New scientific data is raising concerns: millions of people born in recent decades are at risk of developing stomach cancer. According to estimates published in leading journals, up to 76% of these cases will be directly triggered by a single bacterium—Helicobacter pylori. This widespread, yet often overlooked infection is coming to the forefront of the global healthcare agenda. Experts emphasize that inaction is unacceptable, as stomach cancer remains one of the leading causes of cancer mortality worldwide, and in this case, the threat is preventable.
Explanations from internal medicine experts help provide a complete picture. Helicobacter pylori is a microorganism that colonizes the stomach lining. Its presence is often associated with gastritis and peptic ulcers. However, the main danger lies in the fact that without adequate treatment, the infection significantly increases the risk of developing malignant tumors. Moreover, infection can be completely asymptomatic, though it sometimes manifests as abdominal pain, nausea, or loss of appetite. The main transmission routes are consumption of contaminated water and food, as well as household contact with an infected person.
The mechanism by which the bacterium triggers cancer is quite insidious. It provokes chronic inflammation in the stomach tissues and releases specific toxins known as VacA and CagA. These substances disrupt the local immune response and cause genetic and epigenetic damage. Over time, such changes create favorable conditions for the malignant transformation of cells. Numerous epidemiological and experimental studies have confirmed a strong link between prolonged infection and the development of distal gastric adenocarcinoma.
It is important to understand that not every infected person is doomed to develop cancer. The transformation into a malignant tumor depends on a range of factors. Among these are the virulence of the bacterial strain itself (the presence of the CagA gene), the host’s genetic predisposition, age, gender, and lifestyle. In particular, a diet high in salt and smoking significantly increase the risks. Statistically, only 1-3% of those infected will eventually develop stomach cancer. Nevertheless, due to the extremely high prevalence of this infection in the population, it remains a key cancer risk factor.
Diagnosing the infection is not particularly difficult. Doctors recommend screening primarily for people in high-risk groups: those with a family history of stomach cancer or who have already developed precancerous changes in the mucosa. Both non-invasive methods, such as a breath test or stool antigen analysis, and invasive methods, which require gastroscopy with biopsy for further analysis, are used to detect the bacteria.
Fortunately, once the diagnosis is confirmed, doctors have effective treatment regimens aimed at completely eliminating the bacteria. Antibiotics form the basis of therapy. There are various protocols, including the classic triple therapy or bismuth-based quadruple therapy, with the choice depending on regional patterns of bacterial resistance and the patient’s medical history. The key point emphasized by specialists is timing. Eradicating Helicobacter pylori before irreversible changes occur in the mucosa can reduce the risk of cancer by an impressive 40–60%, effectively breaking the harmful chain of events.
However, there is a serious obstacle to complete recovery—the growing antibiotic resistance of the bacteria. Resistance to drugs such as clarithromycin and metronidazole significantly reduces the effectiveness of standard treatment protocols. This leads to persistent infection, continued oncological risk, and requires doctors to develop more complex, tailored treatment strategies.
In conclusion, experts outline four fundamental principles to address this issue. First, antibiotics must be used rationally to avoid worsening resistance problems. Second, if treatment fails, bacterial sensitivity testing should be performed. Third, treatment regimens should be chosen based on local resistance data. And finally, patient education and improving adherence to treatment are crucial to prevent failure and the development of secondary resistance.
