Gastritis

GastritisGastritis

Peyman Adibi,MD.Peyman Adibi,MD.

DefinitionDefinition

The term The term gastritisgastritis is used to denote is used to denote inflammation associated with mucosal inflammation associated with mucosal injuryinjury

Gastritis is mostly a histological term that Gastritis is mostly a histological term that needs biopsy to be confirmedneeds biopsy to be confirmed

Gastritis is usually due to infectious agents Gastritis is usually due to infectious agents (such as Helicobacter pylori) and (such as Helicobacter pylori) and autoimmune and hypersensitivity autoimmune and hypersensitivity reactions.reactions.

DefinitionDefinition Epithelial cell damage and regeneration without Epithelial cell damage and regeneration without

associated inflammation is properly referred to associated inflammation is properly referred to as "as "gastropathygastropathy.“.“

Gastropathy may be referred without histological Gastropathy may be referred without histological evidence and just according to gross evidence and just according to gross appearance in endoscopy or radiologyappearance in endoscopy or radiology

Gastropathy is usually caused by irritants such Gastropathy is usually caused by irritants such as drugs (eg, nonsteroidal antiinflammatory as drugs (eg, nonsteroidal antiinflammatory agents and alcohol), bile reflux, hypovolemia, agents and alcohol), bile reflux, hypovolemia, and chronic congestionand chronic congestion..

Gross–histologic Gross–histologic correlation?correlation?

Research evidenceResearch evidence

Among 98 patients with endoscopic Among 98 patients with endoscopic mucosal changes attributed to gastritis, 27 mucosal changes attributed to gastritis, 27 percent had a normal endoscopic biopsy percent had a normal endoscopic biopsy specimen; i.e. specimen; i.e. PPV of 73 percentPPV of 73 percent or at or at least 1 in four false positive diagnosisleast 1 in four false positive diagnosis

Research evidenceResearch evidence

among 69 patients with a normal among 69 patients with a normal endoscopic appearance, 63 percent had endoscopic appearance, 63 percent had histological evidence of gastritis. histological evidence of gastritis. NPV NPV equals to 27 percentequals to 27 percent

ClassificationClassification

Acute vs. chronicAcute vs. chronic Acute refers to short term inflammationAcute refers to short term inflammation Acute refering to neurophilic infiltrateAcute refering to neurophilic infiltrate

Chronic referring to long standing formsChronic referring to long standing forms Chronic referring to mononuclear cell infiltrate Chronic referring to mononuclear cell infiltrate

especially lymphocyte and maccrophagesespecially lymphocyte and maccrophages

Anatomical siteAnatomical site

ANTRUM

CARDIA

BODY

MUCOUS SECRETING ENDOCRINE

SPECIALISED SECRETORY PARIETAL - ACIDCHIEF -

PEPSINOGEN ENDOCRINEHIST,

SOMASTATIN

MUCOUS SECRETING ENDOCRINE GASTRIN, 5HT

1. Chemical gastritis (acute1. Chemical gastritis (acute ・・ chronic)chronic)Alcoholic gastritisAlcoholic gastritisDrug induced gastritis (e.g., NSAID)Drug induced gastritis (e.g., NSAID)Reflux ( due to duodenal juice or bile) gastritisReflux ( due to duodenal juice or bile) gastritisOther chemical gastritisOther chemical gastritis

2. Radiation gastritis2. Radiation gastritis3. Allergic gastritis3. Allergic gastritis4. Autoimmune gastritis4. Autoimmune gastritis5. Special forms of gastritis5. Special forms of gastritis6. Gastritis6. Gastritis ・・ NOSNOS7. Duodenitis7. Duodenitis

Non HP gastritis (Non HP gastritis (ICD10ICD10))

CLASSIFICATIONCLASSIFICATION

GASTRITIS

ACUTE COMMON CHRONIC

EMAG

AMAG

BILE HPSTRESS

NSAID


GASTRITIS


EMAG

AMAG

BILE HPSTRESS

NSAID

Acute hemorrhagic Acute hemorrhagic erosive erosive

hemorrhagic and erosive lesions hemorrhagic and erosive lesions shortly after exposure of the shortly after exposure of the gastric mucosa to various gastric mucosa to various injurious substances or a injurious substances or a substantial reduction in mucosal substantial reduction in mucosal blood flowblood flow

Mucosal congestion, oedema, inflammation &

ulceration

ACUTE GASTRITIS - ACUTE GASTRITIS - MORPHOLOGYMORPHOLOGY

Acute hemorrhagic Acute hemorrhagic erosiveerosive

nonsteroidal antiinflammatory drugs [NSAIDs], nonsteroidal antiinflammatory drugs [NSAIDs], alcohol, or bile acids) or to mucosal hypoxia alcohol, or bile acids) or to mucosal hypoxia (such as in trauma, burns [Curling's ulcers] or (such as in trauma, burns [Curling's ulcers] or sepsis) or to a combination of factors such as sepsis) or to a combination of factors such as with antineoplastic chemotherapywith antineoplastic chemotherapy

Gastric and duodenal ulceroinflammatory Gastric and duodenal ulceroinflammatory ulcers occurring during severe damage to the ulcers occurring during severe damage to the central nervous system (Cushing's ulcers) are central nervous system (Cushing's ulcers) are often considered in this groupoften considered in this group


Gastric and duodenal Gastric and duodenal ulceroinflammatory ulcers ulceroinflammatory ulcers occurring during severe damage occurring during severe damage to the central nervous system to the central nervous system (Cushing's ulcers) are often (Cushing's ulcers) are often considered in this groupconsidered in this group


specific pathogenetic factor in NSAID-specific pathogenetic factor in NSAID-induced acute hemorrhagic and erosive induced acute hemorrhagic and erosive gastropathy is the gastropathy is the inhibition of inhibition of prostaglandin productionprostaglandin production. Prostaglandins, . Prostaglandins, especially those of the E class, protect especially those of the E class, protect against acute mucosal injury due to against acute mucosal injury due to NSAIDs and other injurious substances by NSAIDs and other injurious substances by several mechanisms, including the several mechanisms, including the stimulation of mucus and bicarbonate stimulation of mucus and bicarbonate secretion, and maintenance of mucosal secretion, and maintenance of mucosal blood flowblood flow

NSAID GI toxicity risk NSAID GI toxicity risk factorfactor

Prior history of an adverse GI event (ulcer, Prior history of an adverse GI event (ulcer, hemorrhage) increases risk four to fivefoldhemorrhage) increases risk four to fivefold

Age >60 increases risk five to sixfoldAge >60 increases risk five to sixfold High (more than twice normal) dosage of a High (more than twice normal) dosage of a

NSAID increases risk 10-foldNSAID increases risk 10-fold Concurrent use of glucocorticoids Concurrent use of glucocorticoids

increases risk four to fivefoldincreases risk four to fivefold Concurrent use of anticoagulants Concurrent use of anticoagulants

increases risk 10- to 15-foldincreases risk 10- to 15-fold

HP and NSAIDHP and NSAID

Patients with a history of uncomplicated Patients with a history of uncomplicated or complicated peptic ulcers (gastric, or complicated peptic ulcers (gastric, duodenal) duodenal) should beshould be tested for H. pylori tested for H. pylori prior to beginning a NSAID or low dose prior to beginning a NSAID or low dose aspirinaspirin. If present, H. pylori should be . If present, H. pylori should be treated with appropriate therapy, even if it treated with appropriate therapy, even if it is believed that the prior ulcer was due to is believed that the prior ulcer was due to NSAIDsNSAIDs


Hemorrhagic or erosive Hemorrhagic or erosive gastropathy may be associated gastropathy may be associated with the development of gastric or with the development of gastric or duodenal ulcers. Acute ulceration duodenal ulcers. Acute ulceration is most likely to occur in relation is most likely to occur in relation to shock-induced hemodynamic to shock-induced hemodynamic instability (ie, the stress ulcer instability (ie, the stress ulcer syndrome). syndrome).

NSAID prophylaxisNSAID prophylaxis

For patients who are at high risk for For patients who are at high risk for NSAID-related gastroduodenal NSAID-related gastroduodenal toxicity, primary therapy with a COX-2 toxicity, primary therapy with a COX-2 selective inhibitor such as selective inhibitor such as rofecoxibrofecoxib is is a reasonable option.a reasonable option.

NSAID prophylaxisNSAID prophylaxis

For high-risk patients taking For high-risk patients taking nonselective NSAIDs, nonselective NSAIDs, misoprostolmisoprostol (at a dose of 200 µg four times (at a dose of 200 µg four times daily) and daily) and lansoprazolelansoprazole (15 or 30 (15 or 30 mg daily) have received FDA mg daily) have received FDA approval for prophylaxis against approval for prophylaxis against NSAID-induced ulcer disease and NSAID-induced ulcer disease and its complications. its complications.

Stress ulcer Stress ulcer pathophysiologypathophysiology

HypersecretionHypersecretion of acid –head trauma. of acid –head trauma. Defects in gastric glycoprotein mucusDefects in gastric glycoprotein mucus –In –In

critically ill patients, increased critically ill patients, increased concentrations of refluxed bile salts or the concentrations of refluxed bile salts or the presence of uremic toxins can denude the presence of uremic toxins can denude the glycoprotein mucous barrier glycoprotein mucous barrier

IschemiaIschemia – Shock, sepsis, and trauma can – Shock, sepsis, and trauma can lead to impaired perfusion of the gutlead to impaired perfusion of the gut..

Stress ulcer risk factorsStress ulcer risk factors

Risk factors –two major risk factors Risk factors –two major risk factors for clinically significant bleeding due for clinically significant bleeding due to stress ulcers are: to stress ulcers are: mechanical mechanical ventilationventilation for more than 48 hours for more than 48 hours (odds ratio 15.6); and (odds ratio 15.6); and coagulopathy coagulopathy (odds ratio 4.3) . The risk of clinically (odds ratio 4.3) . The risk of clinically important bleeding in patients without important bleeding in patients without either of these risk factors was only either of these risk factors was only 0.1 percent.0.1 percent.

Stress ulcer risk factorsStress ulcer risk factors • • ShockShock

• Sepsis • Sepsis • Hepatic failure • Hepatic failure • Renal failure • Renal failure • Multiple trauma • Multiple trauma • Burns over 35 percent of total body surface • Burns over 35 percent of total body surface areaarea • Organ transplant recipients • Organ transplant recipients • Head or spinal trauma • Head or spinal trauma • Prior history of peptic ulcer disease or upper • Prior history of peptic ulcer disease or upper GI bleedingGI bleeding

Common type of Common type of gastritidesgastritides


GASTRITIS


EMAG

AMAG

BILE HPSTRESS

NSAID

Helicobacter pylori Helicobacter pylori is a spiral shaped, is a spiral shaped, microaerophilic, microaerophilic, gram negative gram negative bacterium bacterium measuring measuring approximately 3.5 approximately 3.5 microns in length microns in length and 0.5 microns in and 0.5 microns in widthwidth

urease forms urease forms ammonia and ammonia and bicarbonate that bicarbonate that neutralize neutralize gastric acid and gastric acid and form a protective form a protective cloud around the cloud around the organismorganism

Urease appears to Urease appears to be vital for its be vital for its survival and survival and colonization; it is colonization; it is produced in produced in abundance, abundance, making up more making up more than 5 percent of than 5 percent of the organism's total the organism's total protein weight. protein weight.

spiral shape, spiral shape, flagellaflagella

facilitate its facilitate its passage passage through the through the mucus layermucus layer

H. pylori then H. pylori then attaches to attaches to gastric epithelial gastric epithelial cells by means of cells by means of specific receptor-specific receptor-mediated mediated adhesionadhesion

Helicobacter Helicobacter pylori is the most pylori is the most common chronic common chronic bacterial bacterial infection in infection in humans ;50 humans ;50 percent of the percent of the world's world's population is population is affected.affected.

Therefore, the Therefore, the frequency of H. frequency of H. pylori infection for pylori infection for any age group in any age group in any locality reflects any locality reflects that particular that particular cohort's rate of cohort's rate of bacterial bacterial acquisition during acquisition during childhood years childhood years

Factors such as density of housing, Factors such as density of housing, overcrowding, number of siblings, overcrowding, number of siblings, sharing a bed, and lack of running sharing a bed, and lack of running water have all been linked to a water have all been linked to a higher acquisition of H. pylori higher acquisition of H. pylori infectioninfection

The route by which The route by which infection occurs infection occurs remains unknown remains unknown Person-to-person Person-to-person transmission of H. transmission of H. pylori through either pylori through either fecal/oral or oral/oral fecal/oral or oral/oral exposure seems most exposure seems most likelylikely

Humans appear to be Humans appear to be the major reservoir of the major reservoir of infection; however, infection; however, bacteria have been bacteria have been isolated from primates isolated from primates in and from domestic in and from domestic cats and in milk and cats and in milk and gastric tissue of sheepgastric tissue of sheep

Non GI associated Non GI associated disordersdisorders

Coronary heart diseaseCoronary heart disease RosaceaRosacea Iron deficiency Iron deficiency Anorexia in agingAnorexia in aging

Platelet aggregationPlatelet aggregation mediated by an mediated by an H. pylori interaction with von H. pylori interaction with von Willebrand factor is speculated to Willebrand factor is speculated to contribute to infection related ulcer contribute to infection related ulcer disease but also possibly non-GI disease but also possibly non-GI manifestations of infection such as manifestations of infection such as cardiovascular disease and cardiovascular disease and idiopathic thrombocytopeniaidiopathic thrombocytopenia

A B cell response to H. pylori (with A B cell response to H. pylori (with production of IgG and IgA antibodies) production of IgG and IgA antibodies) occurs locally in the gastroduodenal occurs locally in the gastroduodenal mucosa and systemically. The role of local mucosa and systemically. The role of local antibodies in producing tissue injury or antibodies in producing tissue injury or modulating inflammation in H. pylori modulating inflammation in H. pylori infection remains controversial .infection remains controversial .Prolonged Prolonged stimulation of gastric B cells by activated T stimulation of gastric B cells by activated T cells can lead to MALT lymphoma in rare cells can lead to MALT lymphoma in rare casescases

Vac A & Cag AVac A & Cag A

vacuolating cytotoxin (VacA) which causes vacuolating cytotoxin (VacA) which causes cell injury in vitro and gastric tissue damage cell injury in vitro and gastric tissue damage in vivo . All H. pylori contain the gene coding in vivo . All H. pylori contain the gene coding for VacA; however, only those strains with for VacA; however, only those strains with the cytotoxin-associated gene A (cagA)the cytotoxin-associated gene A (cagA)

Strains producing VacA and CagA cause Strains producing VacA and CagA cause more intense tissue inflammation and more intense tissue inflammation and induce cytokine productioninduce cytokine production

Approximately 85 to 100 percent of Approximately 85 to 100 percent of patients with duodenal ulcers have patients with duodenal ulcers have CagA+ strains, compared to 30 to 60 CagA+ strains, compared to 30 to 60 percent of infected patients who do percent of infected patients who do not develop ulcersnot develop ulcers

CagA strains may be associated with CagA strains may be associated with a higher frequency of precancerous a higher frequency of precancerous lesions.lesions.

Host polymorphism of IL-1 betaHost polymorphism of IL-1 beta (and possibly IL-10) appears to (and possibly IL-10) appears to determine the degree of determine the degree of inflammatory response to inflammatory response to infection, resulting alteration in infection, resulting alteration in acid secretion (hyper or hypo acid secretion (hyper or hypo secretion), and risk for secretion), and risk for subsequent gastric cancersubsequent gastric cancer

IgAIgA antibodies may antibodies may modulatemodulate mucosal injury mucosal injury by inhibiting antigen by inhibiting antigen uptake, disrupting bacterial uptake, disrupting bacterial adherence and motility, adherence and motility, and neutralizing various and neutralizing various toxins. toxins. IgGIgG presumably presumably augmentsaugments inflammatory inflammatory injury by activating injury by activating complement and complement and facilitating neutrophil facilitating neutrophil activation.activation.

Bile reflux gastropathyBile reflux gastropathy

Bile reflux gastropathy typically Bile reflux gastropathy typically results from the regurgitation of bile results from the regurgitation of bile into the stomach because of an into the stomach because of an operative stoma, an incompetent operative stoma, an incompetent pyloric sphincter, or abnormal pyloric sphincter, or abnormal duodenal motilityduodenal motility

Bile reflux gastropathyBile reflux gastropathy

The effect of bile salts on gastric The effect of bile salts on gastric mucosa is comparable to that seen mucosa is comparable to that seen after chronic NSAID useafter chronic NSAID use

Chronic Chronic metaplastic metaplastic gastritidesgastritides


GASTRITIS


EMAG

AMAG

BILE HPSTRESS

NSAID

metaplastic atrophic metaplastic atrophic gastritisgastritis

Metaplasia, especially of the intestinal Metaplasia, especially of the intestinal type, is virtually a universal feature of type, is virtually a universal feature of atrophic gastritis and is often the most atrophic gastritis and is often the most dependable defining morphologic dependable defining morphologic feature.feature.

• • Metaplasia is highly relevant to the Metaplasia is highly relevant to the pathogenesis of atrophic gastritis and pathogenesis of atrophic gastritis and to its complications (eg, pernicious to its complications (eg, pernicious anemia, gastric ulcer, and gastric anemia, gastric ulcer, and gastric cancer).cancer).


The term metaplastic atrophic gastritis makes a The term metaplastic atrophic gastritis makes a sharp distinction between metaplastic and sharp distinction between metaplastic and nonmetaplastic forms of gastric atrophy, nonmetaplastic forms of gastric atrophy, especially the atrophic change (gastrinopenic especially the atrophic change (gastrinopenic type) often noted in the oxyntic mucosa (ie, type) often noted in the oxyntic mucosa (ie, mucosa of the body and fundus), which mucosa of the body and fundus), which remains in place after antrectomy for peptic remains in place after antrectomy for peptic ulcer.ulcer.


Endoscopic surveillance in patients from Endoscopic surveillance in patients from developed countries who do not have developed countries who do not have dysplasia is probably unnecessarydysplasia is probably unnecessary


AUTOIMMUNE METAPLASTIC AUTOIMMUNE METAPLASTIC ATROPHIC GASTRITISATROPHIC GASTRITIS (AMAG) is (AMAG) is an inherited form that is associated an inherited form that is associated with an immune response in the with an immune response in the oxyntic mucosa directed against oxyntic mucosa directed against parietal cells and intrinsic factor. parietal cells and intrinsic factor. AMAG is inherited as an autosomal AMAG is inherited as an autosomal dominant disorderdominant disorder

SYNONYMS OF AMAGSYNONYMS OF AMAG

TYPE A GASTRITISTYPE A GASTRITIS AUTOIMMUNE GASTRITISAUTOIMMUNE GASTRITIS DIFFUSE CORPORAL GASTRITISDIFFUSE CORPORAL GASTRITIS


The chronic inflammation, gland The chronic inflammation, gland atrophy, and epithelial metaplasia of atrophy, and epithelial metaplasia of AMAG are closely paralleled by AMAG are closely paralleled by elevated serum antibodies to parietal elevated serum antibodies to parietal cells and to intrinsic factor, reflecting cells and to intrinsic factor, reflecting its autoimmune origin. its autoimmune origin.


The loss of parietal cell mass leads to The loss of parietal cell mass leads to profound hypochlorhydria, while the profound hypochlorhydria, while the inadequate production of intrinsic inadequate production of intrinsic factor leads to factor leads to vitamin B12vitamin B12 malabsorption and pernicious malabsorption and pernicious anemiaanemia. .


Patients with AMAG are at increased Patients with AMAG are at increased risk for the development of gastric risk for the development of gastric carcinoid tumors and carcinoid tumors and adenocarcinomaadenocarcinoma..

CANCER


surveillance strategy for patients diagnosed with surveillance strategy for patients diagnosed with pernicious anemiapernicious anemia

• • Upper endoscopy soon after diagnosisUpper endoscopy soon after diagnosis • • Removal of gastric polyps if possible; most of Removal of gastric polyps if possible; most of

these polyps will be benignthese polyps will be benign • • Frequent reinvestigation in patients whose Frequent reinvestigation in patients whose

polyps are not removed or who have severe polyps are not removed or who have severe mucosal dysplasia; in the remaining patients mucosal dysplasia; in the remaining patients follow-up endoscopies should be performed at follow-up endoscopies should be performed at approximately five-year intervals.approximately five-year intervals.


Patients with AMAG are Patients with AMAG are less likelyless likely to to be infected by H. pyloribe infected by H. pylori than aged- than aged-matched controls . Two possible matched controls . Two possible explanations are that the metaplastic explanations are that the metaplastic epithelium is unsuitable for H. pylori epithelium is unsuitable for H. pylori colonization, and that the associated colonization, and that the associated hypochlorhydria encourages hypochlorhydria encourages overgrowth by other bacterial speciesovergrowth by other bacterial species


Environmental metaplastic atrophic Environmental metaplastic atrophic gastritis (EMAG) is due to gastritis (EMAG) is due to environmental factors, such as diet environmental factors, such as diet and H. pylori infection, on the gastric and H. pylori infection, on the gastric mucosamucosa. .


Unlike AMAG, mucosal changes Unlike AMAG, mucosal changes in patients with EMAG affect both in patients with EMAG affect both the corpus and antrum in a the corpus and antrum in a multifocal distribution, but multifocal distribution, but with with heaviest involvement of the heaviest involvement of the antrum.antrum.


EMAG vs AMAGEMAG vs AMAG

• • Gastric acid production Gastric acid production does notdoes not disappear entirelydisappear entirely • Serum gastrin • Serum gastrin is notis not elevated elevated • Parietal cell and intrinsic factor • Parietal cell and intrinsic factor autoantibodies and pernicious anemia autoantibodies and pernicious anemia are are absentabsent


There is an increased risk for gastric There is an increased risk for gastric ulcer compared to AMAG, ulcer compared to AMAG, presumably due to the accompanying presumably due to the accompanying hypochlorhydria the latter disorderhypochlorhydria the latter disorder

CANCER


diagnosis of EMAG should diagnosis of EMAG should notnot be be made from biopsy specimens made from biopsy specimens unless unless at least 20 percentat least 20 percent of the of the available antral or transitional available antral or transitional mucosa is replaced by mucosa is replaced by metaplastic glands, or there is metaplastic glands, or there is unequivocal atrophyunequivocal atrophy. .


Possible exceptions are nitroso Possible exceptions are nitroso compounds, which may be compounds, which may be important in EMAG and in the important in EMAG and in the development of gastric cancer . development of gastric cancer . Nitroso compounds, which are Nitroso compounds, which are known carcinogens , are known carcinogens , are generated in the gastric lumen by generated in the gastric lumen by bacterial metabolism of bacterial metabolism of nitratesnitrates..


chronic infectionchronic infection

cell injury/ inflammation cell injury/ inflammation susceptibility to susceptibility to mutagenic factors. mutagenic factors.

Hyperplastic Hyperplastic gastropathiesgastropathies

proliferative, inflammatory, and infiltrative conditions are associated with large folds due to excessive number of mucosal epithelial cells

Ménétrier's diseaseMénétrier's disease Epithelial Epithelial

hyperplasia hyperplasia involving the involving the surface and surface and foveolar mucous foveolar mucous cells (ie, foveolar cells (ie, foveolar hyperplasia); the hyperplasia); the oxyntic glands can oxyntic glands can be normal or be normal or atrophic. atrophic.

Zollinger-Ellison syndromeZollinger-Ellison syndrome

Increased numbers Increased numbers of parietal cells of parietal cells with no change in with no change in surface and surface and foveolar mucous foveolar mucous cells. cells.

Hyperplastic Hyperplastic gastropathiesgastropathies

mixed-type in which mixed-type in which both mucous and both mucous and oxyntic glandular oxyntic glandular cells show cells show hyperplasia, may be hyperplasia, may be seen in as seen in as lymphocytic and H. lymphocytic and H. pylori gastritis.pylori gastritis.

Large gastric folds > 1.0 cm Large gastric folds > 1.0 cm

• •Chronic gastritis/lymphoid Chronic gastritis/lymphoid hyperplasia – 40hyperplasia – 40

• •Benign tumors – 16 Benign tumors – 16 • •Gastric malignancy – 12Gastric malignancy – 12 • •Zollinger-Ellison Zollinger-Ellison

syndrome – 10syndrome – 10 • •Menetrier's disease – 8Menetrier's disease – 8

Ménétrier'sMénétrier's Epigastric pain – 65 percentEpigastric pain – 65 percent Asthenia – 60 percentAsthenia – 60 percent Anorexia – 45 percentAnorexia – 45 percent Weight loss – 45 percentWeight loss – 45 percent Edema – 38 percentEdema – 38 percent Vomiting – 38 percentVomiting – 38 percent

80 percent of patients had 80 percent of patients had hypoalbuminemiahypoalbuminemia

Ménétrier'sMénétrier's Surgery has been Surgery has been

advocated for patients advocated for patients with intractable pain, with intractable pain, hypoalbuminemia with hypoalbuminemia with edema, hemorrhage, edema, hemorrhage, pyloric obstruction, and pyloric obstruction, and for those in whom a for those in whom a malignancy cannot be malignancy cannot be excluded excluded

Ménétrier'sMénétrier's

Gastric Gastric atrophy?>atrophy?>

Gastric Gastric cancer?>cancer?>

Zollinger-Ellison syndromeZollinger-Ellison syndrome

0.1 to 1 percent of patients with peptic 0.1 to 1 percent of patients with peptic ulcer disease . ulcer disease .

Underestimation! Underestimation! symptoms similar to typical peptic ulcer . symptoms similar to typical peptic ulcer . symptoms may be controlled by symptoms may be controlled by

standard doses of an antisecretory drugstandard doses of an antisecretory drug patients may not be tested for patients may not be tested for

hypergastrinemia hypergastrinemia

ZESZES

Most patients are diagnosed Most patients are diagnosed between the ages of 20 and 50. between the ages of 20 and 50. The male to female ratio ranges The male to female ratio ranges between to 2:1 . between to 2:1 .

ZESZES

Gastrinomas can be either Gastrinomas can be either sporadic (80 percent) or sporadic (80 percent) or associated with multiple associated with multiple endocrine neoplasia typeendocrine neoplasia type 1 1

Diarrhea in ZESDiarrhea in ZES

• • The high rate of acid volume load that The high rate of acid volume load that cannot be cannot be absorbed by the intestineabsorbed by the intestine

• • The excess acid The excess acid exceeds the neutralizing capacity exceeds the neutralizing capacity of pancreatic bicarbonateof pancreatic bicarbonate . The exceptionally low pH . The exceptionally low pH of the intestinal contents inactivates pancreatic of the intestinal contents inactivates pancreatic digestive enzymes, interferes with the emulsification digestive enzymes, interferes with the emulsification of fat by bile acids, and damages intestinal epithelial of fat by bile acids, and damages intestinal epithelial cells and villi.cells and villi.

• • The extremely high serum gastrin concentrations The extremely high serum gastrin concentrations may may inhibit absorption of sodium and waterinhibit absorption of sodium and water by the by the small intestine, small intestine,

Signs of ZESSigns of ZES

Multiple ulcersMultiple ulcersdiarrheadiarrheaulcer in atypical siteulcer in atypical siteresistant ulcerresistant ulcerenlarged foldsenlarged foldssevere esophagirtissevere esophagirtisFH of MEN1FH of MEN1

ZES diagnosisZES diagnosisExclude hpoacidity!Exclude hpoacidity!

Check gastrin, if Check gastrin, if >>1000=ZES1000=ZES..

<1000 but abnormal <1000 but abnormal secretin test to be secretin test to be performedperformed,+200 pg/ml ,+200 pg/ml is ZESis ZES

Localization of Localization of gastrinomagastrinoma

SPECT imaging with pentetreotide should SPECT imaging with pentetreotide should be the be the first testfirst test because of its high because of its high sensitivity for both primary tumors and sensitivity for both primary tumors and hepatic metastaseshepatic metastases

If no tumor or metastases are found but If no tumor or metastases are found but clinical suspicion remains high, clinical suspicion remains high, endoscopic ultrasonography (EUS) or endoscopic ultrasonography (EUS) or dual phase helical CT scan should be dual phase helical CT scan should be performed.performed.

ZES treatmentZES treatment

OmeprazoleOmeprazole effectively controlled effectively controlled acid output in acid output in allall patients. patients.

No patients experienced No patients experienced tachyphylaxis, and no hematologic, tachyphylaxis, and no hematologic, metabolic, or gastric toxicity was metabolic, or gastric toxicity was notednoted..


any patient with a sporadic any patient with a sporadic gastrinoma and without evidence of gastrinoma and without evidence of metastatic spread of disease should metastatic spread of disease should be offered exploratory laparotomy be offered exploratory laparotomy with curative intentwith curative intent


laparotomy is not routinely laparotomy is not routinely recommended for patients with ZES recommended for patients with ZES as part of MEN 1 since the multifocal as part of MEN 1 since the multifocal nature of the tumors in this disorder nature of the tumors in this disorder almost uniformly precludes cure of almost uniformly precludes cure of gastrin hypersecretiongastrin hypersecretion

Portal hypertensive Portal hypertensive gastropathygastropathy

Portal hypertensive gastropathy Portal hypertensive gastropathy characteristically appears as a fine characteristically appears as a fine white reticular pattern separating white reticular pattern separating areas of pinkish mucosa on areas of pinkish mucosa on endoscopy, giving the gastric mucosa endoscopy, giving the gastric mucosa a "a "snakeskinsnakeskin" appearance" appearance

Portal hypertensive Portal hypertensive gastropathygastropathy

Gastritis

Documents

central nervous

mucosal blood

metaplastic

common bile

peptic ulcer

foveolar mucous

acute hemorrhagic

bile reflux