H. pylori is one of the most common chronic bacterial infections worldwide, affecting an estimated 4.4 billion people. Incidence and prevalence of infection vary widely, with the highest rates of infection reported in Latin and South America, Russia, and Asia. Where data are available, rates are generally lower in high-income countries (HICs) than low- and middle-income countries (LMICs). However, H. pylori infection remains reasonably common in HICs, with prevalence rates of up to 30% to 50%.Geographical variability also occurs within countries. For example, within the US, prevalence rates vary substantially by state, from 12% in Washington up to 34% in Mississippi. Variation in prevalence among states is, at least partly, due to sociodemographic factors
In addition to the identified risk factors for the acquisition of H. pylori infection, a number of additional factors increase the risk of severe outcomes from infection, including peptic ulcer and gastric cancer. Since the risk of development of gastric cancer increases with the severity and extent of atrophic gastritis and intestinal metaplasia, timely eradication of the underlying H. pylori infection is important for limiting the risk. Eradication reduces the risk of gastric cancer in individuals who have not already developed severe or extensive atrophy or intestinal metaplasia.
The virulence of the H. pylori strain can also affect the risk of development of more serious outcomes.
H. pylori produces a number of virulence factors depending on the strain.
H. pylori cytotoxin-associated gene A (cagA)-positive strains have been identified as the strongest risk factor for gastric cancer.
After adherence to gastric epithelial cells, H. pylori cagA-positive strains deliver CagA into the host cytoplasm via a pilus-like type IV secretion system (TFSS) syringe.
CagA disrupts a number of signal transduction pathways, as well as inhibiting normal epithelial differentiation, by altering cell adhesion, migration, and polarity.
Among the other virulence factors associated with gastric cancer development are vacuolating cytotoxin A (VacA) and blood group antigen-binding adhesin (BabA).
VacA induces vacuole formation; strains of H. pylori that carry the s1 or m1 genotypes, which are associated with high vacuolation, have been associated with an increased risk of gastric cancer in Western populations.
BabA is an adhesin that binds to Lewis b blood group antigens and determines the colonization density of H. pylori. Both BabA high- and low-producing strains are associated with an increased risk of gastric cancer, compared with BabA-negative strains.
All three of these virulence factors have also been associated with an increased risk of peptic ulcer disease.
Genetic factors and environmental factors also play a key role in H. pylori infection outcome.
Risk of development of peptic ulcer disease is higher in patients with a family history of peptic ulcers.
Furthermore, a number of genetic polymorphisms have been identified as potentially predisposing to the development of gastric atrophy and increased risk of gastric cancer.
Many of these polymorphisms have been identified in genes involved in the immune response, including those encoding interleukins and pro-inflammatory cytokines, such as TNF-α.
Dietary influences have also been noted in the risk of the development of peptic ulcers and gastric cancer from H. pylori infection. Diets high in salt, saturated fat, cholesterol, and refined carbohydrates, and low in vitamin C have been associated with a higher odds of developing gastric cancer.
In regions of the world with a high prevalence of H. pylori and associated diseases, such as the Western Pacific, universal or population screening is being considered, mainly to lower the high burden of gastric cancer cases. As an example, the Chinese National Consensus Report recommends screening and treatment in regions with a high risk of gastric cancer.
Given the relative low prevalence of H. pylori infection in the US, the ACG recommends against universal or population-based screening.
However, there are specific populations within the US, principally immigrants from high gastric cancer risk areas (Western Pacific, Central and South America, Eastern Europe), who might benefit from targeted H. pylori screening efforts.