Peptic ulcer disease

A peptic ulcer is a break in the lining of the stomach or duodenum that extends through the muscularis mucosae. It is a common condition that has been transformed within a single generation: what was once a chronic surgical disease, treated by operations designed to reduce acid production, is now in most cases cured by a course of antibiotics. Surgery today is almost entirely reserved for the complications.

How they form

The lining of the stomach and duodenum sits in a hostile environment and survives it through a balance. On one side are the aggressive factors — hydrochloric acid and pepsin. On the other are the defences: a layer of mucus, bicarbonate secreted beneath it, a tight epithelial barrier, a rich mucosal blood supply, and prostaglandins that maintain all of these. An ulcer forms when that balance fails, and in practice it fails for one of two reasons.

Helicobacter pylori

This spiral bacterium colonises the gastric mucus layer, surviving the acid by producing urease, which converts urea into ammonia and creates an alkaline microenvironment around itself. It is responsible for the great majority of duodenal ulcers and a large proportion of gastric ulcers.

What it does depends on where it settles, and this explains an apparent paradox:

  • Antral-predominant infection damages the D cells that produce somatostatin, the brake on acid secretion. Without that brake, gastrin rises, acid output rises, and the excess acid delivered into the duodenum causes gastric metaplasia there, which H. pylori then colonises in turn, producing duodenitis and duodenal ulceration. These patients have high acid output.
  • Body-predominant or pangastritis damages the acid-producing parietal cells themselves. Acid output falls. These patients develop gastric ulcers, atrophic gastritis, intestinal metaplasia — and are the group at increased risk of gastric cancer.

So the same organism produces duodenal ulcers with high acid in one pattern and gastric ulcers with low acid and cancer risk in another. It is the distribution of infection, not the organism alone, that determines the disease.

Non-steroidal anti-inflammatory drugs and aspirin

These inhibit cyclo-oxygenase, and with it prostaglandin synthesis. Prostaglandins maintain mucus, bicarbonate and mucosal blood flow, so their loss removes the defence rather than increasing the attack. The damage is systemic, not local contact injury — which is why enteric-coated or injected preparations still cause ulcers.

NSAID ulcers are characteristically gastric, often multiple, and frequently silent until they bleed or perforate. Risk rises with age, with dose and duration, and sharply when combined with anticoagulants, corticosteroids, SSRIs or H. pylori infection.

Other causes

  • smoking, which impairs healing and increases recurrence
  • physiological stress — major burns (Curling's ulcer), head injury (Cushing's ulcer), critical illness
  • Zollinger-Ellison syndrome — a gastrin-secreting tumour causing profound acid hypersecretion. Suspect it with multiple ulcers, ulcers beyond the duodenal bulb, ulcers that recur after eradication and adequate acid suppression, ulcers with diarrhoea, or a family history suggesting MEN1.
  • Crohn's disease, viral infection in the immunosuppressed, cocaine use, and malignancy presenting as an ulcer

Symptoms

  • Epigastric pain — burning or gnawing. The classical pattern for duodenal ulcer is pain when the stomach is empty, two to three hours after eating and at night, relieved by food or antacids. Gastric ulcer pain is more often provoked by eating, which is why some patients lose weight.
  • nausea, bloating, early satiety
  • heartburn, often indistinguishable from reflux
  • a substantial minority, particularly older patients on NSAIDs, have no symptoms at all until they present with bleeding or perforation

Alarm features requiring prompt endoscopy: weight loss, difficulty swallowing, persistent vomiting, anaemia, black or bloody stools, vomiting blood, a palpable mass, or new dyspepsia in a patient over fifty-five.

How the diagnosis is made

  • Endoscopy confirms the ulcer, allows biopsy and treats bleeding. Every gastric ulcer must be biopsied — from multiple points around the rim — because gastric cancer can present as an ulcer indistinguishable from a benign one. Duodenal ulcers are essentially never malignant and do not require biopsy for that purpose.
  • Testing for H. pylori — urea breath test or stool antigen test, both of which also confirm eradication; biopsy-based rapid urease testing and histology at endoscopy. Proton pump inhibitors must be stopped for two weeks and antibiotics for four weeks before testing, or false negatives result. Serology indicates exposure, not current infection, and is not used to confirm cure.
  • Fasting gastrin where Zollinger-Ellison syndrome is suspected.
  • Full blood count, and review of all medication including over-the-counter analgesics, which patients frequently omit unless asked directly.

Treatment

Eradication of H. pylori

Where infection is present, eradication is the treatment, and it cures the disease rather than suppressing it: recurrence falls from the majority of patients within a year to a very small minority.

Regimens combine a proton pump inhibitor with two or three antibiotics for fourteen days. Rising clarithromycin resistance means that quadruple therapy — bismuth-based, or concomitant — is increasingly preferred as first-line treatment, guided by local resistance patterns. Completing the full course matters, and patients should be told this plainly, because incomplete treatment breeds resistance.

Eradication must be confirmed by breath or stool antigen test at least four weeks after finishing treatment. This step is frequently omitted and should not be.

Acid suppression

Proton pump inhibitors heal the great majority of ulcers. Duodenal ulcers are treated for four weeks, gastric ulcers for eight, with repeat endoscopy for gastric ulcers to confirm healing and re-biopsy any that persist.

Removing the cause

Stopping the NSAID is the most effective measure where one is implicated. Where it cannot be stopped — low-dose aspirin for cardiovascular protection, for example — long-term proton pump inhibitor cover is given. Smoking cessation improves healing and reduces recurrence.

Surgery

Elective surgery for uncomplicated peptic ulcer is now very rare. It is considered for the genuinely refractory ulcer that fails to heal despite confirmed eradication, full acid suppression and withdrawal of NSAIDs — and in that situation the first duty is to reconsider the diagnosis: malignancy, Zollinger-Ellison syndrome, Crohn's disease, or continued covert NSAID use account for most such cases.

Surgery remains the treatment for complications — perforation, bleeding that endoscopy cannot control, and gastric outlet obstruction — which are covered on their own pages.

Follow-up

Confirmation of eradication in all treated patients. Repeat endoscopy for gastric ulcers to document healing and exclude malignancy. Patients requiring long-term NSAIDs or anticoagulation need a considered gastroprotection plan rather than an unexamined prescription.

When to seek an opinion

Persistent indigestion lasting more than a few weeks, indigestion with any alarm feature, or indigestion in a patient taking anti-inflammatory tablets. Vomiting blood, or black tarry stools, requires emergency assessment, as does sudden severe abdominal pain.

Common questions

Is my ulcer caused by stress?

Not in the way the word is usually meant. The great majority are caused by a bacterial infection of the stomach lining or by anti-inflammatory painkillers. Severe physical stress — major burns, serious illness in intensive care — can cause ulcers, but everyday pressure at work does not. This matters because the real causes are treatable and the imagined one is not.

Can an ulcer be cured for good?

Yes. If the bacterium is present and is successfully eradicated, and anti-inflammatory tablets are avoided, most ulcers never return. This is why it is worth taking the full course of antibiotics and having a test afterwards to confirm the infection has gone.

How did I catch this bacterium?

Usually in childhood, through close contact within the household. It is common worldwide and most people who carry it never develop an ulcer. Having it does not reflect poor hygiene now.

Should my family be tested?

Not routinely. Testing is reasonable for close family members who have symptoms, and is more actively considered where there is a family history of stomach cancer, since eradication reduces that risk.

Can an ulcer be cancer?

An ulcer in the stomach can occasionally be a cancer that looks like an ulcer, which is why samples are always taken from a stomach ulcer and why a repeat endoscopy is arranged to confirm it has healed. Ulcers in the duodenum, just beyond the stomach, are not cancerous.

Do I have to stop my aspirin?

Not necessarily, and not without discussion. If you take aspirin to protect your heart, stopping it carries its own risk. The usual approach is to continue it while taking a stomach-protecting tablet long term. Anti-inflammatory painkillers taken for aches and pains are a different matter and are usually best stopped.

Will I need an operation?

Almost certainly not. Operations for ulcers are now uncommon and are reserved for complications — a hole in the stomach or duodenum, bleeding that cannot be stopped at endoscopy, or scarring that blocks the stomach outlet.

Is it safe to take acid tablets for a long time?

For most people, yes. Various concerns have been raised in observational studies, but the effects are small and cause has not been established. Where there is a clear reason to take them — protection alongside aspirin, for instance — the benefit generally outweighs the theoretical risk. The sensible approach is the lowest effective dose, reviewed periodically.

Related conditions

Other conditions of the stomach covered on this site:

This page provides general information and does not replace an individual medical consultation. Assessment and treatment are decided for each patient after review of their history, examination and investigations.

Previous
Previous

Perforated and bleeding peptic ulcer

Next
Next

Oesophageal perforation and Boerhaave syndrome