Additive Effect of Pronase on the Eradication Rate of First-Line Therapy for Helicobacter pylori Infection

Chang Seok Bang, Yeon Soo Kim, Sang Hyun Park, Jin Bong Kim, Gwang Ho Baik, Ki Tae Suk, Jai Hoon Yoon, Dong Joon Kim, Chang Seok Bang, Yeon Soo Kim, Sang Hyun Park, Jin Bong Kim, Gwang Ho Baik, Ki Tae Suk, Jai Hoon Yoon, Dong Joon Kim

Abstract

Background/aims: Helicobacter pylori colonizes on the apical surface of gastric surface mucosal cells and the surface mucous gel layer. Pronase is a premedication enzyme for endoscopy that can disrupt the gastric mucus layer. We evaluated the additive effects of pronase combined with standard triple therapy for H. pylori eradication.

Methods: This prospective, single-blinded, randomized, controlled study was conducted between June and October 2012. A total of 116 patients with H. pylori infection were enrolled in the study (n=112 patients, excluding four patients who failed to meet the inclusion criteria) and were assigned to receive either the standard triple therapy, which consists of a proton pump inhibitor with amoxicillin and clarithromycin twice a day for 7 days (PAC), or pronase (20,000 tyrosine units) combined with the standard triple therapy twice a day for 7 days (PACE).

Results: In the intention-to-treat analysis, the eradication rates of PAC versus PACE were 76.4% versus 56.1% (p=0.029). In the per-protocol analysis, the eradication rates were 87.5% versus 68.1% (p=0.027). There were no significant differences concerning adverse reactions between the two groups.

Conclusions: According to the interim analysis of the trial, pronase does not have an additive effect on the eradication of H. pylori infection (ClinicalTrial.gov NCT01645761).

Keywords: Helicobacter pylori; Pronase.

Figures

Fig. 1
Fig. 1
Flow chart of the study design.

References

    1. Graham DY, Lu H, Yamaoka Y. A report card to grade Helicobacter pylori therapy. Helicobacter. 2007;12:275–278. doi: 10.1111/j.1523-5378.2007.00518.x.
    1. Graham DY, Shiotani A. New concepts of resistance in the treatment of Helicobacter pylori infections. Nat Clin Pract Gastroenterol Hepatol. 2008;5:321–331. doi: 10.1038/ncpgasthep1138.
    1. Graham DY, Fischbach L. Helicobacter pylori treatment in the era of increasing antibiotic resistance. Gut. 2010;59:1143–1153. doi: 10.1136/gut.2009.192757.
    1. Fujii T, Iishi H, Tatsuta M, et al. Effectiveness of premedication with pronase for improving visibility during gastroendoscopy: a randomized controlled trial. Gastrointest Endosc. 1998;47:382–387. doi: 10.1016/S0016-5107(98)70223-8.
    1. Koga M, Arakawa K. On the application of enzymatic mucinolysis in X-ray diagnosis of the stomach. Nihon Igaku Hoshasen Gakkai Zasshi. 1964;24:1011–1031.
    1. Ida K, Okuda J, Nakazawa S, et al. Clinical evaluation of premedication with KPD (pronase) in gastroendoscopy: placebo-controlled double blind study in dye scattering endoscopy. Clin Rep. 1991;25:1793–1804.
    1. Gotoh A, Akamatsu T, Shimizu T, et al. Additive effect of pronase on the efficacy of eradication therapy against Helicobacter pylori. Helicobacter. 2002;7:183–191. doi: 10.1046/j.1523-5378.2002.00079.x.
    1. Hashimoto Y, Tsuiki S, Nisizawa K, Pigman W. Action of proteolytic enzymes on purified bovine submaxillary mucin. Ann N Y Acad Sci. 1963;106:233–246. doi: 10.1111/j.1749-6632.1963.tb16641.x.
    1. Taniguchi Y, Yoshida Y, Kimura K, Mato M. Cytoprotection by 16,16-dimethylprostaglandin E2. Role of gastric juice and mucus gel layer. J Clin Gastroenterol. 1992;14(Suppl 1):S52–S58. doi: 10.1097/00004836-199206001-00009.
    1. Hazell SL, Lee A, Brady L, Hennessy W. Campylobacter pyloridis and gastritis: association with intercellular spaces and adaptation to an environment of mucus as important factors in colonization of the gastric epithelium. J Infect Dis. 1986;153:658–663. doi: 10.1093/infdis/153.4.658.
    1. Shimizu T, Akamatsu T, Sugiyama A, Ota H, Katsuyama T. Helicobacter pylori and the surface mucous gel layer of the human stomach. Helicobacter. 1996;1:207–218. doi: 10.1111/j.1523-5378.1996.tb00041.x.
    1. Chung JW, Lee GH, Han JH, et al. The trends of one-week first-line and second-line eradication therapy for Helicobacter pylori infection in Korea. Hepatogastroenterology. 2011;58:246–250.
    1. Kimura K, Ido K, Saifuku K, et al. A 1-h topical therapy for the treatment of Helicobacter pylori infection. Am J Gastroenterol. 1995;90:60–63.
    1. Endo H, Yoshida H, Ohmi N, Ohta K, Higuchi S. Localization of [14C]amoxicillin in rat gastric tissue when administered with lansoprazole and clarithromycin. J Antimicrob Chemother. 2001;48:923–926. doi: 10.1093/jac/48.6.923.
    1. Patel JK, Chavda JR. Formulation and evaluation of stomach-specific amoxicillin-loaded carbopol-934P mucoadhesive microspheres for anti-Helicobacter pylori therapy. J Microencapsul. 2009;26:365–376. doi: 10.1080/02652040802373012.
    1. Lee GJ, Park SJ, Kim SJ, Kim HH, Park MI, Moon W. Effectiveness of premedication with pronase for visualization of the mucosa during endoscopy: a randomized, controlled trial. Clin Endosc. 2012;45:161–164. doi: 10.5946/ce.2012.45.2.161.
    1. Chang CC, Chen SH, Lin CP, et al. Premedication with pronase or N-acetylcysteine improves visibility during gastroendoscopy: an endoscopist-blinded, prospective, randomized study. World J Gastroenterol. 2007;13:444–447. doi: 10.3748/wjg.v13.i3.444.
    1. Sherwood PV, Wibawa JI, Atherton JC, et al. Impact of acid secretion, gastritis, and mucus thickness on gastric transfer of antibiotics in rats. Gut. 2002;51:490–495. doi: 10.1136/gut.51.4.490.
    1. Whitley E, Ball J. Statistics review 4: sample size calculations. Crit Care. 2002;6:335–341. doi: 10.1186/cc1521.

Source: PubMed

Sponsors and Collaborators

Medical Conditions

Drug Interventions

3
Subscribe