Helicobacter Pylori Infection and Peptic
Ulcers
Majumdar D, Consultant Physician and Gastroenterologist and Hepatobiliary Lead at Ashford and St Peter’s Hospital NHS Foundation Trust, Chertsey, UK. Compenting
interests. Bebb J, Consultant Physician and Gastroenterologist at The Royal Comwall Hospital, Comwall Hospital, Comwall, UK. Compenting interests.
https://doi.org/10.1016/j.mpmed.2019.02.008
Tiur Maris Panjaitan (1815046)
Preceptor :
dr. Mellisa Valensia,Sp.PD
SMF Ilmu Penyakit Dalam
RS Immanuel – Universitas Maranatha
Bandung
2019
Nearly all peptic ulcers are caused by either Helicobacter pylori
infection or the use of non-steroidal anti-inflammatory drugs
(NSAIDs), which include aspirin.
15% of H. pylori-infected people develop an ulcer in their lifetime,
with the risk determined by virulence of the H. pylori strain, host
genetics and environment
NSAID-induced ulcers are largely the result of suppression of
gastro- protective cyclooxygenase (COX)-1.
For H. pylori-associated ulcers, H. pylori eradication treatment
induces healing and prevents relapse.
A peptic ulcer is a breach in the gastric or
duodenal mucosa with penetration of the
muscularis mucosa
Gastritis is defined as inflammation of the
gastric mucosa. It is diagnosed and
classified histologically because endoscopic
appearances such as erythema are
frequently subjective and misleading.
Helicobacter pylori
Can cause either antral-predominant gastritis, which predisposes to duodenal ulceration, or
corpus-predominant or pangastritis, which predisposes to gastric ul- ceration and distal
gastric adenocarcinoma.
Aspirin/NSAIDs
Cause a ‘chemical gastritis’, which is characterized by mucosal hyperplasia and oedema but
minimal inflammatory cell infiltration.
Autoimmune gastritis
Can result in vitamin B12 deficiency and pernicious anaemia
Gastric ulcers and, later, The prevalence of gastric and
duodenal ulcers were duodenal ulceration has
increasingly described in the decreased in Western Europe
late 19th century, the and the USA in recent
incidence of duodenal ulcers decades, after a decrease in
increasing progressively the prevalence of H. pylori
It is mostly acquired in Helicobacter pylori is acquired
childhood, up to the age of by human contact, usually
12, and strongly associated oro-oral rather than faecal-
with greater age oral transmission.
Aspirin and other non-selective NSAIDs are independent
causes of duodenal and gastric ulceration
Concomitant use of gastroprotective agents reduces the risk,
although suboptimal adherence to such treatment is also
associated with an increased risk of upper gastrointestinal (GI)
events.
British Society of Gastroenterology has suggested that if acid
suppression is required after H. pylori eradication, H2-re-
ceptor antagonists should be used first.
Chronic H. pylori-associated gastritis can cause
abdominal pain, nausea and vomiting that resolve
within a few days, and also dyspeptic symptoms
Uncomplicated peptic ulcers typically cause epigastric
pain and, less commonly, nausea, vomiting and
weight loss, whereas some ulcers are asymptomatic.
The differential diagnosis of peptic ulcer disease
Gastro-oesophageal
Reflux Disease Functional Dyspepsia Gallstone Disease
(GORD)
Gastric Cancer Or Irritable Bowel
Crohn’s Disease
Lymphoma Syndrome
Pancreatitis Pancreatic Cancer
H. pylori ulcers usually heal and relapse spontaneously
Ulcers of any cause, particularly NSAID-induced ulcers, can cause
serious complications
Acutely bleeding ulcers cause haematemesis and/or melaena, and
chronic bleeding can cause anaemia
Perforation results in peritonism, and gastric outlet obstruction
causes persistent vomiting
Dyspepsia in the community
• A ‘test-and- treat’ approach is cost-effective and is
advocated over more invasive investigations, such as
Young upper GI endoscopy
patients • Patients should be non-invasively tested for H. pylori
and given treatment to eradicate H. pylori if the results
are positive
• Those whom presenting for the first time with recent-onset,
Older unexplained and persistent dyspepsia , and those with
‘alarm’ symptoms or signs should be referred for upper GI
patients endoscopy and/or other investigations, both to exclude
malignancy and to make a positive diagnosis
Upper gastrointestinal endoscopy
The investigation of choice in older patients with
dyspepsia and those with ‘alarm’ symptoms because
it enables diagnosis of ulceration and other
macroscopic abnormalities such as malignancy and
oesophagitis
Patients with persistent, non-responsive gastro-
oesophageal symptoms, those considering surgery
for GORD and those with H. pylori colonization not
responding to second-line eradication therapy should
probably be referred to specialist services for
consideration of upper GI endoscopy
Tests for Helicobacter pylori not requiring
endoscopy
Serology
involve detection of immunoglobulin G antibodies against H. pylori, and the best are
very accurate.
Urea breath test (UBT)
is a simple, non- invasive test based on H. pylori urease. It is particularly useful for
checking the success of treatment and It is also more accurate than serology so is
often used as a first-line diagnostic test.
Stool antigen test
It assesses active infection so can be used for assessing treatment success, although
with the same caveats relating to its use
Tests for Heliobacter pylori requiring
endoscopy
Biopsy • The biopsy is placed in a urea solution or gel with a pH indicator; when
urease H. pylori is present, the urea is hydrolysed by its urease, resulting in a
test colour change.
• H. pylori infection can be diagnosed accurately by histology if special
stains are used.
Histology
• The distribution of gastritis can give information on disease risk if
biopsies are taken from antrum and corpus.
• Endoscopic mucosal biopsy specimens can be cultured for H. pylori.
Culture • This is not useful as a purely diagnostic test as H. pylori is not
straightforward to grow, and culture is often falsely negative.
Treatment of peptic ulcers and non-ulcer
dyspepsia
Surgery is now reserved for complications that cannot be
controlled pharmacologically and endoscopically
In H. pylori-negative non-NSAID- associated duodenal ulcers, H.
pylori and NSAIDs are still the main etiological causes, and they are
still a common cause in apparently H. pylori-negative non-NSAID-
associated gastric ul- cers.
Although simple H. pylori-induced ulcers heal with H. pylori
treatment alone, other ulcers and large or complicated H. pylori
ulcers are usually treated with a longer course of acid suppression
therapy.
Gastric ulcers
Taking a PPI for 6-8 weeks and removing
the underlying cause, usually by treating
H. pylori or stopping NSAIDs.
If the ulcer is still present, biopsies
should be taken from the ulcer edge to
exclude malignancy and other causes.
Duodenal ulcer
Helicobacter pylori-positive ulcers usually
require a course of H. pylori eradication
therapy, and then no further acid suppression
unless the ulcer has been complicated
Refractory peptic ulcer
Is the patient
Is this a simple Has H. pylori
compliant with
peptic ulcer or eradication/testing
prescribed
something else? been adequate?
treatment?
Is there
Does the patient
surreptitious or Does the patient
have a high body
continuing NSAID smoke?
mass index (BMI)?
use?
.
The most clear-cut indications for eradication of H. pylori
• Active gastric or duodenal ulcer
• History of previous gastric/duodenal ulcer
• Gastric MALT lymphoma
• History of resection of early gastric cancer.
Patients
• In patients taking long or frequent intermittent courses of
who are NSAIDs, especially where dyspeptic symptoms or previous
ulcers have been observed, long-term PPI prophylaxis
positive for should be used
H. pylori
• Given eradication therapy
H. pylori • This strategy benefits those who have an ulcer underlying
positive their symptoms and also 1 in about 14 of those with
functional dyspepsia.
Low clarithromycin resistance areas: first-line treatment remains triple
combination therapy with twice-daily PPI, clarithromycin and amoxicillin or
metronidazole for 1 or 2 weeks.
Metronidazole resistance is also common, in particular among migrants
from developing countries who have frequently had exposure to
metronidazole and other nitroimidazoles.
If treatment failure is confirmed with UBT or stool antigen, second-line
therapy with a bismuth-containing quadruple therapy or 10-day course
of PPI, levofloxacin and amoxicillin is recommended .
High clarithromycin resistance areas: first-line therapy is bismuth-containing
quadruple therapy, avoiding clarithromycin.
Treatment of non-ulcer dyspepsia
There is a high incidence of anxiety disorders, which should be addressed.
Underlying pathophysiological disturbances are not fully understood but include
impaired gastric accommodation, delayed gastric emptying, and visceral
hypersensitivity.
Most experts advocate a trial of PPI and/or H. pylori eradication, if present.
Meta-analysis of antidepressants in the treatment of functional dyspepsia
suggested an effectiveness of tricyclic anti- depressants compared with placebo
Most authorities previously recommended a trial of prokinetic agents such as
domperidone.
Limited data suggest benefit from bismuth, miso- prostol, sucralfate and
pirenzepine.
Prevention of ulcers, gastritis and gastric
cancer
Helicobacter pylori infection is a major risk factor for non-cardiac gastric cancer and is thought
to increase the risk 2.5-5-fold.
Mass eradication trials in Asia have reported excellent compliance, minor adverse events and
low cost along with a 30 -40% reduction in gastric cancer risk with successful eradication.
Challenging research suggests that H. pylori reduces the severity of complications of gastro-
oesophageal reflux, including reducing the incidence of oesophageal adenocarcinoma.
There is also evidence that child- hood H. pylori infection offers some protection against
modern diseases such as asthma and allergy, possibly via the hygiene hypothesis.
However, the current view is that the number of lives saved from gastric cancer is likely to
more than balance these risks.
