stoke sub Hamdon, Somerset, TA14 6QE
Date: April 2007. This document supersedes all previous documents.
www.protexin.com
Sixty-five patients took the yoghurt for four weeks before the quadruple therapy and
64 patients did not. Both groups took the quadruple therapy for one week, and the
results were compared. Of those in the ‘yoghurt + quadruple therapy’ group, 90.8%
had their H. pylori eradicated, compared to 76.6% of the ‘quadruple therapy only’
group (p<0.05). Furthermore, the adverse effects of quadruple therapy were lower in
the yoghurt.
An additional benefit of the probiotic was in its effect against antibiotic-resistant
strains of H. pylori. Such resistant strains are increasingly common, and make
antimicrobiable therapy of gastritis ‘unmanageable’. In the Sheu (2006) study, slightly
more than half of the patients (who had failed ‘triple therapy’) had strains of H. pylori
that were resistant to either clarithromycin or metronidazole.
In the Sheu (2006) study, it was found that among those receiving the quadruple
therapy only, the eradication rate was much lower among those with metronidazoleresistant H. pylori (57.8%) compared with those with metronidazole-sensitive H.
pylori (90.5%) (p<0.01).
Among those patients receiving the yoghurt, it was found that the yoghurt had a
greater effect in reducing the numbers of H. pylori in people with strains that were
both clarithromycin- and metronidazole-resistant compared with those that had other
strains. This result may be because such resistant strains were more densely populated
on the stomach mucosa.
Summary
The Sheu (2006) study strengthens previous evidence of probiotics:
 improving the eradication rates of gastritis standard antimicrobial drug
treatment (triple or quadruple therapy)
 decreasing the amount of adverse effects caused by the standard drug
treatment
 overcoming problems in eradicating certain antibiotic-resistant strains of H.
pylori.
Background to H. pylori
H. pylori is a Gram-negative, non-sporing, microaerophilic bacterium. It has a
vibrioid shape (ie: a rod shape that is curved with a twist). H. pylori has a tuft of 4-6
flagella at one end of the cell body [A flagellum is a thread-like structure, often longer
than the length of the bacterium, that moves like a whip and enables the bacterium to
swim through its fluid environment]. The flagella make the H. pylori highly motile
and enable the bacterium to move easily even within mucus. The flagella of H. pylori
are unique in being sheathed (a covering which is an extension of the outer membrane
of the bacterium) and it is thought this may be a protection against stomach acid.
Research Review – Helicobacter pylori
Probiotics International Ltd., Matts Lane, Stoke sub Hamdon, Somerset, TA14 6QE
Date: April 2007. This document supersedes all previous documents.
www.protexin.com
H. pylori occur only in humans and other primates, and occasionally in cats. It is the
most common human bacterial infection and is present in about 70% of people with
stomach ulcers and about 90% of those with duodenal ulcers.
It is not known how H. pylori is transmitted, but one route may be by saliva.
In developing countries, H. pylori infection may occur in up to 80% of the population.
In developed countries it is present in about 20% of people under age 30, and in 4060% of those aged 60. The higher prevalence in the older age group may be due to a
lower-level of stomach acid-production as people reach middle age.
The survival of H. pylori within the stomach and duodenum is also aided by its
production of urease. Urease is an enzyme that coverts urea to ammonia, which is an
alkaline compound. The local environment of the H. pylori colony increases in pH
making the environment less harmful to the H. pylori (which prefer a pH of 8). Urea
is a waste product of human cell metabolism and, although most is transported in the
bloodstream to the kidneys, to be added to urine, some urea passes from the
bloodstream into the stomach, and is available for use by H. pylori.
H. pylori colonise the mucosa of the stomach and the duodenum. In the stomach there
are two important different types of mucosa, and ulcers form mainly in the border
between the two types (although the precise mechanisms by which damage is caused
is not clear). One type of mucosa secretes gastric acid and the other doesn’t. H. pylori
colonise the non-acid-secreting mucosa. This mucosa has mucus laying over it and the
H. pylori are protected from the effects of stomach acid by the mucus layer. Within
gastric mucus the pH is about 7.4, compared with pH 1-2 within the stomach lumen.
H. pylori swim in the mucus and attach to the epithelial surface of the mucosa, where
they multiply. H. pylori do not invade the mucosal tissues or the bloodstream.
Colonisation of the epithelium by H. pylori leads to inflammation, tissue destruction
and ulceration. [Ulceration of the stomach and/or duodenum is known as peptic
ulcer.]
Research Review – Helicobacter pylori
Probiotics International Ltd., Matts Lane, Stoke sub Hamdon, Somerset, TA14 6QE
Date: April 2007. This document supersedes all previous documents.
www.protexin.com