Helicobacter pylori and cancer risk

The main cause of stomach and duodenal ulcers is an infection with Helicobacter pylori, or, simply, H. pylori. This bacterium is also linked to a higher risk of two kinds of stomach cancer.

H. pylori infection is common—up to 67 percent of people worldwide have it, according to the American Cancer Society. Most don’t develop peptic ulcers, and even fewer develop cancer as a result. Oddly enough, this infection may lower the risk of two cancers: one of the upper stomach (called the cardia) and another of the esophagus.

What is H. pylori, and how does it cause cancer?

H. pylori lives in the mucus layer of your stomach’s lining, where it’s protected from harsh stomach acid and immune system cells that attack bacterial infections. Most people probably become infected in childhood by swallowing contaminated food or water, or by mouth-to-mouth contact.

The two types of cancer associated with H. pylori infection are:

• Non-cardia gastric adenocarcinoma, which affects the portion of the stomach not near the esophagus
• Gastric mucosa-associated lymphoid tissue (MALT) lymphoma, an uncommon type of non-Hodgkin lymphoma that develops outside of lymph nodes 

It’s thought that inflammation and injury of the stomach lining by H. pylori infection may lead to cancer. Studies have found infected people have six to eight times greater risk of non-cardia gastric cancer than uninfected people, according to the National Cancer Institute (NCI).

Similarly, H. pylori infection may cause immune system (lymphoid) tissue to grow in the stomach lining. In rare cases, this tissue may become MALT lymphoma. Infected patients are six times more likely to develop MALT lymphoma than uninfected people, according to the NCI.

Infection may lower the risk of some cancers

Scientific evidence suggests H. pylori infection may decrease the chances of esophageal adenocarcinoma and gastric cardia cancer (stomach cancer that grows near the connection to the esophagus).

A meta-analysis of 13 studies found that the risk of esophageal adenocarcinoma is 45 percent lower among infected patients, according to the NCI.

Further support for the phenomenon is the observation that rates of both esophageal carcinoma and gastric cardia cancer have climbed as rates of H. pylori infection have dropped in Western nations, likely as a result of better hygiene and use of antibiotic treatment.

A possible explanation for lower risks of these two cancers is that long-term infection decreases stomach acidity. This would reduce damage done by acid reflux, which happens when stomach acid leaks into the esophagus. When acid reflux is long-standing or chronic, it’s known as gastroesophageal reflux disease (GERD), a condition associated with higher chances of developing adenocarcinomas of the upper stomach and esophagus.

About 10 percent to 15 percent of people who experience GERD develop Barrett’s esophagus, according to the National Institute of Diabetes and Digestive and Kidney Diseases, but being infected with H. pylori may lower your risk. Having Barrett’s esophagus elevates your risk of developing adenocarcinoma of the esophagus.

The association of increased risks of non-cardia gastric cancer and lower risks of cardia gastric cancer and esophageal adenocarcinoma become greater if you’re infected with strains of H. pylori called cagA-positive. Among H. pylori-infected patients, those with cagA-positive strains had double the chances of non-cardia gastric cancer than those with cagA-negative strains, according to the NCI.

Risk factors

You’re more likely to become infected with H. pylori if you live in a developing nation or are older. Of 62 nations included in a review of data from 1970 to 2016 published in Gastroenterology, the highest incidence of infection found was 87.7 percent in Nigeria and the lowest was 18.9 percent in Switzerland.

Though rates have lowered in recent years in the United States, ethnicity may play a role. For example, more than 60 percent of Mexican-Americans are infected, compared with 30 percent of non-Hispanic white Americans, according to a study in Missouri Medicine. Some evidence that genetics may influence infection rates comes from data showing Black Americans with more African ancestry have higher rates than those with less African ancestry.

Risk factors for infection include:

• Lower socioeconomic status
• Larger number of siblings
• Infected parent—especially mother
• Contaminated water supply

Diagnosis and treatment

The American College of Gastroenterology recommends the following groups of patients be tested for H. pylori infection:

• Those who have peptic ulcer disease or a history of it, unless there’s documented proof of successful treatment of H. pylori infection
• Those who have MALT lymphoma
• Those who’ve had endoscopic resection (surgical removal of growths using an endoscope) of early gastric cancer
• Those who have dyspepsia (discomfort in upper abdomen) of uncertain cause, are younger than 60, and have no alarming symptoms
• Those who are starting long-term treatment with non-steroidal anti-inflammatory drugs (NSAIDs), including aspirin, ibuprofen (Advil^®, Motrin^®), celecoxib (Celebrex^®) and naproxen (Aleve^®)
• Those who have iron-deficiency anemia of unknown cause
• Those who have idiopathic thrombocytopenic purpura (ITP, also called immune thrombocytopenic purpura), in which your immune system attacks platelets, so your blood doesn’t clot normally

Tests may be offered to people who:

• Are long-term users of low-dose aspirin (testing may help lower the risk of ulcer bleeding)

Tests may not be necessary for people with:

• Symptoms of GERD but no history of peptic ulcers
• A family history of gastric cancer, but who have no symptoms
• Lymphocytic gastritis, hyperplastic gastric polyps or hyperemesis gravidarum

Your doctor may test for H. pylori infection via a variety of tests:

• A blood test looks for antibodies to H. pylori in a sample drawn from a vein.
• A breath test (called a urea breath test) looks for evidence of infection. You breathe into a collection bag, swallow a radioactive material in a pill or liquid, and breathe into a second collection bag. The two samples are compared, and infection is indicated if you have higher than normal levels of carbon dioxide in the second sample.
• Stool tests can look for both H. pylori antigens (substances that trigger your body’s immune system to respond) and H. pylori bacteria. Your doctor gives you instructions on how to collect a sample of your stool and put it in a container for laboratory examination.
• An endoscopic sample (biopsy) uses a flexible lighted tube that is placed down your throat and into the esophagus, stomach and first part of the small intestine. From these areas, one or more small tissue samples are taken. You first would be given sedative medicine to relax you and local anesthetic to reduce discomfort during the procedure. Your doctor may discuss the procedure with you in advance and advise you to stop using certain medicines (such as blood thinners) in the weeks before it. You will likely also be told not to eat or drink anything for about 12 hours leading up to the endoscopy. You may need a ride home after the procedure.

Standard treatment of H. pylori infection consists of antibiotics in combination with a proton pump inhibitor—drugs that reduce stomach acid production, including Nexium^® (esomeprazole), Prevacid^® (lansoprazole) and Prilosec^® (omeprazole)—for three to 14 days.

While this treatment may be beneficial, none of the various drug combinations employed always eliminates infection, and none has a success rate above 90 percent, according to an article in The American Journal of Gastroenterology.