Helicobacter pylori (H. pylori) is a bacterium that has adapted to colonize the harsh, acidic environment of the human stomach. This common infection affects over half of the global population, often acquired in childhood and persisting for life if left untreated. While many individuals remain asymptomatic carriers, the infection sets the stage for a progressive disease state. Untreated H. pylori infection poses a risk not just through immediate symptoms but through slow, cumulative damage that can lead to severe gastrointestinal pathology and systemic complications over time.
Chronic Inflammation and Ulcer Development
The presence of H. pylori immediately triggers a persistent inflammatory response in the stomach lining, a condition known as chronic gastritis. To survive the stomach’s highly acidic conditions, the bacterium produces a large amount of the enzyme urease. Urease hydrolyzes urea, which is naturally present in the stomach, into carbon dioxide and ammonia.
The resulting ammonia is alkaline, effectively neutralizing the stomach acid in the immediate area surrounding the bacteria, creating a protective microenvironment. This process is also damaging to the gastric mucosa and stimulates the production of more stomach acid elsewhere. The continuous inflammation and the toxic effects of ammonia weaken the protective mucosal barrier that normally shields the stomach and duodenal walls from digestive acids and enzymes.
When this protective mechanism is overwhelmed, concentrated acid and pepsin begin to erode the compromised tissue, leading to the formation of open sores called peptic ulcers. Ulcers most commonly form in the stomach or the duodenum. Symptoms often include a burning or gnawing abdominal pain, which may be accompanied by nausea, bloating, or vomiting. Untreated ulcers can lead to serious, life-threatening complications such as internal bleeding or perforation.
Nutritional Deficiencies Caused by Infection
The systemic consequences of chronic H. pylori infection impact the body’s ability to absorb essential nutrients. Persistent inflammation, particularly in the stomach, can lead to chronic atrophic gastritis. This results in reduced or absent stomach acid production, known as hypochlorhydria or achlorhydria.
This altered stomach environment significantly impairs the absorption of iron, leading to iron deficiency anemia. Stomach acid is required to release iron from food and keep it in a soluble form necessary for absorption. Furthermore, the chronic inflammatory state increases the production of hepcidin, a peptide that regulates iron metabolism by blocking its absorption and release from storage.
H. pylori infection also contributes to a deficiency in Vitamin B12, which can result in megaloblastic anemia. Long-term chronic gastritis damages the parietal cells in the stomach lining, which produce intrinsic factor. Intrinsic factor is a protein necessary for the absorption of Vitamin B12 in the small intestine. Without sufficient intrinsic factor, the body cannot process B12 from the diet, leading to malabsorption and subsequent neurological and hematological issues.
Progression to Malignancy
Untreated H. pylori infection represents the greatest risk factor for the development of gastric cancers. This progression begins with chronic inflammation (gastritis) and slowly advances through a multi-stage process known as the Correa Cascade, leading to chronic atrophic gastritis.
As the tissue continues to change, the damaged tissue is replaced with cells that resemble those found in the intestine, a pre-cancerous condition called intestinal metaplasia. Over time, these metaplastic cells can become increasingly abnormal, progressing to dysplasia and eventually to Gastric Adenocarcinoma, the most common form of stomach cancer. Certain virulent strains of H. pylori that possess the cagA gene are associated with an increased risk of this malignancy.
Distinct from adenocarcinoma, H. pylori is also directly linked to the development of Mucosa-Associated Lymphoid Tissue (MALT) Lymphoma in the stomach. The chronic presence of the bacteria causes an abnormal accumulation of lymphoid tissue in the stomach wall. This sustained antigenic stimulation triggers the uncontrolled proliferation of B-cells, which can transform into a low-grade MALT lymphoma. In a majority of early-stage MALT lymphoma cases, successful eradication of the H. pylori infection with antibiotics can lead to the regression of the lymphoma.
Continued Risk of Transmission
An individual who harbors an untreated H. pylori infection continues to serve as a reservoir for the bacteria. This continued carriage poses a persistent public health concern, maintaining the cycle of infection within close-knit communities, especially families. The primary routes of transmission are person-to-person, mainly through the fecal-oral and oral-oral pathways.
The oral-oral route involves transmission through saliva or vomitus, while the fecal-oral route is associated with poor hygiene and sanitation. The clustering of H. pylori infection within households suggests that intrafamilial spread is a major factor, with infected parents posing a risk to their children. Treating the infection is therefore not only a matter of personal health protection but also a measure to prevent the infection of close contacts. Eradicating the bacteria in the infected individual is the most effective way to break this chain of transmission and reduce the overall prevalence of the infection.