Treating chronic gastritis depends entirely on what’s causing it. The three most common culprits are a bacterial infection called H. pylori, long-term use of painkillers like ibuprofen or aspirin, and an autoimmune condition where your body attacks the stomach lining. Each requires a different approach, but the core goal is the same: remove the source of irritation, reduce stomach acid, and give the lining time to heal.
Identify the Cause First
Chronic gastritis isn’t a single disease. It’s an umbrella term for ongoing inflammation of the stomach lining, and it comes in two broad forms: atrophic (where the lining thins and loses some of its acid-producing cells) and nonatrophic (where the lining is inflamed but structurally intact). Treatment that works for one type can be useless or even counterproductive for another, so getting the right diagnosis matters more than any single medication.
Diagnosis typically involves an upper endoscopy, where a thin camera is passed into your stomach and small tissue samples are taken from multiple sites. These biopsies are examined under a microscope to determine the type and severity of inflammation, whether atrophy has developed, and whether H. pylori bacteria are present. Blood tests and breath tests can also detect H. pylori, and blood work can reveal vitamin deficiencies that point toward autoimmune gastritis.
Treating H. Pylori Infection
H. pylori is the most common cause of chronic gastritis worldwide. Clearing the infection usually resolves the inflammation over time, and in many cases prevents it from progressing to more serious stomach changes. The current recommendation from the American College of Gastroenterology (updated in 2024) is a 14-day course of quadruple therapy that combines a proton pump inhibitor (a strong acid-reducing pill taken twice daily), tetracycline four times daily, metronidazole three or four times daily, and a bismuth compound four times daily.
This is a lot of pills, and the side effects can be unpleasant, including nausea, metallic taste, and dark stools from the bismuth. But the 14-day duration is important. Shorter courses have lower success rates, and antibiotic resistance is a growing problem. Notably, the older approach of using clarithromycin-based triple therapy is no longer recommended as a first-line treatment unless testing has confirmed the bacteria are sensitive to that particular antibiotic. Resistance to clarithromycin has become too common for it to be a reliable starting point.
If the first round of treatment doesn’t work, alternative regimens exist, including ones built around different antibiotics. Your doctor will typically retest you about four weeks after finishing treatment to confirm the infection is gone.
Managing NSAID-Related Gastritis
If your gastritis is tied to regular use of nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen, naproxen, or aspirin, the most effective step is stopping the drug. When that isn’t possible, because you need daily aspirin for heart protection, for example, adding a proton pump inhibitor (PPI) provides strong protection. PPIs reduce stomach acid production dramatically, and studies have shown they lower the risk of recurrent gastrointestinal bleeding by roughly 90% in people who continue NSAIDs after a previous bleed. Endoscopy studies have also found that PPIs cause fewer ulcers and are better tolerated than older protective medications.
Another option is switching from a traditional NSAID to acetaminophen (Tylenol), which doesn’t irritate the stomach lining. If you need the anti-inflammatory effect specifically, your doctor may consider a COX-2 selective NSAID, which carries a lower risk of stomach damage, though it isn’t zero.
Autoimmune Gastritis and B12 Deficiency
Autoimmune gastritis is a less common but distinct condition. Your immune system targets the cells in the stomach lining that produce acid and a protein called intrinsic factor, which is essential for absorbing vitamin B12. Over time, this leads to atrophy of the stomach lining and, eventually, B12 deficiency that can cause fatigue, nerve tingling, memory problems, and anemia.
There’s no treatment that stops the autoimmune attack itself. Management centers on replacing what’s lost. The UK’s National Institute for Health and Care Excellence (NICE) recommends lifelong intramuscular B12 injections for anyone whose B12 deficiency is caused by autoimmune gastritis. Oral supplements alone often aren’t enough, because the underlying problem is absorption, not intake. If symptoms worsen or don’t improve sufficiently, the frequency of injections can be increased. Importantly, injections should continue for life even after symptoms resolve, since the cause is permanent.
Iron deficiency is also common with autoimmune gastritis, because stomach acid is needed to absorb iron efficiently. Your doctor will monitor both nutrients over time.
Acid Suppression and Mucosal Protection
Regardless of the underlying cause, reducing stomach acid gives inflamed tissue the chance to heal. PPIs are the most potent option and are typically prescribed for 4 to 8 weeks, sometimes longer. H2 blockers (like famotidine) are a milder alternative that works well for less severe cases or as a step-down after a PPI course.
Mucosal protectants take a different approach. Sucralfate, for instance, doesn’t reduce acid at all. Instead, it forms a physical barrier over damaged tissue, shielding it from acid and digestive enzymes while healing occurs. It’s taken on an empty stomach, either one hour before or two hours after meals. Bismuth compounds work similarly and are sometimes used alongside acid-reducing medications for added protection, particularly during H. pylori treatment.
Over-the-counter antacids (like calcium carbonate or magnesium hydroxide) can provide quick symptom relief by neutralizing existing acid, but they don’t promote healing on their own and wear off within an hour or two.
Diet and Lifestyle Adjustments
Spicy and greasy foods don’t cause gastritis, which surprises many people. But they absolutely can worsen symptoms in an already-inflamed stomach. While the inflammation is active, it helps to avoid common irritants: spicy dishes, fried or greasy foods, highly processed foods, carbonated drinks, acidic foods like citrus and tomatoes, and anything high in added sugar.
Alcohol and smoking both directly damage the stomach lining and slow healing. Cutting them out, or at least reducing them significantly, is one of the most impactful changes you can make. Smaller, more frequent meals also tend to be easier on an irritated stomach than two or three large ones, because they keep acid levels more stable throughout the day.
Caffeine is worth mentioning separately. It stimulates acid production, so cutting back on coffee, strong tea, and energy drinks can reduce symptoms. You don’t necessarily need to eliminate caffeine permanently, but dialing it back while your stomach heals makes a noticeable difference for most people.
Why Treatment Matters Long-Term
Chronic gastritis isn’t just about discomfort. Left untreated, ongoing inflammation can progress through a sequence of changes: from gastritis to atrophic gastritis, then to intestinal metaplasia (where stomach cells are replaced by intestinal-type cells), and potentially to dysplasia (abnormal cell growth). Each stage carries a higher risk of gastric cancer. A large observational study published in The BMJ tracked these risks over 20 years: roughly 1 in 85 people with gastritis developed stomach cancer, compared to 1 in 50 with atrophic gastritis, 1 in 39 with intestinal metaplasia, and 1 in 19 with dysplasia.
These numbers are still relatively small in absolute terms, particularly in Western countries where gastric cancer rates are lower overall. But they underscore why treating the underlying cause, not just managing symptoms, is important. Eradicating H. pylori, stopping NSAID damage, and monitoring autoimmune gastritis can all interrupt this progression before it reaches a concerning stage. If you’ve been diagnosed with atrophic gastritis or intestinal metaplasia, your gastroenterologist will likely recommend periodic endoscopies to monitor for changes.