Chronic gastritis is long-term inflammation of the stomach lining, and it has three primary causes: infection with the bacterium H. pylori, an autoimmune reaction against your own stomach cells, or repeated chemical injury from medications, bile, or alcohol. Globally, over 38 million people were living with gastritis and duodenitis in 2021, with H. pylori and long-term use of anti-inflammatory drugs responsible for the vast majority of cases.
H. pylori Infection
The single most common cause of chronic gastritis worldwide is infection with Helicobacter pylori, a spiral-shaped bacterium that colonizes the stomach lining and can persist for decades if untreated. Most people pick up the infection in childhood, often through contaminated water or close household contact, and many never develop symptoms. But the bacteria are far from passive tenants.
H. pylori survives the stomach’s harsh acid environment by producing an enzyme that generates ammonia, which neutralizes the acid in its immediate surroundings. Once established, strains carrying certain virulence factors cause the most damage. The bacterium uses a needle-like structure to inject a protein called CagA directly into the cells of your stomach lining. Inside those cells, CagA disrupts normal signaling: it breaks apart the junctions between neighboring cells, alters cell shape, and triggers inflammatory responses. The result is a cascade of immune chemicals, including several that recruit white blood cells to the area and sustain ongoing inflammation.
H. pylori also produces a toxin called VacA that punches holes in stomach lining cells and can suppress local immune responses, helping the bacterium evade clearance. Meanwhile, fragments of the bacterial cell wall activate a separate arm of the immune system, prompting cells to release even more inflammatory signals. This sustained, low-grade inflammation is what defines chronic gastritis and, over years, can thin the stomach lining and reduce its ability to produce acid and protective mucus.
Autoimmune Gastritis
In autoimmune gastritis, your immune system mistakenly attacks the acid-producing cells (parietal cells) in your stomach. The primary target is the proton pump on these cells, the same pump that acid-blocking medications are designed to shut down. Your body generates antibodies against both parts of this pump, and specialized immune cells infiltrate the stomach lining, releasing inflammatory signals like TNF-alpha and interferon-gamma that drive parietal cell death.
As more parietal cells are destroyed, the stomach produces progressively less acid. This matters for digestion, but it also creates a specific nutritional problem. Parietal cells produce intrinsic factor, a protein essential for absorbing vitamin B12 in the small intestine. Without it, B12 absorption drops dramatically. Because the body stores 2 to 5 mg of B12 and only uses about 2 to 3 micrograms per day, deficiency develops slowly, often over years. Iron deficiency typically shows up first, especially in premenopausal women, sometimes many years before B12 levels fall low enough to cause pernicious anemia. By the time pernicious anemia is diagnosed, it is usually in older adults whose stores have finally been depleted.
Autoimmune gastritis often coexists with other autoimmune conditions, particularly thyroid disease and type 1 diabetes.
Long-Term NSAID Use
Nonsteroidal anti-inflammatory drugs like ibuprofen, naproxen, and aspirin are among the most widely used medications in the world, and chronic use is a well-established cause of gastritis. These drugs work by blocking enzymes called COX-1 and COX-2, which produce prostaglandins. In most of the body, reducing prostaglandins means reducing pain and inflammation. In the stomach, though, prostaglandins play a protective role: they stimulate mucus production, promote blood flow to the lining, and keep stomach contractions smooth and regular.
When NSAIDs suppress prostaglandin production in the stomach, the consequences unfold in a specific sequence. First, the stomach begins contracting more forcefully and erratically. This hypermotility compresses the tiny blood vessels in the stomach wall, disrupting normal blood flow and creating cycles of reduced oxygen followed by reperfusion. These cycles generate damaging free radicals and trigger lipid breakdown in cell membranes. The mucosal barrier becomes more permeable, white blood cells stick to the inner walls of blood vessels, and tissue damage accumulates. Over weeks and months of regular NSAID use, this process produces chronic inflammation and erosion of the protective lining.
Bile Reflux
Bile is produced by the liver to help digest fats in the small intestine. Normally, the pyloric valve at the bottom of the stomach prevents bile from flowing backward. When that valve doesn’t close properly, bile washes into the stomach and damages the lining through a chemical process distinct from acid injury.
Bile acids and a compound called lysolecithin dissolve the phospholipids and cholesterol that make up the stomach’s protective mucus barrier. Once that barrier is compromised, stomach acid penetrates into the lining itself, causing inflammation and cell damage. Several conditions increase the risk of bile reflux:
- Stomach or gallbladder surgery: Procedures that alter the stomach’s anatomy or remove the gallbladder can eliminate the pyloric valve’s function entirely. After gallbladder removal, bile flows continuously into the duodenum rather than being released in controlled bursts, which can overwhelm the normal clearing mechanisms and push bile back into the stomach.
- Diabetic gastroparesis: Long-term high blood sugar damages the nerves controlling stomach movement, slowing emptying and disrupting the coordinated motion between the stomach and duodenum. Bile stays in contact with the stomach lining for longer periods.
- Smoking and heavy alcohol use: Both relax the pyloric sphincter, allowing bile to flow backward more easily.
- Chronic stress: Through the brain-gut axis, stress and emotional disturbance can alter the release of hormones that coordinate stomach and intestinal movement, contributing to disordered motility.
Chronic Alcohol Use
Heavy, long-term alcohol consumption is an independent cause of chronic gastritis. Alcohol directly irritates and erodes the stomach’s mucosal barrier with each exposure. Over time, the lining loses its ability to regenerate the surface cells that are stripped away, leading to a progressive thinning of the stomach wall. Studies of patients with alcohol dependence show that gastric atrophy advances with age, and the shrinking of the secretory area reduces the stomach’s capacity to produce acid and digestive enzymes. In these patients, atrophic and erosive gastritis are common even in the absence of H. pylori infection or NSAID use.
Less Common Causes
A small number of chronic gastritis cases stem from systemic inflammatory diseases. Crohn’s disease, which most people associate with the intestines, can involve the stomach and produce a granulomatous pattern of inflammation. Sarcoidosis, an inflammatory condition that usually affects the lungs, involves the stomach in only about 2.5% of cases found at autopsy. Isolated gastric sarcoidosis, where the stomach is the only organ affected, is rarer still. Because these cases look similar under the microscope to infections and even certain cancers, diagnosis typically requires ruling out more common causes first.
Radiation therapy to the upper abdomen and certain infections in people with weakened immune systems (such as cytomegalovirus) can also produce chronic gastritis, though these are relatively uncommon.
How Chronic Gastritis Is Diagnosed
Symptoms alone can’t confirm chronic gastritis. The gold standard is endoscopy with biopsy, where a thin camera is passed into the stomach and small tissue samples are taken for examination under a microscope. Pathologists look at the number and type of immune cells present. In healthy stomach tissue, you’d expect to see only 2 to 5 immune cells per high-power microscope field. Increases above that threshold are graded as mild, moderate, or marked.
The most widely used classification system calls for at least five biopsies: two from the lower stomach (antrum), two from the upper stomach (corpus), and one from the curve connecting them. This mapping helps determine not just whether gastritis is present but where it’s most severe, whether the lining has started to thin, and whether precancerous changes like intestinal metaplasia have begun. Two staging systems, OLGA and OLGIM, combine these findings to assign a risk level for progression toward stomach cancer.
Why the Cause Matters for Outcomes
Chronic gastritis, regardless of its cause, can progress through a well-described sequence: normal lining gives way to chronic inflammation, then thinning (atrophy), then a change in cell type called intestinal metaplasia, and in rare cases, stomach cancer. The annual risk of progressing from intestinal metaplasia to gastric cancer is estimated at about 0.12%, according to American Gastroenterological Association guidelines. That figure is low in any given year, but it accumulates over decades, which is why identifying and treating the underlying cause early matters.
H. pylori-driven gastritis can be halted and often reversed with antibiotic treatment. NSAID-related gastritis improves when the medication is stopped or switched. Autoimmune gastritis can’t be cured, but monitoring B12 and iron levels prevents the worst nutritional complications. Bile reflux may require medications that bind bile acids or, in severe post-surgical cases, a procedure to reroute intestinal flow. In every case, knowing the specific cause shapes both treatment and the surveillance schedule needed to catch progression early.