conditions, particularly thyroid disease, may be present.

There is a
fourfold increase in gastric cancer.

Peptic ulcer disease

' Peptic ulcer' means an ulcer in the lower oesophagus, stomach or
duodenum, in the jejunum after gastrojejunostomy or, rarely, in the
ileum adjacent to a Meckel's diverticulum. Ulcers in the stomach or
duodenum may be acute or chronic; both penetrate the museularis
mucosae but acute ulcers show no evidence of fibrosis. Erosions do
not penetrate the muscularis mucosae.
Gastric and duodenal ulcer
The prevalence of peptic ulcer is decreasing in many Western
communities as a result of H. pylori eradication therapy but it
remains high in d eveloping countries. The male to female ratio for
duodenal ulcer varies from 5: 1 to 2: 1, whilst that for gastric ulcer
is ~ 2 :1.
Chronic gastric ulcer is usually single; most are situated on the
lesser curve within the antrum. Duodenal ulcer usually occurs in the
first part of the duodenum just distal to the junction of pyloric and
duodenal mucosa. Gastric and duodenal ulcers coexist in 10% of
patients and mul.tiple ulcers occur in 10-15%.
H. pylori: In the UK, the prevalence of H. pylori infection rises with
age (reaching 50% in those aged >50); in the developing world, it
affects up to 90%. Infections are probably acquired in childhood by
person-to-person contact. Most colonised people remain healthy and
asymptomatic. Around 90% of duodenal ulcer patients and 70% of
gastric ulcer patients are infected with H. pylori; the re maining 30%
of gastric ulcers are due to NSAIDs.
H. pylori is a motile Gram-negative organism that uses multiple
flagellae to burrow beneath the epithelial mucus layer. Here the pH
is nearly neutral and any acidity is buffered by the organism's pro-
duction of ammonia from urea. H. pylori exclusively colonises
gastric-type epithelium and is only found in the duodenum at
patches of gastric metaplasia. It stimulates chronic gastritis by pro-
voking an inflammatory response in the epithelium.
In most people, H. pylori causes antral gastritis with depletion of
somatostatin. The subsequent hypergastrinaemia stimulates parietal
cell acid production, but usually without clinical consequences. In a
few patients, particularly smokers, this process is exaggerated,
leading to duodenal ulceration. The pathogenesis of gastric ulcer is
less clear but H. pylori probably acts by reducing gastric mucosa!
resistance to acid and pepsin. Occasionally, H. pylori causes a pan-
gastritis, leading to gastric atrophy and hypochlorhydria, with bac-
terial proliferation in the stomach, predisposing to gastric cancer.
NSAIDs: See page 789.
Smoking: This increases the risk of gastric and, to a lesser extent,
duodenal ulcer. Once the ulcer has formed, it is more likely to cause
complications and less likely to heal if the patient smokes.
Clinical features and investigations
Peptic ulcer disease is a chronic condition with spontaneous relapse
and remission extending over decades. Duodenal and gastric ulcers
share common symptoms:
• Recurrent episodes of epigastric pain in relation to meals.
• Occasionally, vomiting; persistent daily vomiting suggests gastric
outlet obstruction.
In one-third of patients, especially elderly subjects taking NSAIDs,
the history is less characteristic. Pain may be absent or experienced
only as vague epigastric unease. Occasionally, the only symptoms
are anorexia and nausea, or a sense of undue repletion after meals.
The ulcer may even be 'silent', presenting with anaemia from chronic
undetected blood loss, haematemesis or acute perforation. The diag-
nostic value of individual symptoms of ulcer disease is poor.
Endoscopy is the preferred investigation. Gastric ulcers may occa-
sionally be malignant and therefore must always be biopsied and
followed up to ensu.r e healing.
Patients should be screened for H. pylori infection (Box 12.7). Some
tests requi.r e endoscopy; others are non-invasive. Overall, breath or
faecal antigen tests are best because of their accuracy, simplicity and
non-invasiveness.
Management
The aims of management are to relieve symptoms, induce healing
and prevent recurrence.
H. pylori eradication: All patients with acute or chronic duodenal
ulcer disease and those with gastric ulcers who are H. pylori-positive
should receive eradication therapy. This hea ls ulcers, prevents

12.7 ll111G111 tar . . dllli,lD 111 of ff. _ , II.....

Test Adwa11tages Dlllclnntages

Non-Invasive
Serology Rapid office kits Lacks sensitivity and
available; good for specificity; cannot differentiate
population studies current from past infection
1
3c urea breath High sensitivity and Requires expensive mass
tests specificity spectrometer
Faecal antigen test Cheap, > 95% specificity Acceptability
Invasive (antral biopsy)
Histology Sensitivity and specificity False negatives occur; takes
several days to process
Rapid urease tests Cheap, quick; > 95% 85% sensitivity
specificity
Microbiological 'Gold standard'·• defines Slow Md laborious; lacks
culture antibiotic sensitivity sensitivity
relapse and elimina tes the need for long-term treatment in >90% of
patients. A PPI is taken with two antibiotics (from amoxicillin, clari-
thromycin and metronidazole) for 7 days. First-line therapy is a PPI
(twice daily), clarithromycin 500 mg twice daily, and amoxicillin
1 g twice daily or metronidazole 400 mg twice daily, for 7 days.
Compliance, side-effects (usually diarrhoea, nausea, vomiting) and
metroni-d azole resistance iinfluence success rates.
Patients who remain infected after initial therapy should be
offered :second-line therapy. For those who are still colonised after
two treatments, the choice lies between a third attempt (guided by
antibiotic sensitivity testing) and long-term acid suppression.
H. pylori and NSAIDs are independent risk factors for ulcers, and
patients requiring Jong-term NSAID therapy should fi rst undergo
eradication therapy to reduce ulcer risk. Subsequent co-prescription
of a PPI with the NSAlD is ad vised but is not always necessary for
patients being given low-dose aspirin.
General measures: Cigarette smoking, aspirin and NSAIDs should
be avoided. Alcohol in moderation is no t harmful and no special
dietary advice is required.
Maintena nce treatt11e11t: This should not be necessary after suc-
cessful H. pylori eradication.
Surgica l treah 11e11 t: Surgery is now rarely required for peptic
ulcer, unless there is perforation, persis ting haemorrhage, gastric
outflow obstruction or persisting or recurrent ulcer after medical
treatment. Non-healing gastric ulcer is treated by partial gas-
trectomy, in which the uJcer and the ulcer-bearing area of the stom-
ach are :resected to exclude an underlying cancer. In the emergency
situation, biopsies are taken, and then 'unde r-running' the ulcer for
bleeding or 'oversewing' (patch repair) for perforation is sufficient.
Complications of peptic ulcer
Perforation: This allows stomach contents to escape into the peri-
toneum, causing peritonitis. It is more common in duodena] than in
gastric ulcers. About one-quarter of cases •occur in acute ulcers, often
with NSAIDs. It causes:
• Sudden, severe pain, often the first sign of ulcer, starting in the
upper abdomen and becoming generalised. Shoulder tip pain due
to diaphragmatic irritation, shallow respiration due to pain, and
shock are common. • Generalised rigidity. • Absent bowel sounds.
• Los:s of liver dullness due to gas under the diaphragm.
Rigidity persists, and although pain may temporarily improve,
the patient's condition later deteriorates with general peritonitis.
In at least 50% of cases, an erect CXR shows free air beneath the
diaphragm. If not, a water-soluble contrast swallow will confirm
perforation.
After resuscitation, the acute perforation is closed surgically.
Following surgery, H. pylori should be treated (if present) and
NSAIDs avoided. The mortality from perforation is 25%, reflecting
the age and comorbidity of the popuJation affected.
Gastric 011tlet obstn,ction: The most common cause is an ulcer
near the pylorus, but occas ional cases are due to antral cancer or
adult hypertrophic pyloric stenosis. Clinical features include:
• Nausea. • Vomiting of large quantities of gastric content.
• Abdominal distension.
Examination reveals wasting, dehydration and a succussion
splash persisting 4 hrs or more after the last meal. Visible gastric
peristalsis is diagnostic.
 Investigations show:
• Low serum chloride and potassium. • Raised bicarbonate and urea:
dehydration results in enhanced renal absorption of Na• in exchange
for H· and paradoxical aciduria. • Nasogastric aspiration of at least
200 mL after an overnight fast: suggests the diagnosis. • Endoscopy:
performed after the stomach has been emptied by wide.bore
nasogastric tube.
Management includes:
• Nasogastric suction and the administration of large volumes of IV
isotonic saline with potassium. • PPis: may heal ulcers, relieve
pyloric oedema and overcome the need for surgery. • Balloon dilata-
tion of ben ign stenosis: may be possible. • Partial gastrectomy after
a 7-day period of nasogastric aspiration: necessary in other patients.
Bleeding: See pages -116-418.