1. GASTRO-OESOPHAGEALGASTRO-OESOPHAGEAL
REFLUX DISEASEREFLUX DISEASE
Gastro-oesophageal refluxGastro-oesophageal reflux resultingresulting
in heartburn affects approximately 30% ofin heartburn affects approximately 30% of
the general population.the general population.

2. AnatomyAnatomy
 The oesophagus is a muscular tube 25 cmThe oesophagus is a muscular tube 25 cm
long which extends from the cricoidlong which extends from the cricoid
cartilage to the cardiac orifice of thecartilage to the cardiac orifice of the
stomach.stomach.
 It has an upper and a lower sphincter.It has an upper and a lower sphincter.
 A peristaltic swallowing wave propels theA peristaltic swallowing wave propels the
food bolus into the stomach.food bolus into the stomach.

3. PathophysiologyPathophysiology
 Occasional episodes of gastro-oesophagealOccasional episodes of gastro-oesophageal
reflux are common in health.reflux are common in health.
 Reflux is followed by oesophageal peristalticReflux is followed by oesophageal peristaltic
waves which efficiently clear the gullet, alkalinewaves which efficiently clear the gullet, alkaline
saliva neutralises residual acid, and symptomssaliva neutralises residual acid, and symptoms
do not occur.do not occur.
 Gastro-oesophageal reflux disease developsGastro-oesophageal reflux disease develops
when the oesophageal mucosa is exposed towhen the oesophageal mucosa is exposed to
gastric contents for prolonged periods of time,gastric contents for prolonged periods of time,
resulting in symptoms and, in a proportion ofresulting in symptoms and, in a proportion of
cases, oesophagitis.cases, oesophagitis.

4. EtiologyEtiology
1. abnormal of the lower oesophageal sphincter:1. abnormal of the lower oesophageal sphincter:
A. reduced tone:A. reduced tone:
 dietary factors (coffee, tea),dietary factors (coffee, tea),
 smoking,smoking,
 alcohol,alcohol,
 pregnancy, obesity (resulting in increased intra-abdominalpregnancy, obesity (resulting in increased intra-abdominal
pressure);pressure);
 preparations (Papaverin, Nitrats, Teophyllin, etc.)preparations (Papaverin, Nitrats, Teophyllin, etc.)
B. inappropriate relaxation:B. inappropriate relaxation:
 hiatus hernia;hiatus hernia;
 dietary factors (fried, fatty food, macaroni; these food result indietary factors (fried, fatty food, macaroni; these food result in
delayed gastric emptying, increased intra-gastric acidity)delayed gastric emptying, increased intra-gastric acidity)
2. defective oesophageal clearance;2. defective oesophageal clearance;

5. Factors associated with the developmentFactors associated with the development
of gastro-oesophageal reflux diseaseof gastro-oesophageal reflux disease ..

6. Abnormalities of the lowerAbnormalities of the lower
oesophageal sphincter:oesophageal sphincter:
 In health, the lower oesophageal sphincter isIn health, the lower oesophageal sphincter is
tonically contracted, relaxing only duringtonically contracted, relaxing only during
swallowing.swallowing.
 Some patients with gastro-oesophageal refluxSome patients with gastro-oesophageal reflux
disease have reduced lower oesophagealdisease have reduced lower oesophageal
sphincter tone, permitting reflux when intra-sphincter tone, permitting reflux when intra-
abdominal pressure rises.abdominal pressure rises.
 In others, basal sphincter tone is normal butIn others, basal sphincter tone is normal but
reflux occurs in response to frequent episodes ofreflux occurs in response to frequent episodes of
inappropriate sphincter relaxation.inappropriate sphincter relaxation.

7. Hiatus hernia:Hiatus hernia:
 Hiatus hernia causes reflux because theHiatus hernia causes reflux because the
pressure gradient between the abdominal andpressure gradient between the abdominal and
thoracic cavities, which normally pinches thethoracic cavities, which normally pinches the
hiatus, is lost. In addition, the oblique anglehiatus, is lost. In addition, the oblique angle
between the cardia and oesophagus disappears.between the cardia and oesophagus disappears.
 Many patients who have large hiatus herniasMany patients who have large hiatus hernias
develop reflux symptoms, but the relationshipdevelop reflux symptoms, but the relationship
between the presence of a hernia and symptomsbetween the presence of a hernia and symptoms
is poor.is poor.
 Hiatus hernia is very common in individuals whoHiatus hernia is very common in individuals who
have no symptoms, and some symptomatichave no symptoms, and some symptomatic
patients have only a very small or no hernia.patients have only a very small or no hernia.

8. Important features of hiatusImportant features of hiatus
herniahernia
 Occurs in 30% of the population over theOccurs in 30% of the population over the
age of 50 years;age of 50 years;
 Often asymptomatic;Often asymptomatic;
 Heartburn and regurgitation can occur;Heartburn and regurgitation can occur;
 Gastric volvulus may complicate largeGastric volvulus may complicate large
para-oesophageal hernias.para-oesophageal hernias.

9. Types of hiatus herniaTypes of hiatus hernia ..

10. Delayed oesophagealDelayed oesophageal
clearance:clearance:
 Defective oesophageal peristaltic activityDefective oesophageal peristaltic activity
is commonly found in patients who haveis commonly found in patients who have
oesophagitis.oesophagitis.
 It is a primary abnormality, since it persistsIt is a primary abnormality, since it persists
after oesophagitis has been healed byafter oesophagitis has been healed by
acid-suppressing drug therapy.acid-suppressing drug therapy.
 Poor oesophageal clearance leads toPoor oesophageal clearance leads to
increased acid exposure time.increased acid exposure time.

11.  Gastric contents:Gastric contents: Gastric acid isGastric acid is
the most important oesophagealthe most important oesophageal
irritant and there is a closeirritant and there is a close
relationship between acid exposurerelationship between acid exposure
time and symptoms.time and symptoms.
 Defective gastric emptying:Defective gastric emptying:
Gastric emptying is delayed inGastric emptying is delayed in
patients with gastro-oesophagealpatients with gastro-oesophageal
reflux disease.reflux disease.

12.  Increased intra-abdominal pressure:Increased intra-abdominal pressure:
Pregnancy and obesity are establishedPregnancy and obesity are established
predisposing causes. Weight loss maypredisposing causes. Weight loss may
improve symptoms.improve symptoms.
 Dietary and environmental factors:Dietary and environmental factors:
Dietary fat, chocolate, alcohol and coffeeDietary fat, chocolate, alcohol and coffee
relax the lower oesophageal sphincter andrelax the lower oesophageal sphincter and
may provoke symptoms. There is littlemay provoke symptoms. There is little
evidence to incriminate smoking orevidence to incriminate smoking or
NSAIDs as causes of gastro-oesophagealNSAIDs as causes of gastro-oesophageal
reflux disease.reflux disease.

13. Clinical featuresClinical features
 The major symptoms areThe major symptoms are heartburnheartburn andand
regurgitationregurgitation, often provoked by bending,, often provoked by bending,
straining or lying down.straining or lying down.
 'Waterbrash', which is salivation due to reflex'Waterbrash', which is salivation due to reflex
salivary gland stimulation as acid enters thesalivary gland stimulation as acid enters the
gullet, is often present.gullet, is often present.
 A history of weight gain is common.A history of weight gain is common.
 Some patients are woken at night by choking asSome patients are woken at night by choking as
refluxed fluid irritates the larynx.refluxed fluid irritates the larynx.
 Others develop dysphagia.Others develop dysphagia.
 A few present with atypical chest pain whichA few present with atypical chest pain which
may be severe, can mimic angina and ismay be severe, can mimic angina and is
probably due to reflux-induced oesophagealprobably due to reflux-induced oesophageal
spasm.spasm.

14. ComplicationsComplications
1. Oesophagitis1. Oesophagitis
 A range of endoscopic findings, from mildA range of endoscopic findings, from mild
redness to severe, bleeding ulcerationredness to severe, bleeding ulceration
with stricture formation, is recognised.with stricture formation, is recognised.
 There is a poor correlation betweenThere is a poor correlation between
symptoms and histological andsymptoms and histological and
endoscopic findings.endoscopic findings.
 A normal endoscopy and normalA normal endoscopy and normal
oesophageal histology are perfectlyoesophageal histology are perfectly
compatible with significant gastro-compatible with significant gastro-
oesophageal reflux disease.oesophageal reflux disease.

15. Reflux oesophagitisReflux oesophagitis . The gullet is inflamed and. The gullet is inflamed and
ulcerated (small arrows) and there is early stricturing (largeulcerated (small arrows) and there is early stricturing (large
arrow).arrow).

16. 2. Barrett's oesophagus2. Barrett's oesophagus
 Barrett's oesophagus ('columnar linedBarrett's oesophagus ('columnar lined
oesophagus'-CLO) is a pre-malignant glandularoesophagus'-CLO) is a pre-malignant glandular
metaplasia of the lower oesophagus, in whichmetaplasia of the lower oesophagus, in which
the normal squamous lining is replaced bythe normal squamous lining is replaced by
columnar mucosa composed of a cellular mosaiccolumnar mucosa composed of a cellular mosaic
containing areas of intestinal metaplasia.containing areas of intestinal metaplasia.
 It occurs as an adaptive response to chronicIt occurs as an adaptive response to chronic
gastro-oesophageal reflux and is found in 10%gastro-oesophageal reflux and is found in 10%
of patients undergoing gastroscopy for refluxof patients undergoing gastroscopy for reflux
symptoms.symptoms.

17.  CLO principally occurs in Western CaucasianCLO principally occurs in Western Caucasian
males and is rare in other racial groups.males and is rare in other racial groups.
 It is the major risk factor for oesophagealIt is the major risk factor for oesophageal
adenocarcinoma, with a lifetime cancer risk ofadenocarcinoma, with a lifetime cancer risk of
around 10%.around 10%.
 The prevalence is increasing, and it is moreThe prevalence is increasing, and it is more
common in men (especially white) and thosecommon in men (especially white) and those
over 50 years of age.over 50 years of age.
 It is weakly associated with smoking but notIt is weakly associated with smoking but not
alcohol.alcohol.
 Recent studies suggest that cancer risk isRecent studies suggest that cancer risk is
related to the severity and duration of refluxrelated to the severity and duration of reflux
rather than the presence of CLO per se but thisrather than the presence of CLO per se but this
remains to be proven.remains to be proven.
 DiagnosisDiagnosis requires multiple systematicrequires multiple systematic
biopsies to maximise the chance of detectingbiopsies to maximise the chance of detecting
intestinal metaplasia and/or dysplasia.intestinal metaplasia and/or dysplasia.

18. ManagementManagement
 Neither potent acid suppression nor antirefluxNeither potent acid suppression nor antireflux
surgery will stop progression or inducesurgery will stop progression or induce
regression of CLO, and treatment is onlyregression of CLO, and treatment is only
indicated for symptoms of reflux or complicationsindicated for symptoms of reflux or complications
such as stricture.such as stricture.
 Endoscopic ablation therapy or photodynamicEndoscopic ablation therapy or photodynamic
therapy can induce regression but 'buriedtherapy can induce regression but 'buried
islands' of glandular mucosa may persistislands' of glandular mucosa may persist
underneath the squamous epithelium andunderneath the squamous epithelium and
cancer risk is not eliminated.cancer risk is not eliminated.
 At present these therapies remain experimentalAt present these therapies remain experimental
but show promise; they are used in patients withbut show promise; they are used in patients with
high-grade dysplasia (HGD) or early malignancyhigh-grade dysplasia (HGD) or early malignancy
that is not suitable for surgery.that is not suitable for surgery.

19. Barrett's oesophagusBarrett's oesophagus . Pink columnar mucosa extends up. Pink columnar mucosa extends up
the gullet. Small islands of squamous mucosa remain (arrow).the gullet. Small islands of squamous mucosa remain (arrow).

20. AnaemiaAnaemia
 Iron deficiency anaemia occurs as aIron deficiency anaemia occurs as a
consequence of chronic, insidious blood lossconsequence of chronic, insidious blood loss
from long-standing oesophagitis.from long-standing oesophagitis.
 Almost all such patients have a large hiatusAlmost all such patients have a large hiatus
hernia.hernia.
 Nevertheless, hiatus hernia is very common andNevertheless, hiatus hernia is very common and
other causes of blood loss, particularly colorectalother causes of blood loss, particularly colorectal
cancer, must be considered in anaemic patients,cancer, must be considered in anaemic patients,
even when endoscopy reveals oesophagitis andeven when endoscopy reveals oesophagitis and
a hiatus hernia.a hiatus hernia.

21. Benign oesophageal strictureBenign oesophageal stricture
 Fibrous strictures develop as a consequence ofFibrous strictures develop as a consequence of
long-standing oesophagitis.long-standing oesophagitis.
 Most patients are elderly and have poorMost patients are elderly and have poor
oesophageal peristaltic activity.oesophageal peristaltic activity.
 They present with dysphagia which is worse forThey present with dysphagia which is worse for
solids than for liquids.solids than for liquids.
 Bolus obstruction following ingestion of meat canBolus obstruction following ingestion of meat can
lead to absolute dysphagia.lead to absolute dysphagia.
 A history of heartburn is common but notA history of heartburn is common but not
invariable; many elderly patients presenting withinvariable; many elderly patients presenting with
strictures have no preceding heartburn.strictures have no preceding heartburn.

22. DiagnosisDiagnosis ofof
benign oesophageal stricturebenign oesophageal stricture
 Endoscopy and biopsies of the strictureEndoscopy and biopsies of the stricture
are taken to exclude malignancy.are taken to exclude malignancy.
 Endoscopic balloon dilatation orEndoscopic balloon dilatation or
bouginage is undertaken.bouginage is undertaken.

23. ManagementManagement ofof
benign oesophageal stricturebenign oesophageal stricture
 Subsequently, long-term therapy with aSubsequently, long-term therapy with a
proton pump inhibitor drug at full doseproton pump inhibitor drug at full dose
should be started to reduce the risk ofshould be started to reduce the risk of
recurrent oesophagitis and stricturerecurrent oesophagitis and stricture
formation.formation.
 The patient should be advised to chewThe patient should be advised to chew
food thoroughly, and it is important tofood thoroughly, and it is important to
ensure adequate dentition.ensure adequate dentition.

24. InvestigationsInvestigations
 Investigation is advisable if patients present in middle orInvestigation is advisable if patients present in middle or
late age, if symptoms are atypical or if a complication islate age, if symptoms are atypical or if a complication is
suspected.suspected.
 Endoscopy is the investigation of choiceEndoscopy is the investigation of choice . This is. This is
performed to exclude other upper gastrointestinalperformed to exclude other upper gastrointestinal
diseases which can mimic gastro-oesophageal reflux,diseases which can mimic gastro-oesophageal reflux,
and to identify complications. A normal endoscopy in aand to identify complications. A normal endoscopy in a
patient with compatible symptoms should not precludepatient with compatible symptoms should not preclude
treatment for gastro-oesophageal reflux disease.treatment for gastro-oesophageal reflux disease.
 When, despite endoscopy, the diagnosis is unclear or ifWhen, despite endoscopy, the diagnosis is unclear or if
surgical intervention is under consideration,surgical intervention is under consideration, 24-hour24-hour
pH monitoringpH monitoring is indicated. A pH of less than 4 foris indicated. A pH of less than 4 for
more than 6-7% of the study time is diagnostic of refluxmore than 6-7% of the study time is diagnostic of reflux
disease.disease.

25. ManagementManagement
Lifestyle advice, including:Lifestyle advice, including:
 weight loss,weight loss,
 avoidance of dietary items which theavoidance of dietary items which the
patient finds worsen symptoms,patient finds worsen symptoms,
 elevation of the bed head in those whoelevation of the bed head in those who
experience nocturnal symptoms,experience nocturnal symptoms,
 avoidance of late meals,avoidance of late meals,
 giving up smoking.giving up smoking.

26. AntacidsAntacids
Antacids widely available for self-Antacids widely available for self-
medication and are used for relief of minormedication and are used for relief of minor
dyspeptic symptoms.dyspeptic symptoms.
 Magnesium Trisilicate Mixture 10 – 20 mlMagnesium Trisilicate Mixture 10 – 20 ml
3 – 4 times daily before meals;3 – 4 times daily before meals;
 Aluminium Hydroxide 300 mg5 ml LiquidAluminium Hydroxide 300 mg5 ml Liquid
300 – 600 mg as needed between meals300 – 600 mg as needed between meals
and at bedtime or as directed byand at bedtime or as directed by
physician.physician.

27. The majority are based on combinations ofThe majority are based on combinations of
calcium, aluminium and magnesium salts,calcium, aluminium and magnesium salts,
all of which have individual side-effects.all of which have individual side-effects.
 Calcium compounds cause constipation,Calcium compounds cause constipation,
 Magnesium-containing agents causeMagnesium-containing agents cause
diarrhoea,diarrhoea,
 Aluminium compounds block absorption ofAluminium compounds block absorption of
digoxin, tetracycline and dietarydigoxin, tetracycline and dietary
phosphates.phosphates.
 Most have a high sodium content and canMost have a high sodium content and can
exacerbate congestive heart failure.exacerbate congestive heart failure.

28. Histamine H2-receptorHistamine H2-receptor
antagonist drugsantagonist drugs ..
 Cimetidine 800 mg at bedtime; treatment should beCimetidine 800 mg at bedtime; treatment should be
continued for at least 4 – 8 weeks; maintenance: 400mgcontinued for at least 4 – 8 weeks; maintenance: 400mg
at bedtime;at bedtime;
 Ranitidine (Zantac) 150 mg twice a day or 300 mg atRanitidine (Zantac) 150 mg twice a day or 300 mg at
night for 4 – 8 weeks; maintenance: 150 – 300 mg atnight for 4 – 8 weeks; maintenance: 150 – 300 mg at
night;night;
 Dyspeptic symptoms remit promptly, usually within daysDyspeptic symptoms remit promptly, usually within days
of starting treatment.of starting treatment.
 They are moderately effective for the management ofThey are moderately effective for the management of
reflux disease.reflux disease.
 H2-receptor antagonist drugs help symptoms withoutH2-receptor antagonist drugs help symptoms without
healing oesophagitis.healing oesophagitis.
 They are well tolerated, and the timing of medication andThey are well tolerated, and the timing of medication and
dosage should be tailored to individual need.dosage should be tailored to individual need.

29. H+/K+ ATPase ('protonH+/K+ ATPase ('proton
pump') inhibitorspump') inhibitors ..
 Omeprazole (Losec) 20 – 80 mg once daily or twice dailyOmeprazole (Losec) 20 – 80 mg once daily or twice daily
up to 8 – 12 weeks;up to 8 – 12 weeks;
 Lansoprazole (Prevacid) 30 mg once daily or twice dailyLansoprazole (Prevacid) 30 mg once daily or twice daily
for 4 – 8 weeks;for 4 – 8 weeks;
 They are the most powerful inhibitors of gastric secretionThey are the most powerful inhibitors of gastric secretion
yet discovered, with maximal inhibition occurring 3-6yet discovered, with maximal inhibition occurring 3-6
hours after an oral dose. They have an excellent safetyhours after an oral dose. They have an excellent safety
profile.profile.
 Proton pump inhibitors (omeprazole and lansoprazole)Proton pump inhibitors (omeprazole and lansoprazole)
are also much more effective than H2-antagonists forare also much more effective than H2-antagonists for
healing and maintenance of reflux oesophagitis.healing and maintenance of reflux oesophagitis.
 Proton pump inhibitors are the treatment of choice forProton pump inhibitors are the treatment of choice for
severe symptoms and for complicated reflux disease.severe symptoms and for complicated reflux disease.
 Recurrence of symptoms is common when therapy isRecurrence of symptoms is common when therapy is
stopped and some patients require life-long treatment atstopped and some patients require life-long treatment at
the lowest acceptable dose.the lowest acceptable dose.

30. Treatment of gastro-oesophagealTreatment of gastro-oesophageal
reflux disease: a 'step-down'reflux disease: a 'step-down'
approachapproach..

31. Anti-reflux surgeryAnti-reflux surgery
 Patients who fail to respond to medical therapy,Patients who fail to respond to medical therapy,
 those who are unwilling to take long-term proton pumpthose who are unwilling to take long-term proton pump
inhibitors,inhibitors,
 those whose major symptom is severe regurgitationthose whose major symptom is severe regurgitation
should be considered forshould be considered for anti-reflux surgery.anti-reflux surgery.
 This can be undertaken by an open operation but isThis can be undertaken by an open operation but is
increasingly being carried out laparoscopically.increasingly being carried out laparoscopically.
 Although heartburn and regurgitation are alleviated inAlthough heartburn and regurgitation are alleviated in
most patients, a proportion develop complications suchmost patients, a proportion develop complications such
as inability to vomit and abdominal bloating ('gas-bloatas inability to vomit and abdominal bloating ('gas-bloat
syndrome').syndrome').

32. Issues in older people gastro-Issues in older people gastro-
oesophageal reflux diseaseoesophageal reflux disease
 The prevalence of gastro-oesophageal refluxThe prevalence of gastro-oesophageal reflux
disease is higher in older people anddisease is higher in older people and
complications are more common.complications are more common.
 The severity of symptoms does not correlateThe severity of symptoms does not correlate
with the degree of mucosal inflammation in oldwith the degree of mucosal inflammation in old
age.age.
 Late complications such as peptic strictures orLate complications such as peptic strictures or
bleeding from oesophagitis are more common inbleeding from oesophagitis are more common in
older people.older people.
 Aspiration from occult gastro-oesophageal refluxAspiration from occult gastro-oesophageal reflux
disease should be considered in older patientsdisease should be considered in older patients
with recurrent pneumonia.with recurrent pneumonia.

33. GASTRITISGASTRITIS
 Gastritis is a histological diagnosis,Gastritis is a histological diagnosis,
although it can sometimes be recognisedalthough it can sometimes be recognised
at endoscopy.at endoscopy.

34. Common cause of gastritisCommon cause of gastritis

35. Acute gastritisAcute gastritis
 Acute gastritis is often erosive and haemorrhagic.Acute gastritis is often erosive and haemorrhagic.
 Neutrophils are the predominant inflammatory cell in theNeutrophils are the predominant inflammatory cell in the
superficial epithelium.superficial epithelium.
 Acute gastritis often produces no symptoms but mayAcute gastritis often produces no symptoms but may
cause dyspepsia, anorexia, nausea or vomiting,cause dyspepsia, anorexia, nausea or vomiting,
haematemesis or melaena.haematemesis or melaena.
 Many cases resolve quickly and do not meritMany cases resolve quickly and do not merit
investigation; in others, endoscopy and biopsy may beinvestigation; in others, endoscopy and biopsy may be
necessary to exclude peptic ulcer or cancer.necessary to exclude peptic ulcer or cancer.
 Treatment should be directed to the underlying cause.Treatment should be directed to the underlying cause.
 Short-term symptomatic therapy with antacids, acidShort-term symptomatic therapy with antacids, acid
suppression (e.g. H2-receptor antagonists) orsuppression (e.g. H2-receptor antagonists) or
antiemetics (e.g. metoclopramide 10 mg 3 times a day)antiemetics (e.g. metoclopramide 10 mg 3 times a day)
may be necessary.may be necessary.

36. Chronic gastritis due toChronic gastritis due to
Helicobacter pylory infectionHelicobacter pylory infection
 The predominant inflammatory cells areThe predominant inflammatory cells are
lymphocytes and plasma cells.lymphocytes and plasma cells.
 Correlation between symptoms and endoscopicCorrelation between symptoms and endoscopic
or pathological findings is poor.or pathological findings is poor.
 Most patients are asymptomatic and do notMost patients are asymptomatic and do not
require any treatment.require any treatment.
 Patients with dyspepsia and H. pylori-associatedPatients with dyspepsia and H. pylori-associated
gastritis may benefit from H. pylori eradication.gastritis may benefit from H. pylori eradication.

37. Autoimmune chronic gastritisAutoimmune chronic gastritis
 This involves the body of the stomach, spares the antrumThis involves the body of the stomach, spares the antrum
and results from autoimmune activity against parietal cells.and results from autoimmune activity against parietal cells.
 The histological features are diffuse chronic inflammation,The histological features are diffuse chronic inflammation,
atrophy and loss of fundic glands, intestinal metaplasia andatrophy and loss of fundic glands, intestinal metaplasia and
sometimes hyperplasia of enterochromaffin-like (ECL)sometimes hyperplasia of enterochromaffin-like (ECL)
cells.cells.
 Circulating antibodies to parietal cell and intrinsic factorCirculating antibodies to parietal cell and intrinsic factor
may be present.may be present.
 In some patients the degree of gastric atrophy is severe,In some patients the degree of gastric atrophy is severe,
and loss of intrinsic factor secretion leads to perniciousand loss of intrinsic factor secretion leads to pernicious
anaemia.anaemia.
 The gastritis itself is usually asymptomatic but someThe gastritis itself is usually asymptomatic but some
patients have evidence of other organ-specificpatients have evidence of other organ-specific
autoimmunity, particularly thyroid disease.autoimmunity, particularly thyroid disease.
 There is a fourfold increase in the risk of gastric cancerThere is a fourfold increase in the risk of gastric cancer
development.development.

38. Menetrie`s diseaseMenetrie`s disease
 In this rare condition the gastric pits are elongated andIn this rare condition the gastric pits are elongated and
tortuous, with replacement of the parietal and chief cellstortuous, with replacement of the parietal and chief cells
by mucus-secreting cells. As a result, the mucosal foldsby mucus-secreting cells. As a result, the mucosal folds
of the body and fundus are greatly enlarged.of the body and fundus are greatly enlarged.
 Most patients are hypochlorhydric.Most patients are hypochlorhydric.
 Whilst some patients have upper gastro-intestinalWhilst some patients have upper gastro-intestinal
symptoms, the majority present in middle or old age withsymptoms, the majority present in middle or old age with
protein-losing enteropathy due to exudation from theprotein-losing enteropathy due to exudation from the
gastric mucosa.gastric mucosa.
 Barium meal shows enlarged, nodular and coarse foldsBarium meal shows enlarged, nodular and coarse folds
which are also seen at endoscopy.which are also seen at endoscopy.
 Treatment with anti-secretory drugs may reduce proteinTreatment with anti-secretory drugs may reduce protein
loss but unresponsive patients require partialloss but unresponsive patients require partial
gastrectomy.gastrectomy.