Download ABC of the Upper Gastrointestinal Tract - R. Logan (BMJ, 2002) WW PDF

TitleABC of the Upper Gastrointestinal Tract - R. Logan (BMJ, 2002) WW
TagsMedical
LanguageEnglish
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Total Pages63
Table of Contents
                            ABC of the Upper Gastrointestinal Tract
1 Implications of dyspepsia for the NHS
2 Oesophagus: Heartburn
3 Oesophagus: Atypical chest pain and motility disorders
4 Dysphagia
5 Epidemiology and diagnosis of Helicobacter pylori infection
6 Pathophysiology of duodenal and gastric ulcer and gastric cancer
7Management of Helicobacter pylori infection
8 Indigestion and non-steroidal anti-inflammatory drugs
9 Upper gastrointestinal haemorrhage
10 Indigestion: When is it functional?
11 Upper abdominal pain: Gall bladder
12 Cancer of the stomach and pancreas
13 Anorexia, nausea, vomiting, and pain
                        
Document Text Contents
Page 2

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Page 31

7 Management of Helicobacter pylori infection
Adam Harris, J J Misiewicz

This article discusses the current management of Helicobacter
pylori infection in patients with dyspepsia with or without
endoscopic abnormalities. We take an evidence based approach
when possible and consider recent guidelines from national and
international bodies pertaining to primary and secondary care.

Duodenal ulcer disease
In patients who are not taking non-steroidal anti-inflammatory
drugs (NSAIDs) duodenal ulcer will be due to H pylori infection
in 95% of cases, and eradication treatment can be prescribed
without testing for H pylori. If there is any doubt about the
diagnosis, such as a possible ulcer crater on a barium meal,
endoscopic confirmation of duodenal ulcer and H pylori
infection should be sought before prescribing treatment.

H pylori eradication treatment, if successful, will be effective
in curing the ulcer diathesis regardless of whether a patient is
seen at the initial presentation of the disease or at a recurrence.
Patients taking long term (maintenance) treatment with H2
receptor antagonists or proton pump inhibitors should also be
offered H pylori eradication treatment regardless of whether
they are free of symptoms or still experiencing indigestion. In
most cases eradication of H pylori cures the duodenal ulcer
disease, and maintenance treatment can be stopped.

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Uncomplicated duodenal ulcers heal quickly and completely
after eradication of H pylori. Further antisecretory treatment,
repeat endoscopy, or formal assessment of eradication is not
necessary, and one can await the clinical outcome.

Recurrent symptoms indicate either eradication failure or
the presence of some other disease. Subsequent management
will not be clear unless the outcome of eradication treatment is
known, and this is best assessed by a 13C-urea breath test
performed more than four weeks after the antimicrobial
treatment. Recurrent symptoms after documented H pylori
eradication are often due to gastro-oesophageal reflux disease,
the symptoms of which may be misattributed to duodenal ulcer.

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Complicated duodenal ulcers (such as bleeding or perforated)
are associated with appreciable morbidity and mortality,
especially in elderly people. Therefore, in patients with
complicated duodenal ulcers, eradication of H pylori and
complete epithelialisation of the ulcer crater need to be
confirmed by the 13C-urea breath test and endoscopy, after
which maintenance antisecretory treatment can be stopped.
The prevalence of H pylori infection in patients with
complicated duodenal ulcer may be lower than in those with
simple duodenal ulcer, and H pylori status should therefore be
assessed before prescribing eradication treatment.

Duodenal ulcers recur in about 5% of patients initially
infected with H pylori even after eradication and in the absence
of reinfection or use of NSAIDs. Duodenal ulcers are also found
occasionally in people not infected with H pylori. After exclusion
of surreptitious use of ulcerogenic drugs and the rarer causes of
duodenal ulcer, such patients need long term maintenance
treatment with antisecretory drugs.

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x H pylori infection
x Non-steroidal anti-inflammatory drugs


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x Zollinger-Ellison syndrome
x Hypercalcaemia
x Granulomatous diseases (Crohn’s disease, sarcoidosis)
x Neoplasia (carcinoma, lymphoma, leiomyoma, leiomyosarcoma)
x Infections (tuberculosis, syphilis, herpes simplex, cytomegalovirus)
x Ectopic pancreatic tissue

pH

2

Gastric
juice

Adherent
layer of
mucus

H pylori

Epithelium

Gastric
gland

Blood

5

6.8

7.4

.���
� >�� Microanatomy of gastric mucosa indicating the pH gradient

Known duodenal ulcer or ulcer found at endoscopy or barium meal

1 week of triple therapy for H pylori eradication

Second line
eradication treatment

Urea breath test >4 weeks
after treatment

Urea breath test >4 weeks after treatment or re-investigate if symptoms recur

Assume infection with H pylori

H pylori negative

H pylori negative

H pylori positive

H pylori positive

No further
treatment

Maintenance
antisecretory

treatment

Patient still
symptomatic

Patient
asymptomatic

No further
treatment

Consider:
False negative result
Gastro-oesophageal reflux disease
Functional dyspepsia
H pylori negative duodenal ulcer
Gall stones

.���
� >�- Management plan for uncomplicated duodenal ulcer in patients
not taking NSAIDs

22

Page 32

Gastric ulcer
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The main difference in the management of gastric ulcers from
that of duodenal ulcers is the need to exclude malignancy in an
apparently benign gastric ulcer. Endoscopy is mandatory, with
targeted biopsies of the ulcer rim and base. About eight weeks
after treatment is started, endoscopy should be repeated to
confirm healing, obtain further biopsies from the original ulcer
site, and if clinically indicated ascertain H pylori infection status.


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As with duodenal ulcer, eradication of H pylori leads to healing
of gastric ulcer and markedly decreases the incidence of relapse.
Eradication of H pylori also seems to reduce the complications
associated with gastric ulcer, but the supporting evidence is less
strong than for duodenal ulcer. Maintenance treatment with
antisecretory drugs should therefore be started after successful
eradication of H pylori in those patients with gastric ulcer who
have a history of haemorrhage or perforation until complete
healing of the ulcer is confirmed at endoscopy.

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�!� ��� ���� H pylori �� #1�)�
Most gastric ulcers associated with H pylori infection or with use
of NSAIDs occur in elderly women. Despite several studies, no
clearly defined guidelines have emerged. NSAIDs and H pylori
seem to be independent risk factors for increased risk of
gastrointestinal bleeding. If a patient infected with H pylori has
ulceration then H pylori should be eradicated before treatment
with NSAIDs is started. There is no evidence that H pylori
eradication relieves NSAID induced dyspepsia.

Gastro-oesophageal reflux disease
The interaction between H pylori, gastro-oesophageal reflux
disease (GORD), and treatment with antisecretory drugs is
extremely complex and highly contentious. Epidemiological
studies have shown that the prevalence of H pylori infection is
no higher in patients with GORD than in healthy controls
matched for age and sex. Indeed,H pylori infection may be less
common in patients with GORD, particularly those with more
severe (erosive) disease, suggesting that the bacterium may have
a protective role, perhaps by producing corpus gastritis and
thus decreasing the output of acid. Moreover, proton pump
inhibitors used to treat GORD seem to be more effective at
suppressing acid and healing oesophagitis in the presence of
H pylori. After eradication of the bacterium, patients with
GORD may require higher doses and longer duration of proton
pump inhibitor treatment.

However, patients with GORD and H pylori infection who
need prolonged treatment with standard doses of proton pump
inhibitors may be at increased risk of developing atrophic
gastritis. It is well recognised that chronic atrophic pangastritis
is associated with increased risk of proximal gastric
adenocarcinoma. During profound acid suppression with
proton pump inhibitors,H pylori infection spreads from the
antrum to the gastric body and fundus and causes a chronic
active pangastritis that, with time, may progress to atrophic
gastritis. The actual lifetime risk of subsequent gastric cancer is
unknown and needs to be evaluated against the potentially
detrimental effects of eradicating H pylori infection in patients
with GORD. Further studies are needed before these
contradictory considerations can be resolved.

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x H pylori infection
x Non-steroidal anti-inflammatory drugs
x Neoplasia (carcinoma, lymphoma, leiomyosarcoma)
x Stress
x Crohn’s disease
x Infections (herpes simplex, cytomegalovirus)

Gastric ulcer found after barium meal

1 week of triple therapy for H pylori eradication

Endoscopy: Multiple targeted biopsies to exclude malignancy and test for H pylori

Benign and H pylori positive

Urea breath test >4 weeks after treatment

Benign and H pylori negative

8 weeks of antisecretory treatment

Repeat endoscopy

Repeat endoscopy >4 weeks after treatment

Repeat biopsies and 4 weeks of antisecretory treatment

Ulcer healed and
H pylori positive

Ulcer healed Ulcer not healed
Second line

eradication treatment

H pylori positive

No further treatment

Ulcer healed Ulcer not healed

Repeat biopsiesNo further treatment

Maintenance
antisecretory

treatment

Ulcer healed and
H pylori negative

No further treatment

No further treatment

H pylori negative

.���
� >�3 Management plan for gastric ulcer

.���
� >�4 Benign gastric ulcer (arrow) in upper part of
stomach

Proton pump inhibitors + H pylori infection increases atrophic gastritis Proved?

Barrett's oesophagus and GORD are risk factors for oesophageal cancer Important?

Important?

H pylori eradication reduces efficacy of proton pump inhibitors and H2
receptor antagonists

H pylori pangastritis may protect against Barrett's oesophagus and GORD

True?H pylori may cause reflux

Relevant?

.���
� >�5 Interactions between H pylori, GORD, and antisecretory drugs

Management of Helicobacter pylori infection

23

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palliative treatment
in gastric cancer 42
in pancreatic cancer 44

pancreatectomy procedures 44
pancreatic cancer 41, 43–4

prognosis 44
treatment 44

pancreatic pseudocyst 46
pancreatitis

chronic, differential diagnosis 43
nausea and vomiting 46
upper abdominal pain ,,

pangastritis 17
Barrett’s oesophagus and GORD and 23
chronic atrophic, and gastric cancer 23, 41

pantoprazole, proton pump inhibitor 7
parietal cells, in gastric acid secretion 19, 20
Parkinson’s disease, dysphagia caused by 1.
patient counselling, in �������� infection 24–5
peptic stricture

dysphagia caused by 14
postoperative 13

peptic ulcer 1–3
dyspepsia in 1–3, 33–4
haemorrhage and 30–1
�������� and 16, 17
nausea and vomiting 46–7
�������� duodenal ulcer; gastric ulcer

periampullary tumours 43
pernicious anaemia 19, 21
pharyngeal pouch, dysphagia caused by 12
pH monitoring (oesophageal) 5, /

in acid reflx 8, 10
in GORD 33
in nausea and vomiting 48

pigment stones 37
piroxicam, gastrointestinal toxicity 27
polidoconal, sclerosant intravariceal injection 32
potassium supplements, peptic stricture and 13
pregnancy

gallstones and 37
nausea and vomiting 46

prokinetic drugs
for functional dyspepsia 36
for nausea and vomiting 48

propranolol, beta-adrenoceptor blocker,
in variceal haemorrhage 32

prostaglandin E1 analogue 27
proton pump inhibitors

action of 19
costs of .
for chest pain 10
for duodenal ulcer 22
for functional dyspepsia 36
for nausea and vomiting 47
for NSAID-associated ulcers 28
for oesophagitis 6–7
for peptic stricture 13
in low dose triple therapy 24, 25
interactions between �������� and GORD 6, 23

psychological factors
in achalasia 9, 11
in chest pain 8, 9, 11
in dyspepsia 35, 36

psychotherapy
for functional dyspepsia 36

Index

53

for nausea and vomiting in functional
dyspepsia 48

psychotropic drugs, in functional dyspepsia 23, 46

quadruple therapy, �������� eradication 24, 25

radiology, in dysphagia 12
radiotherapy, for oesophageal tumours 14
ranitidine, H2 receptor antagonist 7
ranitidine-bismuth-citrate, �������� eradication 24
reflux, �������� gastro-oesophageal reflux
reflux oesophagitis, pain in 33
reflux related dysmotility, dysphagia in 15
renal disorders

nausea and vomiting 46
upper abdominal pain ,,

respiratory symptoms, in GORD 4
resuscitation, haemorrhage and 31
rofecoxib, COX-2 inhibitor 29
rupture, after oesophageal dilatation 13, 15

salt, dietary factor in �������� infection 21
sarcoidosis 22
Schatzki’s ring 13
sclerosants, intravariceal injection 32
selective seretonin reuptake inhibitor ,/
Sengstaken-Blakemore (Minnesota) tube 32
serology, �������� diagnosis 3, 18
smoking 21, 24, .-, 46
sodium tetradecyl sulphate, sclerosant intravariceal

injection 32
somatisation, dyspepsia and nausea and vomiting 46, 47
spasm, oesophageal 9, 11, 15
sphincter of Oddi, high pressure 39
stents, oesophageal 14
stomach

cancer of 41–2
oesophagogastrectomy 14
�������� gastric

stool antigen tests, �������� diagnosis 3, 18
strictures

oesophageal 4, -
peptic 13, 14

stroke, dysphagia caused by 1.
sucralfate, for functional dyspepsia 36
sulindac, gastrointestinal toxicity .-
sumatriptan, chest pain caused by 9
syphilis 22

terlipressin, vasoactive drug 32
tolmetin, gastrointestinal toxicity .-
transjugular intrahepatic portosystemic

shunt (TIPPS) 32
tricyclic antidepressants

for achalasia 9, 11
for functional dyspepsia ,/

Troisier’s sign 41
tuberculosis 22
tumour markers, in pancreatic cancer 43
tumours ��� adenocarcinoma; carcinoma; gallbladder

cancer; gastric cancer; gastrointestinal cancer;
oesophageal tumours; pancreatic cancer

tumours, duodenal ulcer caused by 22

ulcer
NSAID-associated 27–8, 28–9
�������� duodenal ulcer; gastric ulcer; peptic ulcer

Page 63

ultrasonography
gall stone test 38
in jaundice 43

upper abdominal pain
gall bladder 37–40
nausea and vomiting with 45–8

urea breath test, H pylori diagnosis 18
urease tests, H pylori diagnosis 17–18

vacuolating toxin (Vac A toxin), in H pylori
phenotype 21

Index

54

variceal haemorrhage, treatment 32
vasoactive drugs, gastrointestinal haemorrhage 32
vomiting 45–8

in GORD $
in hernia torsion 4

weight loss, in dyspepsia 45, 46
Whipple’s procedure 44

Zollinger-Ellison syndrome, gastrin-secreting
tumour 19, ��

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