Management of Helicobacter pylori infection

Abstract

Helicobacter pylori infection exhibits a wide disease spectrum ranging from asymptomatic gastritis, peptic ulcer disease, to gastric cancer. H. pylori can induce dysbiosis of gastric microbiota in the pathway of carcinogenesis and successful eradication can restore gastric homeostasis. Diagnostic testing and treatment for H. pylori infection is recommended in patients with active or past history of peptic ulcer, chronic dyspepsia, chronic non-steroidal anti-inflammatory drugs (NSAID) or aspirin use, precancerous gastric lesions, gastric cancer, mucosa-associated lymphoid tissue (MALT) lymphoma, family history of gastric cancer, family history of peptic ulcers, household family member having active H. pylori infection, iron deficiency anemia, idiopathic thrombocytopenic purpura, or vitamin B12 deficiency. Recommended first-line regimens for H. pylori eradication are classified according to clarithromycin resistance. In areas of high clarithromycin resistance (≥15%), we recommend 14-day concomitant therapy or 14-day bismuth quadruple therapy (BQT) as first-line regimen. In areas of low clarithromycin resistance (<15%), we recommend 14-day triple therapy or 14-day BQT as first-line treatment. Second-line regimens are 14-day levofloxacin triple therapy or 14-day BQT if BQT is not previously used. For patients with multiple treatment failure, antimicrobial susceptibility testing (AST) should be performed. If AST is not available, we recommend using antibiotics not previously used or for which resistance is unlikely, such as amoxicillin, tetracycline, bismuth, or furazolidone. High-dose potent proton pump inhibitor or vonoprazan is recommended to achieve adequate acid suppression. Probiotics can be used as an adjuvant treatment to reduce the side effects of antibiotics and enhance eradication rate.

Keywords: Helicobacter pylori; management; treatment.

Figure 1

Global prevalence (upper panel), regional prevalence of H. pylori infection (lower left panel), and age‐standardized incidence rate of gastric cancer in ASEAN (lower right panel).

Figure 2

Interplays between H. pylori infection and gastric microbiome. In normal condition, the mucus layer over gastric epithelial cells is the habitat of highly diverse bacteria phyla. The most abundant phylum is Firmicutes, followed by Proteobacteria, and Bacteroidetes. In H. pylori‐associated chronic gastritis, dysbiosis develops with decreased microbial diversity. There is higher abundance of Proteobacteria, but lower number of other phyla. As carcinogenesis continues, reduced H. pylori abundance and higher degree of dysbiosis are observed in intestinal metaplasia and dysplasia. In gastric cancer, oropharyngeal or intestinal commensals (Streptococcus, Lactobacillus, Veillonella, and Prevotella) are enriched.

Figure 3

Algorithm for H. pylori management.

Figure 4

Algorithm for management of multiple H. pylori treatment failure.