Peptic ulcer disease and gastritis

Essentials

1
Helicobacter pylori is responsible for 70% to 90% of peptic ulcers, with non-steroidal anti-inflammatory drugs (NSAIDs) accounting for most of the remainder.
2
Emergency presentations of peptic ulcer disease vary from mild indigestion to severe life-threatening complications.
3
Endoscopy is the investigation of choice for definitive diagnosis.
4
Most patients can be managed medically with a combination of anti-secretory drugs and antibiotics as indicated.
5
Surgical treatment may be indicated for complications, such as haemorrhage, perforation and obstruction.
6
A ‘negative’ erect chest x-ray does not exclude ulcer perforation.

Introduction

Peptic (gastroduodenal) ulcers are defects in the gastrointestinal mucosa that extend through the muscularis mucosa. The term ‘gastritis’ is used to denote inflammation associated with mucosal injury. Gastropathy is defined as epithelial cell damage and regeneration without associated inflammation.

The discovery of the organism Helicobacter pylori has resulted in a dramatic change in our understanding of the aetiology and pathophysiology of peptic ulcer disease. What was once a chronic disease prone to relapse and recurrence has now become eminently treatable and curable.

Patients presenting to emergency departments may do so with ‘classic’ ulcer symptoms, undifferentiated abdominal or chest pain or, more dramatically, with life-threatening complications, such as perforation or haemorrhage.

Aetiology, genetics, pathogenesis and pathology

Aetiology

Peptic ulcer disease is associated with two major factors: H. pylori infection and the consumption of NSAIDs. Smoking is also an important contributory element but does not appear to be a risk factor for H. pylori recurrence or ulcer relapse following eradication of H. pylori .

Gastritis is usually due to infectious agents (such as H. pylori ), autoimmune conditions and hypersensitivity reactions. In contrast, gastropathy is usually caused by irritants, such as drugs (e.g. NSAIDs and alcohol), bile reflux, hypovolaemia, ischaemia or chronic congestion.

Genetics

There seems to be a distinct familial aggregation of peptic ulcer disease in pre– H. pylori studies, suggesting a polygenic inheritance of peptic ulcer disease. It remains uncertain whether genetic factors predispose to H. pylori infection or whether the genetic factors function independently.

Pathogenesis and pathology

H. pylori disrupts the mucous layer of the gastroduodenal tissue, adheres to the gastric epithelium and releases enzymes and toxins. This causes the underlying mucosa to be susceptible to acid damage and incites an inflammatory response by the host.

NSAIDs cause ulcers by inhibiting the production of prostaglandins in the stomach and duodenum. The decreased synthesis of prostaglandins leads to the generation of increased amounts of gastric acid, decreased production of bicarbonate and glutathione and reduced blood flow to the gastric mucosa. NSAIDs are more commonly associated with gastric ulceration.

Epidemiology

H. pylori infects about 50% of the world’s population. There are significant regional differences in the prevalence of peptic ulcer disease not explained by H. pylori alone, purportedly due to dietary variations. Populations with poor hygiene and low socioeconomic status are predisposed to a higher prevalence of H. pylori infection.

The vast majority of patients harbouring H. pylori are asymptomatic. Although decreasing in incidence in developed regions, H. pylori is the major cause of peptic ulceration or, at least, a major cofactor in its development. H. pylori has been isolated from 20% to 50% of patients with symptoms of dyspepsia. More importantly, 90% to 95% of patients with duodenal ulcers and 70% of those with gastric ulcers are infected with the organism. Eradication of H. pylori has been shown to markedly reduce the recurrence rate for ulceration. At least 50% of patients taking NSAIDs will have endoscopic evidence of erythema, erosions or ulcers even if they are asymptomatic.

Several risk factors influence gastrointestinal toxicity due to NSAIDs, the most important being a prior history of clinical ulcer disease or ulcer complications. Other risk factors are the dose and duration of therapy with NSAIDs, age above 75 years and cardiovascular disease. The risk of peptic ulcer disease is highest on commencement of NSAIDs. Combined therapy of NSAIDs with corticosteroids, anticoagulants, other NSAIDs or low-dose aspirin dramatically increases the risk of ulcer complications.

Some NSAIDs are more likely to produce ulcers than others. In general, shorter-acting agents, such as ibuprofen and diclofenac, are less likely to lead to ulcers than longer-acting agents. Even though cyclo-oxygenase (COX)-2 selective inhibitors (coxibs) have shown a reduction in the risk of peptic ulcers and their complications compared with traditional NSAIDs, this risk is increased compared with placebo. Studies have shown that the combination of a proton pump inhibitor (PPI) with a coxib decreases the incidence of peptic ulcers. However, there is no evidence that coxibs have advantages over other NSAIDs for patients with unhealed ulcers. Coxibs appear to inhibit the healing of peptic ulcers.

The interaction between NSAIDs and H. pylori is controversial and complex, but evidence from two meta-analyses of case-controlled trials identified synergism between H. pylori and NSAIDs in producing peptic ulcers and ulcer bleeding. Traditional risk factors—such as smoking, alcohol and stress—may increase the risk of ulceration and delay healing, but their relative importance as aetiological agents has fallen considerably with the discovery of H. pylori . Other causes of peptic ulceration, such as Zollinger-Ellison syndrome, are rare.

Clinical features

History

Peptic ulcers may present with a wide variety of symptoms, and over two thirds may be completely asymptomatic until complications, such as haemorrhage or perforation, occur. ‘Indigestion’ is the most common symptom in patients found to have peptic ulcer disease. Patients classically describe a burning or gnawing pain in the epigastrium that may radiate into the chest or straight through to the back. This may be associated with belching, early satiety, nausea and vomiting. Food may either exacerbate or relieve the pain. The pain is classically both fluctuating and periodic, with bouts of discomfort of variable severity interspersed with symptom-free periods.

The symptoms ‘indigestion’ or ‘dyspepsia’, however, have relatively poor sensitivity and specificity for diagnosing the various peptic syndromes. Less than 25% of patients with dyspepsia have peptic ulcer disease proven by gastroscopy and 20% to 60% of patients presenting with complications of ulcer disease report no antecedent symptoms.

Other presentations include chest or abdominal pain that must be differentiated from conditions such as myocardial ischaemia, biliary tract disease, pancreatitis and other abdominal emergencies.

Patients also present with the two most common complications of ulcer disease: acute gastrointestinal haemorrhage and acute perforation. The former gives symptoms of melaena with or without haematemesis, and the latter presents with sudden, severe abdominal pain.

Examination

In uncomplicated peptic ulcer disease, abdominal findings may be limited to epigastric tenderness without peritoneal signs. If perforation has occurred, patients experience severe pain and look unwell. Abdominal findings include generalized tenderness, widespread peritonism and ‘board-like’ rigidity. Those with gastrointestinal bleeding will usually have melaena on rectal examination.

Differential diagnosis

The differential diagnosis of upper abdominal pain is broad. Functional (idiopathic, non-ulcer) dyspepsia is the commonest (up to 60%), and the diagnosis is one of exclusion. Other important differential diagnoses include gastric, oesophageal or pancreatic cancer; pancreatitis; biliary tract disease; gastro-oesophageal reflux disease; ischaemic bowel disease; and metabolic diseases such as hypercalcaemia and hyperkalaemia.

Clinical investigations

The extent of investigations depends greatly on the patient’s presentation and the degree of severity of symptoms. There are no blood tests that can reliably predict the presence of peptic ulcer disease. Pathology investigations are aimed primarily at eliminating alternative diagnoses or identifying the complications of peptic ulceration.

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