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New england journal of medicine
New England Journal of Medicine
December 24, 1998
Vol. 339, No.26
Mastic Gum Kills Helicobacter pylori
Farhad U. Huwez, M.R.C.P., Ph.D.
Barnet General Hospital, Barnet, Herts EN5 3DJ, United Kingdom
Debbie Thirlwell, B.Sc., Alan Cockayne, Ph.D.,
Dlawer A.A. Ala'Aldeen, Ph.D., M.R.C.Path.
University Hospital, Nottingham NG7 2UH, United Kingdom
To the Editor:
Even low doses of mastic gum - 1 g per day for two weeks - can cure peptic
ulcers very rapidly, but the mechanism responsible has not been clear. We have found that mastic is active against Helicobacter pylori, which could explain its therapeutic effect in patients with peptic ulcers.
Mastic is a resinous exudate obtained from the stem and the main leaves of Pistacia lentiscus. It
is used as a food ingredient in the Mediterranean region. Clinically, mastic has been effective in the treatment of benign gastric ulcers1 and duodenal ulcers2. In rats, mastic showed cytoprotective and mild antisecretory properties3. We assessed the antibacterial properties of mastic against H. pylori.
The H. pylori strains NCTC 11637 (a standard reference strain) and six fresh clinical isolates
(three were sensitive and three were resistant to metronidazole) were maintained by passage on 7 percent horse chocolate blood agar or in IsoSensitest broth (with 5 percent fetal-calf serum) at 37°C in a microaerobic atmosphere (6 percent oxygen and 5 percent carbon dioxide in nitrogen).
Mastic was prepared as a stock solution in ethanol at a concentration of 50 mg per milliliter and
diluted in the broth culture (containing 107 cells of H. pylori per milliliter) for a final concentration ranging from 0.0075 to 1.0 mg per milliliter. Ethanol was added to control cultures at appropriate concentrations. The cultures were incubated, 10-µl aliquots were obtained and seeded on agar plates at various times for up to 48 hours, and the minimal bactericidal concentrations (the minimal concentration of drug required to kill 99.9 percent of the organisms in the medium after overnight incubation) were determined.
Mastic killed the H. pylori NCTC 11637 strain and the six clinical isolates (reduction in the
viable count by a factor of 1000) irrespective of the organism's level of susceptibility to nitroimidazoles. The minimal bactericidal concentration at 24 hours for all strains that were studied was 0.06 mg of the crude mastic per milliliter. At lower concentrations, bacterial growth was still significantly inhibited, with a clear postantibiotic effect even at the lowest concentration used, 0.0075 mg per milliliter. Mastic induced clear ultrastructural changes in the organism, as demonstrated by transmission electron microscopy (data not shown).
These results suggest that mastic has definite antibacterial activity against H. pylori. This
activity may at least partly explain the anti-peptic-ulcer properties of mastic1,2. Examination of the anti-H. pylori effect of the various constituents of mastic, which have been recently identified4, may pinpoint the active ingredient. Mastic is cheap and widely available in Third World countries; therefore, our data should have important implications for the management of peptic ulcers in developing countries. References: 1. Huwez FU, Al-Habbal MJ. Mastic in treatment of benign gastric ulcers. Gastroenterol Japon 1986;21:273-4. 2. Al-Habbal MJ, Al-Habbal Z, Huwez FU. A double-blind controlled clinical trial of mastic and placebo in the treatment of duodenal ulcer. J Clin Exp Pharm Physiol 1984;11:541-4. 3. Al-Said MS, Ageel AM, Parmar NS, Tariq M. Evaluation of mastic, a crude drug obtained from Pistacia lentiscus for gastric and duodenal anti-ulcer activity. J Ethnopharmacol 1986;15:271-8. 4. Papageorgiou VP, Bakola-Christianopoulou MN, Apazidou KK, Psarros EE. Gas chromatographic-mass spectroscopic analysis of the acidic triterpenic fraction of mastic gum. J Chromatogr 1997;769:263-73.
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