Bactericidal action of mastic gum on H. pylori.
(Care and treatment)
Medicine, Botanic (Research)
Medicine, Herbal (Research)
|Publication:||Name: Australian Journal of Medical Herbalism Publisher: National Herbalists Association of Australia Audience: Academic Format: Magazine/Journal Subject: Health Copyright: COPYRIGHT 2010 National Herbalists Association of Australia ISSN: 1033-8330|
|Issue:||Date: Summer, 2010 Source Volume: 22 Source Issue: 2|
|Topic:||Event Code: 310 Science & research|
|Product:||SIC Code: 2861 Gum and wood chemicals|
|Geographic:||Geographic Scope: Australia Geographic Code: 8AUST Australia|
Dabos K, Sfika E, Vlatta L, Giannikopoulos G. 2010. The effect of
mastic gum on Helicobacter pylori: A randomized pilot study. Phytomed
Helicobacter pylori is now well known as a gram negative bacteria that plays a role in the pathogenesis of peptic ulcers, gastritis, primary B cell gastric lymphoma and adenocarcinoma of the stomach. Eradication is difficult and generally requires a triple drug regime to achieve. This is related to a number of side effects and there is the concern of the development of bacterial resistance. Thus natural alternatives are needed. Mastic gum is a natural resin that is excreted from Pistacia lentiscus var. chia, which has shown some activity in healing peptic ulcers and treating gastrointestinal upsets. The active consitutents may include mono and sesquiterpenoids (essential oils) and triterpenoids (e.g. masticadienonic acid).
The current randomised controlled trial was designed to assess the efficacy of this natural gum as a monotherapy or in combination with pantoprazole (a proton pump inhibitor) and compare this with the standard regime. Fifty two patients with H. pylori (as assessed by a C urea breath test) but no active ulcers were randomised into four groups which received:
* Group A--Low dose mastic gum monotherapy: 350 mg three times daily for 14 days;
* Group B--High dose mastic gum monotherapy: 1 g three times daily for 14 days;
* Group C--Mastic gum 350 mg three times daily and pantoprazole twice daily for 14 days; or
* Group D--Standard therapy of pantoprazole 20 mg twice daily, amoxicillin 1 g twice daily and clarithromycin 500 mg twice daily for 10 days.
The mastic gum was supplied in capsule form without any additives or flavourings. One week into the study patients were telephoned to assess compliance and adverse effects. Following treatment (5 weeks later) they were physically examined and routine laboratory tests were undertaken. The following percentages of patients achieved eradication:
* Group A--30.8%
* Group B--38.5%
* Group C--0%
* Group D--76.92%
Groups A and B also showed reduced urea breath test values which correspond to a reduced bacterial load. The only group to achieve statistically significant results was the conventional treatment group, but there was a trend towards significance in both mastic gum monotherapy groups, with dose increases producing increased efficacy. Only two patients in the mastic gum groups complained of adverse effects (diarrhea and nausea) compared with three patients in group D (abdominal cramping and diarrhea), one of which was so severe it caused the participant to cease the trial.
Previous studies have shown conflicting results on the bactericidal activity (against H. pylori) of mastic gum in vivo. This study displays the ability to eradicate the bacteria, but not to the same extent as allopathic triple therapy. It may be worth considering as an adjunctive herbal treatment or a monotherapy in those patients unwilling to undergo conventional eradication programs.
Tessa Finney-Brown mnhaa
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