In 1982, Australian scientists Dr. Barry Marshall and Dr. Robin Warren discovered Helicobacter pylori, a spiral-shaped bacterium that thrives in the harsh acidic environment of the human stomach.
This groundbreaking discovery earned them the Nobel Prize in Medicine in 2005, as they demonstrated that H. pylori causes stomach ulcers and, later, its connection to stomach cancer.
Dr. Marshall even drank a solution containing the bacteria to prove its link to gastritis and ulcers, which led to antibiotics becoming the standard treatment.
Decades after the discovery, researchers at the National Taiwan University College of Medicine sought to determine if testing for H. pylori in stool samples could help identify individuals at higher risk for stomach cancer.
Their study, published in JAMA, involved tens of thousands of participants and aimed to assess whether adding H. pylori stool antigen tests (HPSA) to the standard fecal immunochemical test (FIT), which screens for colon cancer, could better predict stomach cancer risk.
Stomach cancer, also called gastric cancer, is not a leading cause of cancer in Western countries but remains a major health concern in Asia, including Japan and Taiwan.
Globally, H. pylori-associated stomach adenocarcinoma ranks as the third leading cause of cancer, with approximately 800,000 new cases each year.
An estimated 90% of gastric cancer cases are linked to H. pylori, which has been classified as a Class 1 carcinogen by the World Health Organization, meaning there is strong evidence that it causes cancer.
In the Taiwan study, led by Dr. Yi-Chia Lee, researchers invited over 150,000 residents aged 50–69 to participate. Of these, 63,508 were randomized to undergo both HPSA and FIT screening, while 88,995 were screened with FIT alone.
FIT detects hidden blood in stool and has shown some effectiveness in identifying stomach cancer, even though it is primarily used for colon cancer screening. The study aimed to see if combining HPSA and FIT could improve detection and reduce stomach cancer rates and mortality.
- pyloriis a tricky target for screening because it infects about half the world’s population, yet most people never develop symptoms. Factors like genetics, diet, and environment play a role in whether the infection leads to chronic inflammation, ulcers, or cancer.
The bacteria survive stomach acid by producing urease, an enzyme that neutralizes acid by creating a more alkaline environment. Over time, chronic inflammation caused by H. pylori can lead to precancerous changes in the stomach lining.
To combat this, combination therapy using antibiotics and proton pump inhibitors (PPIs) is often prescribed to eradicate H. pylori and reduce cancer risk.
PPIs lower stomach acid, allowing antibiotics to work more effectively. However, the overuse of antibiotics poses the risk of resistance, so treatments are carefully designed to balance effectiveness with this concern.
The results of the study were mixed. The combined HPSA and FIT group had a slightly lower stomach cancer incidence rate (0.032%) compared to the FIT-alone group (0.037%).
However, mortality rates were similar between the two groups: 0.015% for the combination group and 0.013% for the FIT-only group. The findings suggest that adding HPSA screening to FIT did not significantly reduce stomach cancer rates or deaths.
The researchers noted that when differences in participation and follow-up times were accounted for, the combined test group showed a slightly lower cancer incidence but no significant impact on mortality.
While the study didn’t demonstrate a clear benefit of HPSA screening over FIT alone, it highlights the complexity of H. pylori as a screening target and the challenges of preventing stomach cancer.
Future research may focus on improving screening methods and exploring how factors like ethnicity and lifestyle influence H. pylori-related cancer risks. For now, the study reinforces the importance of understanding and managing H. pylori infections to reduce the global burden of stomach cancer.
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The findings are published in JAMA.
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