NEW YORK (Reuters Health) – Pretreating antibiotic-resistant Helicobacter pylori with a mucolytic that destroys bacterial biofilm can eradicate infection in many cases, Italian research shows.

“A standard rescue therapy against H. pylori is still lacking, and antimicrobial sensitivity testing is currently recommended for patients who have failed eradication therapy,” Dr. Giovanni Cammarota of A. Gemelli University Hospital in Rome and colleagues note in a paper published online May 17th in Clinical Gastroenterology and Hepatology.

“We carried out a novel approach to achieve H. pylori eradication after multiple treatment failures, based on the hypothesis that microbial biofilm may support H. pylori’s tenacious resistance to antibiotics.”

The researchers first showed that adding n-acetylcysteine, a mucolytic, to H. pylori isolates from 10 patients who had failed at least four earlier eradication attempts inhibited biofilm formation.

Then they randomly assigned 40 such patients to one of two groups: the first received a one-week pretreatment with 600 mg n-acetylcysteine followed by a one-week culture-guided antibiotic regimen, including a proton-pump inhibitor and two antibiotics; the second received only the antibiotic regimen, also including a proton-pump inhibitor and two antibiotics. All patients completed treatment.

At two months after therapy, C13-urea breath testing showed that 13 pretreated patients (65%) were no longer infected with H. pylori, compared to 4 (20%) of the patients receiving only antibiotics (p<0.01). Mild side effects such as diarrhea and stomatitis were reported in both groups. Repeat endoscopy in 60% of patients revealed that H. pylori biofilm had disappeared in all patients in whom the bacteria had been eradicated. VacA and CagA genotypes of H. pylori had no effect on treatment outcome. “Larger studies will be necessary to confirm our results and clarify whether treatment success can be improved by increasing the dosage of or the exposure to (n-acetylcysteine) before or during antibiotic treatment,” Dr. Giovanni Cammarota and colleagues conclude. “New strategies are being envisaged to design substances that can either inhibit biofilm formation or destabilize biofilms.” Reference:
http://www.cghjournal.org/article/S1542-3565%2810%2900454-4/abstract

Clin Gastroenterol Hepatol 2010.