A reliable diagnosis is mandatory for the identification of infection and to confirm eradication of infection. Although bacterial culture from the gastric biopsy is the “gold” standard technique for H. pylori identification, and is recommended for antibiotic susceptibility testing, it is not practical for all patients. Although infrequently indicated, quantitative polymerase chain reaction (PCR) on gastric biopsies can be used to detect low bacterial loads, the use of the testing is limited by its high cost.10 Others have suggested the measurement of decreased plasma pepsinogen II may be a reliable biomarker to confirm successful eradiation of H. pylori infection.11 However, studies are with limited numbers of patients, and inconclusive findings.

Others have suggested that H. pylori infection plays a role in the development of other conditions. Hwang et al12, in a systematic review and meta-analysis, found no evidence that H. pylori infection plays a role in the pathogenesis or development of chronic tonsillitis. Gomes et al13 concluded that recurrent aphthous stomatitis (RAS) ulcers are not associated with the presence of bacteria in the oral cavity and there is no evidence that H. pylori infection drives RAS development. Sun et al14 hypothesized that host genetic factors that control the production of cytokines, including interleukin -1ß, which affect susceptibility to many H. pylori-related diseases. The authors concluded that the findings of their meta-analysis showed that IL1ß-31C>T polymorphism might increase H. pylori risk in Asian and Latin American populations, that TNFa-308G>A and -1031T>C polymorphisms may be protective factors against H. pylori infection15, and that -863C>A may be a risk factor in Asian populations. However, they indicate further studies with different ethnicities and larger samples size are needed to validate their findings.

AmHPR H. pylori antibiotic resistance panel testing examines antibiotic resistance to 6 antibiotic types that are currently used in H. pylori treatment by means of NGS: 23S rRNA for clarithromycin; gyrA for fluoroquinolones; rdxA for metronidazole; pbp1 for amoxicillin; 16S rRNA for tetracycline, and rpoB for rifabutin. Binh et al16 stated that metronidazole resistance is a key factor associated with H. pylori failure. The authors confirmed that the mutations in rdxA were mainly associated with metronidazole resistance, and mutations in frxA were able to enhance H. pylori resistance only in the presence of rdxA mutations. These authors conclude that further work is needed to identify the role of mutations associated with treatment failure. In a large pilot study by17 and colleagues on 849 Indonesian dyspeptic patients, authors showed a high prevalence of metronidazole and levofloxacin resistance with low prevalence of clarithromycin, amoxicillin and tetracycline resistance, largely related to local antibiotic consumption. They noted that resistance is primarily due to the H. pylori genotype, rather than the human genotype.

Multiple regimens are available for treating H. pylori infection. The first-line regimen for H. pylori eradication includes proton pump inhibitor (PPI), clarithromycin (CAM), and amoxicillin (AMX), or metronidazole. Proton pump inhibitors (PPIs) suppress acid production in combination with antibiotic treatment. However, the failure rate of triple anti-H. pylori therapies has increased up to 30%. The known factors for therapy failure include antibiotic resistance, poor compliance, high gastric acidity, and high bacterial load.