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H. pylori infection may increase colorectal cancer risk, particularly among African-Americans
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Helicobacter pylori infection appeared associated with increased risk for colorectal cancer, particularly among African-Americans, according to study results.
Previous data linking H. pylori and CRC risk have lacked consistency, according to Meira Epplein, PhD, co-leader of cancer control and population sciences at Duke Cancer Institute and associate professor of population health sciences at Duke University School of Medicine, and colleagues.
In their study, Epplein and colleagues analyzed 4,063 prediagnosis serum samples from patients who were later diagnosed with colorectal cancer. Investigators also analyzed samples from an equal number of matched controls.
The researchers evaluated antibody responses to 13 H. pylori proteins, including virulence factors VacA and CagA.
Results showed H. pylori seropositivity in 41% of prediagnosis samples and 40% of controls (OR = 1.09; 95% CI, 0.99-1.2). Researchers observed an increased risk for colorectal cancer among patients with H. pylori VacA-specific seropositivity (OR = 1.11; 95% CI, 1.01-1.22), and particularly among African Americans (OR, 1.45; 95% CI, 1.08-1.95).
HemOnc Today spoke with Epplein about the study, the benefits and risks of H. pylori, and the racial disparities that may be responsible for higher colorectal cancer rates among African-American populations.
Question: Why did you choose to explore the association between H. pylori and colorectal cancer?
Answer: H. pylori is the established main cause of stomach cancer. I have been working in Asia, where stomach cancer is very common, and with the Southern Community Cohort Study, which is a study of low-income whites and African-Americans in the southeastern U.S. We found 80% in this subset had evidence of current or past H. pylori infection. This was astounding to us, and I wanted to know the other implications of this high prevalence of infection. People have looked in the literature for associations between H. pylori and a number of comorbidities. After stomach cancer, the one that seemed to hit the most in databases was colorectal cancer. We don’t have any evidence that H. pylori lives in the colon, but you can imagine that there could be some downstream effects from the stomach into the intestines. We sought to look at this somewhat controversial association of infection with colorectal cancer.
Q: You mentioned this a controversial association. Why?
A: What we reported is an association. We can’t say H. pylori causes colorectal cancer. What we can say is that people who have H. pylori, particularly people of color who have high antibody levels to certain H. pylori proteins, have increased odds for developing colorectal cancer. One result could be that we change people’s colonoscopy screening schedule, such as we do based on risk factors like adenomas or the size of the polyps. If this could be another marker for colorectal cancer risk, we could possibly catch cancer earlier.
Q: What were some of the most noteworthy aspects of the way you conducted this work?
A: When we contacted 10 of the largest cancer cohorts in the U.S., all of them said they would participate. We had the Nurse’s Health Cohort at Harvard, the Multiethnic Cohort study out of Hawaii, the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial, and other national and local cohorts. In these big epidemiological cohorts, you collect blood from healthy people at baseline, and then you follow them to cancer. We had more than 4,000 prospectively ascertained cases, which we then matched 1:1 with controls for age, sex, and race. We sent the samples to the German Cancer Research Center in Heidelberg, Germany, which developed the H. pylori multiplex serology assay. This blood was evaluated using the Luminex platform. They have specifically chosen 13 H. pylori proteins that they think are potential virulence factors.
Q: W hat are the potential implications of the results, given that you haven’t established causality?
A: The ability to put patients into different risk-stratification categories would be a big step, allowing us to identify colorectal cancer earlier. The other thing our data show is how different H. pylori prevalence is by race. We have seen that H. pylori — an ancient microbe — is disappearing in certain populations, but it is not disappearing among people of color. This is a big finding that could translate to the clinic.
Q: Is reinfection a significant concern?
A: Reinfection rates tend to vary by location. There are a couple factors at play, including adherence and antibiotic resistance. The overall reinfection rate of H. pylori is less than 5% in the general population, but that can vary greatly depending on the community you live in and what type of education you receive about oral and fecal hygiene issues. Another point to consider is that, if we eliminate the dominant strain, the patient generally is not going to be reinfected with the same strain.
Q: Could you elaborate on the disparities you observed?
A: It is important for individuals at high risk for stomach cancer, and potentially colorectal cancer, to get tested and treated for H. pylori. However, as we think about eradication, we have to consider that H. pylori has some potential benefits. There is evidence suggesting that infection as a child can build immune response, and that those children are less likely to develop allergies, eczema or other atopic diseases. They also may be less likely to get gastroesophageal reflux disease, Barrett’s esophagus or esophageal adenocarcinoma. There are good reasons why H. pylori has survived, but it’s still a burden. If we can impact colorectal cancer screenings and H. pylori testing and treatment at age 40 years and older, we could make a move on a cancer infection that is much more prevalent among African-Americans than whites.
Q: What are the next steps in research?
A: We are looking forward to a multipathogen approach to find out if there is indeed a causal relationship, even an indirect one. We also hope to see if other infections play a role, as well, and may quantify reactions to see if there is a general risk for gastrointestinal disease. – by Rob Volansky
Reference:
Butt J, et al. Gastroenterology. 2018;doi:10.1053/j.gastro.2018.09.054.
For more information:
Meira Epplein, PhD, can be reached at Cancer Control and Population Sciences Program, Duke Cancer institute, 2424 Erwin Road, Suite 602, Room 6026, Durham, NC 27705; email: meira.epplein@duke.edu.
Disclosure: Epplein reports no relevant financial disclosures.