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A peptic ulcer is an erosion in a segment of the gastrointestinal mucosa, typically in the stomach (gastric ulcer) or
the first few centimeters of the duodenum (duodenal ulcer), that penetrates through the muscularis mucosae.1
Symptoms typically include burning epigastric pain that is often relieved by food.1
Nearly all ulcers are caused by Helicobacter pylori (H pylori) infection or non-steroidal anti-inflammatory drug
(NSAID) use. H pylori has been clearly associated with both gastric and duodenal ulcers, and, in the absence of
NSAIDs, eradication of the organism results in long-term healing with re-infection being rare.2 H pylori is said to
account for 80% of all gastric or stomach ulcers and more than 90% of all duodenal ulcers.3,4 Confirmation of the
presence of H pylori prior to eradication therapy is recommended.2
tosis and basophilic leukemias. Very few patients have approximately an hour after eating), and is generally relieved by
hypersecretion of gastrin (Zollinger-Ellison syndrome).1 antacids or food but aggravated by alcohol and caffeine.6,7
• Chronic conditions: Diseases associated with an Weight loss and gastrointestinal bleeding occur more
increased risk of peptic ulcer disease include cirrhosis, frequently with gastric ulcers.6 Patients can experience
chronic obstructive pulmonary disease, renal failure and weight loss of 5 kg to 10 kg and although this could indicate
organ transplantation.8 carcinoma, especially in people over 40 years, on investiga-
• Rare conditions: Other rare, miscellaneous causes tion a benign gastric ulcer is found most of the time.7
include radiation-induced or chemotherapy-induced
ulcers, vascular insufficiency and duodenal obstruction.8 Duodenal ulcers tend to produce more consistent pain. Pain
is absent when the patient awakens but appears mid-
These factors weaken the normal protective barrier of the morning, is relieved by food, but recurs two to three hours
mucous membrane of the stomach and small intestine and after a meal.1 Pain that awakens a person at night, a few
may cause increased secretion of acid and pepsin, with hours after falling asleep, is also common and is highly
resulting inflammation and subsequent ulceration.5 suggestive of duodenal ulcer.1 The pain then usually
subsides by morning and is often relieved after eating.6 This
Diagnosis of peptic ulcer disease is not commonly noticed in gastric ulceration.7 In neonates,
Symptoms depend on ulcer location and patient age. Many perforation or haemorrhage may be the first manifestation of
patients, particularly elderly patients, have few or no symp- duodenal ulcer. Haemorrhage may also be the first recognised
toms.1 Pain is however the most common symptom, often sign in later infancy and early childhood, although repeated
localised to the epigastrium or mid-epigastrium and relieved vomiting or evidence of abdominal pain may be a clue.1
by food or antacids.1,6 The pain is described as burning,
gnawing, constant or annoying, or sometimes a sensation of Diagnosis of peptic ulcer is by patient history, and confirmed by
hunger.1,6 The course is usually chronic and recurrent. Only endoscopy and testing for H pylori. Table II gives a summary of
about 50% of patients present with the characteristic pattern persons that should be tested for H pylori. The following are
of symptoms.1 Table I distinguishes between the symptoms examples of tests that can be done for H pylori8,9,10:
of gastritis, gastric and duodenal ulcer. • Carbon-13 urea breath tests detect active H pylori
infection by testing for the enzymatic activity of bacterial
Gastric ulcer symptoms often do not follow a consistent pattern urease. In the presence of urease produced by H pylori,
(for example, eating sometimes exacerbates rather than labeled carbon dioxide is produced in the stomach,
relieves, pain).1 This is especially true for pyloric channel absorbed into the bloodstream, diffused into the lungs
ulcers, which are often associated with symptoms of obstruction and exhaled.
(for example bloating, nausea and vomiting) caused by • Stool or faecal antigen testing identifies active H pylori
oedema and scarring.1 In general, however, in gastric ulcers, infection by detecting the presence of H pylori antigens in
pain typically starts whenever the stomach is empty (usually stools.
Evidence
•
•
Serology, which is immunoglobulin G (IgG) based, can be
measured in serum, plasma or whole blood. It will,
however, not distinguish between a previous or a current
infection.
Biopsy-based urease tests, which are invasive and can
only be done at gastroscopy or in the acute hospital
setting. There are two methods for this test. In the CLO
test (“Campylobacter-like organisms” test, the rapid
urease test) a fragment of mucosal membrane is placed
Table III: Specific questions to ask the patient with sus-
Aspect
pected peptic ulcer diease
Question
Pattern, duration and se- • Describe the location of the pain
verity of symptoms • Describe the type of pain that you are
experiencing (for example, constant or
intermittent, gnawing or stabbing)
• Are you sometimes awakened by the
into a special jelly which undergoes a colour change in symptoms after a few hours of falling
10 to 20 minutes, or the specimen is sent for histology asleep?
which may take up to 24 hours to obtain the result. • Is the pain relieved or worsened by the
intake of food?
Endoscopy allows for biopsy or cytologic brushing of gastric Onset • When did the symptoms start?
and oesophageal lesions to distinguish between simple • Has there been any change to your
ulceration and ulcerating stomach cancer. Stomach cancer work routine, stress levels, use of medi-
cine, eating or drinking habits?
may present with similar signs and symptoms and must be
excluded, especially in patients who are over 45 years of Associated factors and • Do you have any other symptoms (for
age, have lost weight, or report severe or refractory symp- conditions example, blood in your stools, nausea
or vomiting)?
toms.1 The incidence of malignant duodenal ulcer is ex-
• What current or preceding illnesses do
tremely low, therefore biopsies of lesions in that area are you suffer from?
generally not warranted. Endoscopy can also be used to • What medicine do you take?
definitely diagnose H pylori infection, which should be • Are any other family members experi-
sought when an ulcer is detected. encing similar symptoms?
Previous similar symp- • Have you experienced similar symp-
Gastrin-secreting malignancy and Zollinger-Ellison syn- toms toms before? If yes, what was the
drome should be considered when there are multiple ulcers, cause?
when ulcers develop in atypical locations or are refractory to Previous and current ac- • What are you taking or doing to relieve
treatment, or when the patient has prominent diarrhoea or tions to relieve symptoms the symptoms?
weight loss. Serum gastrin levels should be measured in
these patients.1 treatment. The pharmacist should only offer short-term
symptomatic treatment (one to two days).5
Counselling approach to follow • Since a high percentage of gastric carcinoma occurs as a
A thorough history regarding habits and medica- result of gastric ulceration, early referral of a suspected
tion usage should be taken, a physical examina- gastric ulcer is an urgent necessity.
tion can be performed and, if appropriate, • Any complications such as acute bleeding, perforation or
laboratory/diagnostic tests (often endoscopy) may be obstruction constitute an emergency which necessitates
conducted to exclude other conditions. The overall aim is to urgent medical attention.
reduce epigastric pain, to improve the patient’s quality of life
by identifying, treating and/or eliminating the underlying The following are potential complications of an undiagnosed
cause of the peptic ulceration, and to use pharmacological and untreated peptic ulcer5:
therapy when indicated. This should be accomplished
without adverse effects or with clinically acceptable adverse • Chronic, slow gastrointestinal bleeding with resulting
effects. A list of aspects that should be addressed in a anaemia (tiredness and pallor) and occult blood in the
patient assessment history is given in Table III. stools.
• Reduced food intake due to pain, with resultant weight
If the pharmacist is convinced that a patient is only suffering loss and emaciation.
from gastritis, therapeutic treatment can be offered. If a • Complications specifically in cases of ulceration:
peptic ulcer is suspected, the pharmacist can provide o Acute bleeding with:
temporary, symptomatic treatment, followed by referral to a - Clear blood in stools
medical practitioner. Empiric therapy is therefore often - Haematemesis
begun without a definite diagnosis. - Hypovolaemic shock and death
o Perforation of the ulcer with peritonitis. An acute
When to refer abdomen presents.
The following are indicative of referral: o On healing, fibrosis and stenosis can occur, with
• All patients with a new or recurring ulcer should be partial or complete obstruction.
referred to a medical practitioner for diagnosis and o Gastric carcinoma often presents as a gastric ulcer.
Evidence
Available treatment options for peptic ulcer
disease
The choice of the most appropriate treatment for peptic ulcer
disease depends on the cause. The most effective therapy is
generally to treat or eliminate the underlying cause (in the
majority of cases H pylori).
Gastric ulcer
Stop NSAIDs,
if used 1
Full dose PPI for H pylori positive Test for H pylori Full dose PPI for one
two months H pylori2 or two months
Ulcer associated negative
with NSAID use
H pylori positive
Ulcer not associated
with NSAID use
Eradication
therapy3
H pylori
positive Ulcer healed Low dose treat- Healed
Endoscopy and
ment as required5 Endoscopy4
H pylori test4 H pylori
negative
Ulcer not healed Not healed
H pylori negative
Periodic review 6
Refer to specialist Return to self care Refer to specialist
secondary care secondary care
1 If NSAID continuation is necessary, after ulcer healing offer long term gastric protection or consider substitution to a newer COX-
selective NSAID.
2 Use a carbon-13 urea breath test, stool antigen test or, when performance has been validated, laboratory-based serology.
3 Use a PPI, amoxicillin, clarithromycin 500 mg (PAC500) regimen or a PPI, metronidazole, clarithromycin 250 mg (PMC250) regimen.
Follow guidance found in the British National Formulary for selecting 2nd line therapies.
After two attempts at eradication manage as H pylori negative.
4 Perform endoscopy 6-8 weeks after treatment. If retesting for H pylori use a carbon-13 urea breath test.
5 Offer low dose treatment, possibly used on an as required basis, with a limited number of repeat prescriptions.
6 Review care annually to discuss symptoms, promote stepwise withdrawal of therapy when appropriate and provide lifestyle advice. In
some patients with an inadequate response to therapy it may become appropriate to refer to a specialist.
Duodenal ulcer
Stop NSAIDs,
if used1
Full dose PPI for Test positive Test for Test negative
two months H pylori2
Ulcer associated
with NSAID use
Test positive
Ulcer not associated
with NSAID use
Response
Eradication
therapy 3
No response
or relapse
Full dose PPI
Retest for
for one or two
H pylori4 Negative Response
months
No response
Positive
Low dose Exclude other
Eradication
treatment as causes of DU7
therapy 5 No response No response
or relapse required 6
Response
Response
1 If NSAID continuation is necessary, after ulcer healing offer long term gastric protection or consider substitution to a newer COX-
selective NSAID.
2 Use a carbon-13 urea breath test, stool antigen test or, when performance has been validated, laboratory-based serology.
3 Use a PPI, amoxicillin, clarithromycin 500 mg (PAC500) regimen or a PPI, metronidazole, clarithromycin 250 mg (PMC250) regimen
4 Use a carbon-13 urea breath test.
5 Follow guidance found in the British National Formulary for selecting 2nd line therapies.
6 Offer low dose treatment, possibly used on an as required basis, with a limited number of repeat prescriptions.
7 Consider non-compliance with treatment, possible malignancy, failure to detect H pylori infection due to recent PPI or antibiotic
ingestion, inadequate testing, or simple misclassification; surreptitious or inadvertent NSAID or aspirin use; ulceration due to ingestion
of other drugs; Zollinger-Ellison syndrome; Crohn’s disease.
A small number of patients with chronic, refractory peptic ulceration may require maintenance acid suppression. In some patients with
an inadequate response to therapy it may become appropriate to refer to a specialist for a second opinion.
8 Review care annually to discuss symptoms, promote stepwise withdrawal of therapy when appropriate and provide lifestyle advice.
Evidence
Eradication of H pylori in duodenal ulcers should be checked
by retesting using a carbon-13 urea breath test. There is a
small risk that gastric ulcers may be malignant, therefore
patients should receive repeat endoscopy and biopsy,
retesting for H pylori six to eight weeks after starting treat-
ment. Acid suppression should be stopped two weeks
before retesting since acid suppression therapy increases
the possibility of false negative results. If a patient remains
positive for H pylori after initial treatment, a regimen that uses
example, ibuprofen 400 mg three times daily). For NSAID-
associated ulcers, NSAIDs should be stopped where
possible, and simple analgesics such as paracetamol with or
without a low dose opioid should be prescribed. Those with
inflammatory diseases, for example rheumatoid arthritis, may
however depend on NSAIDs for effective pain relief.
Evidence
In the OMNIUM study4,14, 75% of patients were successfully
treated after eight weeks of omeprazole 20 mg. These rates
were comparable to 400 µg of misoprostol (71%, a non-
significant difference). In the ASTRONAUT study4,15, 80% of
patients were successfully treated after eight weeks, superior
to 150 mg twice daily of ranitidine (63%, P=<0.001). Both
studies, however, included patients with endoscopic ero-
sions as well as ulcers. NICE guidelines recommend four to
eight weeks’ treatment with a PPI, whether or not NSAIDs are
9.
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13.
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Standard Treatment Guidelines and Essential Drugs List for South Africa:
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British Society of Gastroenterology Endoscopy Committee. 2002. Non-
variceal Upper Gastrointestinal Haemorrhage: Guidelines. Gut, 51: iv1-
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North of England Dyspepsia Guideline Development Group. 2004.
Dyspepsia: Managing Dyspepsia in Adults in Primary Care. Evidence-
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25 November 2008).
14. Hawkey CJ, Karrasch JA, Szczepanski L, Walker DG, Barkun A,
Swannell AJ & Yeomans ND for The Omeprazole versus Misoprostol for
Other ulcers NSAID-Induced Ulcer Management (OMNIUM) Study Group. 1998.
The prevalence of H pylori is falling with successive birth Omeprazole compared with misoprostol for ulcers associated with
nonsteroidal anti-inflammatory drugs. New England Journal of Medicine,
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CJ, Swannell AJ & Hawkey CJ for The Acid Suppression Trial: Ranitidine
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