What a Peptic Ulcer Actually Is
The stomach lining is protected from its own acid by a layer of mucus and bicarbonate. A peptic ulcer forms when this protective barrier breaks down and acid erodes through the mucosal lining, creating an open sore. When this happens in the stomach, it is called a gastric ulcer. When it happens in the duodenum (the first section of the small intestine), it is called a duodenal ulcer. Duodenal ulcers are more common.
The two causes responsible for the vast majority of peptic ulcers are H. pylori infection and NSAID use. Both damage the protective mucus layer through different mechanisms. Everything else, including stress, tea, coffee, and spicy food, may worsen existing ulcer symptoms but doesn't cause ulcers in people without H. pylori or NSAID exposure.
All gastric ulcers found on endoscopy should be biopsied. Around 2-5% of gastric ulcers that look benign are actually early gastric cancer. Duodenal ulcers rarely, if ever, undergo malignant transformation. This distinction is why follow-up endoscopy to confirm healing is standard practice for gastric but not duodenal ulcers.
Symptoms and How They Differ by Ulcer Type
Duodenal and gastric ulcers produce the same core symptom (upper abdominal burning pain) but with a different relationship to food that is diagnostically useful.
Comes 2-3 hours after meals, when the stomach has emptied and acid contacts the ulcer. Relieved by eating (food buffers acid), which is why patients often snack at night. Night pain is characteristic.
Comes earlier, often during or soon after eating, as food stimulates acid secretion against the stomach ulcer. Eating may worsen rather than relieve symptoms.
Common in both types, particularly after meals. Can be the dominant symptom when pain is mild or absent.
NSAID-related ulcers are often completely asymptomatic until they bleed or perforate. Elderly patients on NSAIDs are particularly likely to have silent ulcers.
Coffee-ground vomit or haematemesis (vomiting blood). Black tarry stools (melaena) from digested blood. Iron deficiency anaemia from chronic slow bleeding.
Unexplained weight loss, progressive dysphagia, persistent vomiting, palpable abdominal mass, or iron deficiency anaemia warrant urgent endoscopy to exclude gastric cancer.
H. Pylori: Treatment and Eradication
H. pylori eradication requires a combination of a PPI (acid suppressant) with two antibiotics, taken together for 7-14 days. Standard first-line treatment in India is a triple therapy or quadruple therapy protocol. Antibiotic resistance is an increasing problem: clarithromycin resistance in particular is rising in many Indian cities, which reduces the success rate of standard regimens.
Eradication success should always be confirmed, not assumed. The best tests for confirming eradication are the urea breath test or stool antigen test, performed at least four weeks after completing treatment and two weeks after stopping PPIs. Serology (blood antibody test) cannot confirm eradication because antibodies remain positive for months to years after the bacterium has been cleared.
If first-line eradication fails, a different antibiotic combination is used for the second attempt. Bismuth-based quadruple therapy (bismuth, PPI, tetracycline, metronidazole) is often used as salvage treatment where clarithromycin resistance is common.
Long-Term Management and Prevention of Recurrence
Once the cause is addressed (H. pylori eradicated or NSAID stopped), peptic ulcers heal in the majority of patients with 4-8 weeks of PPI therapy. Recurrence after successful eradication is rare. But several practices increase recurrence risk: restarting NSAIDs without gastroprotection, smoking (which impairs mucosal healing), and reinfection with H. pylori in high-prevalence environments.
People who genuinely need long-term NSAIDs for chronic pain or cardiovascular protection should use the lowest effective dose of the least gut-toxic NSAID, combined with a PPI, with periodic review of whether the NSAID is still necessary.