Helicobacter pylori, a spiral-shaped bacterium that colonizes the stomach lining, most commonly causes chronic gastritis (ongoing inflammation of the stomach). It also causes the majority of peptic ulcers and is a recognized risk factor for stomach cancer. Roughly 44% of adults worldwide carry the infection, yet most never develop symptoms. When problems do arise, they range from mild digestive discomfort to serious complications that develop over years or decades.
How H. pylori Damages the Stomach
H. pylori survives in the harsh acidic environment of the stomach by producing an enzyme that breaks down urea into ammonia and carbon dioxide. The ammonia neutralizes stomach acid in the bacterium’s immediate surroundings, creating a protective pocket. But ammonia is also toxic to the cells lining the stomach. It can react with other chemicals in the body to form compounds that directly damage those cells, triggering inflammation.
This inflammation is the root of nearly everything H. pylori causes. In some people, it stays low-grade and never produces noticeable symptoms. In others, it progresses to erode the protective mucus layer, leaving the stomach or upper intestine vulnerable to acid damage. Over many years, sustained inflammation can also change the structure of the stomach lining itself, setting the stage for more serious conditions.
Chronic Gastritis
The single most common consequence of H. pylori infection is chronic gastritis, a persistent inflammation of the stomach lining. Nearly everyone who carries the bacterium develops some degree of gastritis, though many never feel it. When symptoms do appear, they typically include a burning or aching pain in the upper abdomen, bloating, frequent burping, nausea, and a vague sense of feeling full or losing your appetite. The pain often feels worse on an empty stomach.
Left untreated for years, chronic gastritis can progress to atrophic gastritis, a condition where the stomach lining thins and loses some of its acid-producing cells. This matters because reduced acid production impairs the body’s ability to absorb certain nutrients, particularly iron.
Peptic Ulcers
Peptic ulcers are open sores that develop on the inner lining of the stomach or the upper portion of the small intestine (the duodenum). H. pylori is the leading cause of these ulcers. The bacterium weakens the protective mucus barrier, allowing stomach acid to eat into the tissue beneath.
The hallmark symptom is a gnawing or burning pain between the navel and the breastbone, often occurring between meals or during the night when the stomach is empty. Eating or taking antacids may temporarily relieve it. Some people also experience unintentional weight loss. Ulcers can bleed, which may show up as dark or tarry stools, vomiting that looks like coffee grounds, or unexplained fatigue from gradual blood loss. A bleeding ulcer needs prompt medical attention.
Stomach Cancer
H. pylori is classified as a definite carcinogen for stomach (gastric) cancer. The path from infection to cancer is long and involves a chain of changes: chronic gastritis progresses to atrophic gastritis, then to abnormal cell changes, and eventually, in a small percentage of carriers, to cancer. This process typically unfolds over decades. The vast majority of people infected with H. pylori never develop stomach cancer, but the bacterium is involved in a significant share of cases that do occur.
H. pylori is also linked to a type of stomach lymphoma called MALT lymphoma, a rare cancer of the immune tissue in the stomach lining. In early-stage cases, eradicating the infection alone can sometimes cause the lymphoma to regress.
Iron Deficiency Anemia
One of the less obvious consequences of H. pylori is unexplained iron deficiency anemia. The connection is the duodenum, the first section of the small intestine where iron absorption begins. Chronic inflammation from H. pylori interferes with stomach acid production and damages proteins needed to absorb iron from food. Over time, this can leave the body unable to take in enough iron, leading to anemia even when dietary intake seems adequate.
Atrophic gastritis compounds the problem by further reducing acid output. The link is strong enough that guidelines now recommend testing for H. pylori in cases of iron deficiency anemia that can’t be explained by other causes. Studies have shown that anemia often improves after the infection is successfully treated, reinforcing the idea that the bacterium is the underlying driver.
How H. pylori Is Detected
If you’re being evaluated for H. pylori, the most common noninvasive tests are the urea breath test and the stool antigen test. In the breath test, you swallow a substance containing urea. If H. pylori is present, its enzymes break the urea down, and the byproducts show up in your breath. This test has a sensitivity around 96%, making it the most accurate noninvasive option. The stool antigen test looks for bacterial proteins in a stool sample and is highly specific (about 95%) but catches fewer cases overall, with sensitivity around 73%.
Blood tests that check for antibodies are sometimes used for screening, but they can’t distinguish between a current infection and a past one your body has already cleared. For this reason, breath and stool tests are preferred when the goal is to confirm an active infection. Endoscopy with biopsy, where a small tissue sample is taken directly from the stomach lining, serves as the gold standard and is typically used when there’s a need to visually assess the stomach for ulcers, inflammation, or suspicious changes.
Treatment and Antibiotic Resistance
Treating H. pylori requires a combination of antibiotics taken alongside a medication that reduces stomach acid, typically for 14 days. The current recommended first-line approach is a four-drug regimen that includes bismuth (the active ingredient in Pepto-Bismol), two antibiotics, and an acid-suppressing medication. This combination achieves cure rates above 90% in real-world use, even when the bacterium is resistant to one of the antibiotics.
Older treatment approaches that relied on a single antibiotic called clarithromycin are falling out of favor. Resistance to clarithromycin now exceeds 15% in the majority of countries studied, and when the bacterium is resistant, that regimen’s success rate drops to roughly 30%. Current guidelines recommend against using clarithromycin-based treatment unless lab testing has confirmed the specific strain is susceptible to it.
Antibiotic resistance is a growing global challenge for H. pylori treatment. Resistance to metronidazole is the highest of any antibiotic used against the bacterium, and resistance to levofloxacin, a common second-line option, exceeds 15% in more than half the countries where it has been measured. This is why combination therapy using multiple antibiotics remains essential, and why confirming that the infection has been eliminated after treatment (usually with a follow-up breath or stool test) is an important step.
Most People Have No Symptoms
Perhaps the most striking fact about H. pylori is how quietly it operates. The majority of the estimated 44% of adults who carry it will never develop ulcers, cancer, or even noticeable digestive symptoms. The reasons some people progress to serious disease while others carry the bacterium harmlessly for life involve a combination of bacterial strain differences, genetic susceptibility, diet, and other environmental factors that researchers are still working to untangle. What is clear is that when H. pylori does cause problems, those problems are treatable, and eradicating the infection halts the chain of damage before it can progress further.