Evolving Concepts in Helicobacter pylori Management

Abstract

Helicobacter pylori is the most common chronic bacterial infection worldwide and the most significant risk factor for gastric cancer, which remains a leading cause of cancer-related death globally. H pylori and gastric cancer continue to disproportionately impact racial and ethnic minority and immigrant groups in the United States. The approach to H pylori case-finding thus far has relied on opportunistic testing based on symptoms or high-risk indicators, such as racial or ethnic background and family history. However, this approach misses a substantial proportion of individuals infected with H pylori who remain at risk for gastric cancer because most infections remain clinically silent. Moreover, individuals with chronic H pylori infection are at risk for gastric preneoplastic lesions, which are also asymptomatic and only reliably diagnosed using endoscopy and biopsy. Thus, to make a significant impact in gastric cancer prevention, a systematic approach is needed to better identify individuals at highest risk of both H pylori infection and its complications, including gastric preneoplasia and cancer. The approach to H pylori eradication must also be optimized given sharply decreasing rates of successful eradication with commonly used therapies and increasing antimicrobial resistance. With growing acceptance that H pylori should be managed as an infectious disease and the increasing availability of susceptibility testing, we now have the momentum to abandon empirical therapies demonstrated to have inadequate eradication rates. Molecular-based susceptibility profiling facilitates selection of a personalized eradication regimen without necessitating an invasive procedure. An improved approach to H pylori eradication coupled with population-level programs for screening and treatment could be an effective and efficient strategy to prevent gastric cancer, especially in minority and potentially marginalized populations that bear the heaviest burden of H pylori infection and its complications.

Keywords: Antibiotic Resistance; Gastric Cancer; Gastric Cancer Screening; Gastric Intestinal Metaplasia; H pylori Treatment; Helicobacter pylori; Susceptibility Testing; Under-represented Minorities.

Figure 1.. Incorporating antimicrobial resistance testing into practice.

* If not allergic to penicillin and not previously tried ^ Using an optimized regimen if originally not used (rabeprazole 20mg twice daily or esomeprazole 40mg twice daily) and metronidazole 500mg four times daily

Bismuth Quad: bismuth, tetracycline, metronidazole and PPI Rifabutin Triple: rifabutin, amoxicillin, and PPI PCAB Amoxicillin dual: PCAB, amoxicillin PCAB/PPI Amoxicillin dual: PCAB or PPI and amoxicillin Clarithromycin Triple: clarithromycin, amoxicillin (or metronidazole), and PPI or PCAB Metronidazole Triple: metronidazole, amoxicillin and PPI Levofloxacin Triple: levofloxacin, amoxicillin and PPI Notes 1. Modified from algorithms developed by Shah et al and Graham and Moss. 2. Acceptable alternative empiric regimens to bismuth quadruple include rifabutin triple and PCAB amoxicillin dual, if shown to have adequately high local eradication success. 3. This suggested approach is primarily for U.S. patients and is based on some trial data from the U.S. but is mostly at the level of expert opinion. 4. For detailed descriptions of medication doses and frequencies see Chey et al and Shah et al. For PCAB therapy dosing see Chey et al.

Figure 2.. Multifactorial mechanisms contributing to H. pylori eradication failure.