Gastric Microenvironment Enables Persistence of Helicobacter pylori: a Physician's Combat Towards Eradication and Directions for the Future

Abstract

lymphoid tissue (MALT) lymphoma, and gastric carcinoma (Malfertheiner et al., 2009; Kuipers, 1997; IARC monograph, 1994) as being associated with H. pylori infection. Efforts were also focused on instituting modalities to counter these pathologies in the form of reinforcing the gastric wall and killing the causative bacteria. Deep insight into the microbial structure, virulence factors, pathogenesis, and associated pathological states has directed scientists and clinical researchers to design compactly constituted drug regimens comprising antibiotics (amoxicillin, clarithromycin, metronidazole, levofloxacin, etc.), anti-secretory agents (PPIs and H2 blockers), and topical medications (colloidal bismuth preparations) for the eradication of H. pylori. These endeavours should simplify and expedite the process of the absolute eradication of H. pylori from the stomach. However, it proves to be a significant challenge. This bacterial endurance has been attributed to phenotypic and genotypic variations such as the development of drug resistance (Ebinesh and Kailash, 2016; Broutet et al., 2003) and the impotency of antimicrobial agents in the stomach (Vakil and Megraud, 2007; Bloom and Polak, 1980). The role of the stomach and its microenvironment in eradication failure (Table 1) and future prospects for successful eradication will be discussed.