Dyspepsia and chronic gastritis

Definition of dyspepsia
• predominant epigastric pain lasting at least 1 month
• can be associated with any other upper gastrointestinal symptom
such as epigastric fullness, nausea, vomiting, or heartburn, provided
epigastric pain is the patient’s primary concern
• Functional dyspepsia - endoscopy (and other tests where relevant)
has ruled out organic pathology that explains the patient’s
symptoms
Normal endoscopic picture of the stomach
 Recommendations of the World
Gastroenterology Organization (WGO)
• dyspepsia patients aged 60 or over have an endoscopy to exclude
upper gastrointestinal neoplasia
• dyspepsia patients under the age of 60 should have a non-invasive
test for H. pylori, and therapy for H. pylori Infection if positive
• dyspepsia patients under the age of 60 should have empirical PPI
therapy if they are H. pylori-negative or who remain symptomatic
after H. pylori eradication therapy
• dyspepsia patients under the age of 60 not responding to PPI or H.
pylori eradication therapy should be offered prokinetic therapy and
tricyclic antidepressant therapy
Intestinal metaplasia of the stomach
 Recommendations of the World
Gastroenterology Organization (WGO)
• functional dyspepsia patients, if H. pylori positive should be
prescribed eradication therapy
• functional dyspepsia patients, if H. pylori-negative or who remain
symptomatic despite eradication of the infection should be treated
with PPI therapy
• functional dyspepsia patients not responding to ppi or H. pylori
eradication therapy (if appropriate) should be offered tricyclic
antidepressant therapy
 Recommendations of the World
Gastroenterology Organization (WGO)
• functional dyspepsia patients not responding to PPI, H. pylori
eradication therapy or tricyclic antidepressant therapy should be
offered prokinetic therapy
• functional dyspepsia patients not responding to drug therapy should
be offered psychological therapies
• suggest motility studies for selected patients with functional
dyspepsia where gastroparesis is strongly suspected
 Updated American guideline definition
• epigastric pain for at least 1 month with any other upper abdominal
symptom, including heartburn
• This definition varies from the Rome IV criteria, which exclude
symptoms of reflux disease
• Functional dyspepsia is still defined by a normal endoscopy
 Key Recommendations

• endoscopy for patients aged ≥60 years with alarm symptoms or after
failure of empiric testing and treatment
• The latter should undergo noninvasive testing for Helicobacter pylori,
followed by eradication therapy if positive and empiric proton-pump
inhibitor (PPI) therapy if negative or if symptoms persist after H.
pylori eradication
• Offer prokinetic therapy after failure of H. pylori therapy or empiric
PPI therapy
• Offer tricyclic antidepressant therapy to patients who fail prokinetic
therapy, and vice-versa.
 Alarm features for dyspepsia
• Unintentional weight loss
• Dysphagia
• Odynophagia
• Unexplained iron deficiency anemia
• Persistent vomiting
• Palpable mass or lymphadenopathy
• Family history of upper gastrointestinal cancer
 H. pylori testing
• Invasive methods (requiring gastroscopy and biopsies):
1. histological staining (hematoxylin and eosin, the Alcian blue stain and a
modified silver stain)
2. cultures
3. rapid urease test
4. molecular detection (PCR DNA)
• Non-invasive methods (not requiring gastroscopy and biopsies):
1. urease breath test (13C-UBT)
2. fecal antigen test
3. serology
 H. pylori testing
• simultaneous treatment with proton-pump inhibitors leads to false-
negative results in both invasive and non-invasive tests
• Serological tests for detection of antibodies against H. pylori cannot
differentiate between active and past infection
 Eradication of H. pylori infection
• A triple-therapy of clarithromycin/proton-pump
inhibitor/amoxicillin for 14 to 21 days is considered the first line of
treatment.
• Clarithromycin is preferred over metronidazole because the
recurrence rates with clarithromycin are far less compared to a triple-
therapy using metronidazole
• However, in areas where clarithromycin resistance is known,
metronidazole is the option of choice
• Quadruple bismuth containing therapy would be of benefit,
particularly if using metronidazole
 Differential diagnosis for dyspepsia
• Peptic ulcer disease
• Gastroesophageal malignancy
• Biliary pain
• Drug-induced dyspepsia
• Other causes
• Functional dyspepsia
 Dif. Diagnosis with peptic ulcer disease
• Upper abdominal pain or discomfort is the most prominent symptom in patients
with peptic ulcers
• Although discomfort from ulcers is usually centered in the epigastrium, it may
occasionally localize to the right or left upper quadrants
• While classic symptoms of duodenal ulcer occur when acid is secreted in the
absence of a food buffer (ie, two to five hours after meals or on an empty
stomach), peptic ulcers can be associated with food-provoked symptoms, and
thus, the utility of using symptoms related to food ingestion to predict the
presence of an ulcer is unreliable.
• Peptic ulcers can also be associated with postprandial belching, epigastric
fullness, early satiation, fatty food intolerance, nausea, and occasional vomiting.
 Dif. Diagnosis with Gastroesophageal
malignancy
• Gastroesophageal malignancy is an uncommon cause of chronic
dyspepsia in the Western hemisphere but the incidence is higher in
patients of Asian, Hispanic, or Afro-Caribbean extraction.
• The incidence of gastroesophageal malignancy increases with age.
• When present, abdominal pain tends to be epigastric, vague, and
mild early in the disease but more severe and constant as the
disease progresses
• In addition, other symptoms and signs typically evolve with disease
progression (eg, anemia, fatigue, weight loss).
 Dif. Diagnosis with Biliary pain
• Classic biliary pain is characterized by episodic intense dull pain located
in the right upper quadrant, epigastrium, or (less often) substernal area
that may radiate to the back (particularly the right shoulder blade)
• The pain is often associated with diaphoresis, nausea, and vomiting.
The pain is constant and not colicky.
• It is not exacerbated by movement and is not relieved by squatting,
belching, bowel movements, or passage of flatus.
• The pain typically lasts at least 30 minutes, plateauing within an hour.
The pain then starts to subside, with an entire attack usually lasting less
than six hours.
 Drug-induced dyspepsia
• NSAIDs and COX-2 selective inhibitors can cause dyspepsia even in
the absence of peptic ulcer disease.
• Other drugs that have been implicated in drug-induced dyspepsia
include calcium channel blockers, methylxanthines, alendronate,
orlistat, potassium supplements, acarbose, dabigatran, iron, vitamin
D, selective serotonin reuptake inhibitors, sildenafil, sulfonylureas,
and certain antibiotics, including erythromycin
 Other causes
• Celiac disease and chronic pancreatitis may rarely present with
dyspepsia alone.
• Other rare causes for dyspepsia include infiltrative diseases of the
stomach (eg, eosinophilic gastroenteritis, Crohn disease, sarcoidosis,
lymphoma, and amyloidosis, diabetic radiculopathy, metabolic
disturbances (eg, hypercalcemia, heavy metal toxicity), hepatoma,
steatohepatitis, celiac artery compression syndrome, superior
mesenteric artery syndrome, abdominal wall pain, and intestinal
angina
 Other causes
• Granulomatous gastritis
• Crohn disease
• Extrapulmonary manifestations of sarcoidosis
• Celiac artery compression syndrome
• Superior mesenteric artery syndrome
• Chronic mesenteric ischemia
• Celiac disease in adults
 Functional dyspepsia
• Functional (idiopathic or nonulcer) dyspepsia requires exclusion of
other organic causes of dyspepsia
• It is defined by the presence of epigastric pain and no evidence of
structural disease to explain the symptoms
 Evaluation of a patient with new onset of
dyspepsia
• A history, physical examination, and laboratory evaluation are the first
steps
• Identify alarm features for gastroesophageal malignancy
• A detailed history is necessary to determine the underlying cause and
to identify patients with alarm features
 History features
• Aspirin and other NSAID - the possibility of NSAID dyspepsia and
peptic ulcer disease
• Radiation of pain to the back or personal or family history of
pancreatitis may be indicative of underlying chronic pancreatitis
• Significant weight loss, anorexia, vomiting, dysphagia, odynophagia,
and a family history of gastrointestinal cancers suggest the presence
of an underlying gastroesophageal malignancy
 History features
• Nausea and vomiting, with or without weight loss, occurring with
recurrent or persistent upper abdominal pain raises the possibility of
gastroparesis, especially in patients with risk factors
• Severe episodic epigastric or right upper quadrant abdominal pain
lasting at least 30 minutes is suggestive of symptomatic
cholelithiasis
 Physical examination in dyspepsia
• Usually normal, except for epigastric tenderness
• Abdominal tenderness on palpation should be evaluated with the
Carnett sign to determine if it is due to pain arising from the abdominal
wall rather than due to inflammation of the underlying viscera
• The presence of increased local tenderness during muscle tensing
(positive Carnett’s sign) suggests the presence of abdominal wall pain.
However, if the pain is decreased (negative Carnett’s sign), the origin of
pain is not from the abdominal wall and likely from an intra-abdominal
organ, as the tensed abdominal wall muscles protect the viscera.
 Other informative findings on
physical examination
• A palpable abdominal mass (eg, hepatoma)
• Lymphadenopathy (eg, left supraclavicular or periumbilical in gastric
cancer)
• Jaundice (eg, secondary to liver metastasis)
• Pallor secondary to anemia
• Ascites may indicate the presence of peritoneal carcinomatosis or
liver cirrhosis
• Patients with an underlying malignancy may have evidence of muscle
wasting and peripheral edema
 Laboratory tests
• Routine blood counts and blood chemistry including liver function
tests, serum lipase, and amylase, should be performed to identify
patients with alarm features (eg, iron deficiency anemia) and
underlying metabolic diseases that can cause dyspepsia (eg, diabetes,
hypercalcemia)
• (See "Clinical manifestations of hypercalcemia", 'Gastrointestinal
abnormalities' and "Diabetic autonomic neuropathy of the
gastrointestinal tract".)
 Diagnostic approach
• Our approach is largely consistent with the American College of
Gastroenterology and Canadian Association of Gastroenterology
guidelines
• Patient age ≥60 years - perform an upper endoscopy to evaluate
dyspepsia. Biopsies of the stomach should be obtained to rule out H.
pylori. Patients with H. pylori should receive eradication therapy in
addition to treatment based on the underlying diagnosis (eg, peptic
ulcer disease). After H. pylori treatment, eradication should be
assessed
 Diagnostic approach
• A meta-analysis of nine studies with 5389 patients found that the
most prevalent findings in patients with dyspeptic symptoms were
erosive esophagitis and peptic ulcer disease (pooled prevalence 6
and 8 percent, respectively)
• Most patients with a normal upper endoscopy and routine
laboratory tests have functional dyspepsia. However, additional
evaluation may be required based on symptoms
 Diagnostic approach
• Patient age <60 years:
• should be tested and treated for H. pylori, and upper endoscopy should be
performed selectively.
• H. pylori negative or who continue to have symptoms after successful
eradication of H. pylori should be treated with antisecretory therapy with a
proton pump inhibitor (PPI).
• In patients whose symptoms do not improve after eight weeks of PPI
therapy, we initiate a therapeutic trial with a tricyclic antidepressant.
• Given the side effects associated with prokinetics and the limited evidence of
efficacy, we reserve the use of prokinetics for patients who fail tricyclic
antidepressants.
 Upper endoscopy in selected patients
• Endoscopic evaluation of patients <60 years is reserved for patients with any one
of the following:
1. Clinically significant weight loss (>5 percent usual body weight over 6 to 12
months).
2. Overt gastrointestinal bleeding.
3. >1 other alarm feature
4. Rapidly progressive alarm features
• In such patients, upper endoscopy should be performed early, preferably within
two to four weeks. Biopsies of the stomach should be obtained to rule out H.
pylori and patients with evidence of infection should be treated with eradication
therapy
 Alarm features
• Unintentional weight loss
• Dysphagia
• Odynophagia
• Unexplained iron deficiency anemia
• Persistent vomiting
• Palpable mass or lymphadenopathy
• Family history of upper gastrointestinal cancer
 Test and treat for Helicobacter pylori
• The rationale for H. pylori testing in patients with dyspepsia is based
upon the recognition of H. pylori as an etiologic factor in peptic ulcer
disease.
• In patients who do not require an upper endoscopy or in whom
biopsies were not performed at the time of upper endoscopy, testing
for H. pylori should be performed with a test for active infection (eg,
urea breath test or stool antigen assay).
• Serologic testing should not be used due to their low positive
predictive value
 Evaluation of persistent symptoms
• Patients with continued symptoms of dyspepsia fall into the following
categories:
• patients with persistent H. pylori infection
• patients with an alternate diagnosis
• patients with functional dyspepsia
• Patients with continued symptoms of dyspepsia should be carefully
reassessed, paying specific attention to the type of ongoing
symptoms, the degree to which symptoms have improved or
worsened, and compliance with medications.
 Evaluation of persistent symptoms
• An upper endoscopy should be performed in patients with persistent
dyspepsia
• During upper endoscopy, biopsies for H. pylori should be performed
in patients who have not previously been tested, while culture and
sensitivity testing should be performed in patients previously treated
for H. pylori
• Biopsies of the duodenum should also be performed to rule out
celiac disease or inflammatory conditions (Crohn's disease)
 Evaluation of persistent symptoms
• In patients with a normal upper endoscopy, further evaluation should
be performed selectively based on the type of ongoing symptoms:
• abdominal imaging with an ultrasound or computed tomography
scan in patients with concurrent jaundice or pain suggestive of a
biliary/pancreatic source
• a four-hour solid-phase scintigraphic gastric emptying scan for those
with persistent nausea and vomiting)
• Approximately 75 percent of patients with dyspepsia have functional
(idiopathic or nonulcer) dyspepsia with no underlying cause on
diagnostic evaluation
Chronic gastritis
 Chronic gastritis
• Definition of gastritis has its basis in histological features of the
gastric mucosa
• It is not erythema observed during gastroscopy, and there are no
specific clinical presentations or symptoms defining it
• The current classification of gastritis centers on time course (acute
versus chronic), histological features, anatomic distribution, and
underlying pathological mechanisms
 Chronic gastritis
• Acute gastritis will evolve to chronic, if not treated
• Helicobacter pylori (H. pylori) is the most common cause of gastritis
worldwide.
• 60 to 70% of H. pylori-negative subjects with functional dyspepsia or
non-erosive gastroesophageal reflux were also found to have
gastritis
 Chronic gastritis
• Clinical presentation, laboratory investigations, gastroscopy, as well as
the histological and microbiological examination of tissue biopsies are
essential for the diagnosis of gastritis and its causes
• Treatment of H. pylori-associated gastritis results in the rapid
disappearance of polymorphonuclear infiltration and a reduction of
chronic inflammatory infiltrate with the gradual normalization of the
mucosa. Mucosal atrophy and metaplastic changes may resolve
shortly, but it is not necessarily the outcome of treatment of H.
pylori in all treated patients. Other types of gastritis should be
treated based on their causative etiology.
 Etiology of gastritis
• H. pylori-associated gastritis: This is the most common cause of
gastritis worldwide.
• H. pylori-negative gastritis: smoking, alcohol, NSAIDs or steroids
• Autoimmune gastritis
• Gastritis due to infection other than H. pylori
• Gastritis may result from bile acid reflux
• Radiation gastritis
• Collagenous gastritis
• Eosinophilic gastritis
 Etiology of gastritis
• Vasculitis-associated gastritis
• Ménétrier disease:
• Presence of large gastric mucosal folds in the body and fundus of the
stomach
• Massive foveolar hyperplasia of surface and glandular mucous cells
• Protein-losing gastropathy, hypoalbuminemia, and edema in 20 to
100% of patients
• Reduced gastric acid secretion because of loss of parietal cells
 Etiology of gastritis
• Sarcoidosis-associated gastritis: Sarcoidosis is a multisystemic
disorder characterized by the presence of non-caseating granulomas.
Although sarcoidosis can affect any body organ, the gastrointestinal
tract, including the stomach, is rarely affected.
• Lymphocytic gastritis: a rare gastritis. The etiology of lymphocytic
gastritis remains unestablished, but an association with H. pylori
infection or celiac disease has been suggested.
• Ischemic gastritis: This is rare and associated with high mortality
 H. pylori-negative gastritis
• A negative triple staining of gastric mucosal biopsies (hematoxylin and
eosin, Alcian blue stain and a modified silver stain)
• A negative H pylori culture
• A negative IgG H. pylori serology
• No self-reported history of H. pylori treatment
• In these patients, the cause of gastritis may relate to tobacco
smoking, consumption of alcohol, and/or the use of non-steroidal
anti-inflammatory drugs (NSAIDs) or steroids.
 Autoimmune gastritis
• chronic atrophic gastritis and associated with raised serum anti-
parietal and anti-intrinsic factor antibodies
• The loss of parietal cells results in a reduction of gastric acid
secretion, which is necessary for the absorption of inorganic iron
• Therefore, iron deficiency is commonly a finding in patients with
autoimmune gastritis. Iron deficiency in these patients usually
precedes vitamin B12 deficiency
• The disease is common in young women.
Gastritis due to infection other than H.
pylori
• Mycobacterium avium-intracellulare
• Enterococcal infection
• Herpes simplex
• Cytomegalovirus
• Parasitic gastritis may result from cryptosporidium, Strongyloides
stercoralis, or anisakiasis infection
 Epidemiology
• In the western population - declining incidence of H. pylori gastritis
with + increasing prevalence of autoimmune gastritis
• Autoimmune gastritis is more common in women and older people.
The prevalence is estimated to be approximately 2% to 5%
• Chronic gastritis remains a relatively common disease in developing
countries
• The prevalence of H. pylori infection in children in the western
population is approximately 10% but about 50% in developing
countries
 Epidemiology
• prevalence of H. pylori: 69% in Africa, 78% in South America, and 51%
in Asia.
• Socioeconomic and environmental hygiene are the essential factors
in the transmission of H. pylori infection worldwide.
• These factors include family-bound hygiene, household density, and
cooking habits.
• The pediatric origin of H. pylori infection is currently considered the
primary determinant of H. pylori-associated gastritis in a community
 Pathophysiology
• H.pylori-associated gastritis transmission is via the fecal-oral route.
• Chronic gastritis mostly results from H. pylori infection and appears
either as non-atrophic or atrophic form. These two forms are
phenotypes of gastritis at different stages of the same life-long
disease
Severe H. pylori gastritis
Erosive gastritis
Atrophic gastritis after severe
inflammation
Atrophic gastritis with signs of metaplasia
 Pathophysiology
• The progression from acute to chronic gastritis begins in childhood
as a simple chronic superficial mononuclear inflammation of gastric
mucosa which progress in years or decades to atrophic gastritis
characterized by loss of normal mucosal glands in the antrum,
corpus, fundus or all
• Epstein-Barr virus (EBV) and human cytomegalovirus (HCMV) have
been identified in gastric tumors and DNA from H. pylori, EBV, and
PCR determined the presence of HCMV in biopsies from patients
with gastric cancer complicating chronic gastritis
 Histopathology of H. pylori gastritis
• H. pylori gastritis tend to be antral at the beginning of disease.
• The inflammation is superficial and mostly in the upper layers of the
mucosa of the corpus (body of the stomach)
• Chronic gastritis mucosa is associated with neutrophilic inflammation
• The most cytotoxic strains of H. pylori will cause atrophic gastritis.
• The lost mucosal glands in atrophic gastritis become replaced with
new immature glandular and epithelial cells resembling glands of
intestinal tissues
Autoimmune gastritis
 Histopathology of autoimmune gastritis
• In early phases - lymphocytic and plasma cell infiltration of the deeper
glandular portion of mucosa is present
• Hyperplasia of endocrine cells in gastric mucosa is an early feature in
autoimmune gastritis.
• Oxyntic glands may undergo destruction, and parietal cells show
pseudohypertrophy as the disease progress
• In advanced disease, marked atrophy of the oxyntic glands together
with diffuse lymphoblastic infiltration of the lamina propria are
present.
• Intestinal metaplasia is present in end-stage disease
Chronic atrophic gastritis and intestinal
metaplasia
 History and physical examination
of chronic gastritis
• There are no typical clinical manifestations of gastritis.
• Sudden onset of epigastric pain, nausea, and vomiting have been
described to accompany acute gastritis
• Many people are asymptomatic or develop minimal dyspeptic
symptoms
• If not treated the picture may evolve to chronic gastritis
 History and physical examination
of chronic gastritis
• History of smoking, consumption of alcohol, intake of NSAIDs or
steroids, allergies, radiotherapy or gall bladder disorders should all be
considerations.
• A history of treatment for inflammatory bowel disease, vasculitic
disorders, or eosinophilic gastrointestinal disorders might require
exploration if no cause of gastritis is apparent.
 Findings in chronic autoimmune gastritis

• anemia (iron-deficiency) due to hypochlorhydria – even in the early

stages of autoimmune gastritis
• positive histological examination of gastric biopsies
• presence of other autoimmune disorders
• neurological symptoms (related to vitamin B12 deficiency)
• positive family history
 Findings in chronic autoimmune gastritis
• Autoimmune gastritis is associated with other autoimmune
disorders (mainly thyroid diseases) including Hashimoto thyroiditis
but also with Addison disease, chronic spontaneous urticaria,
myasthenia gravis, Diabetes type 1, vitiligo
• The association between chronic atrophic autoimmune gastritis and
autoimmune thyroid disease earned the name in the early 60s of
“thyrogastric syndrome.”
 Evaluation of chronic gastritis
• The diagnosis of gastritis has its basis in histopathological
examination of gastric biopsy tissues.
• While medical history and laboratory tests are helpful, endoscopy
and biopsy is the gold standard in making the diagnosis, identifying
its distribution, severity, and cause
 Tests used for the diagnosis of
H. pylori-associated gastritis
• Invasive methods (requiring gastroscopy and biopsies):
1. histological staining (hematoxylin and eosin, the Alcian blue stain and a
modified silver stain)
2. cultures
3. rapid urease test
4. molecular detection (PCR DNA)
• Non-invasive methods (not requiring gastroscopy and biopsies):
1. urease breath test (13C-UBT)
2. fecal antigen test
3. serology
 Tests used for the diagnosis of
H. pylori-associated gastritis
1. simultaneous treatment with proton-pump inhibitors leads to
false-negative results in both invasive and non-invasive tests
2. Serological tests for detection of antibodies against H. pylori cannot
differentiate between active and past infection
 Diagnosis of autoimmune gastritis
1) atrophic gastritis of gastric corpus (body) and fundus of the stomach
2) autoantibodies against the intrinsic factor and the parietal cells
3) raised serum gastrin levels
4) serum pepsinogen 1 level
5) pepsinogen 1 to pepsinogen 2 ratios
 Diagnosis of autoimmune gastritis
• The most sensitive serum biomarker in autoimmune gastritis is
parietal cell antibodies (as compared to intrinsic factor antibodies).
• The determination of the high risk of gastric cancer in autoimmune
gastritis irrespective of H. pylori infection:
1. low levels of pepsinogen 1
2. high fasting serum gastrin
3. atrophic gastritis of the corpus and fundus
 Diagnosis of autoimmune gastritis
• Pernicious anemia is a condition of macrocytic anemia associated
with low cobalamin levels and atrophic corpus-fundus gastritis
associated with parietal cell antibodies or intrinsic factor
autoantibodies
 Treatment of H. pylori-associated gastritis
• A triple-therapy of clarithromycin/proton-pump
inhibitor/amoxicillin for 14 to 21 days is considered the first line of
treatment.
• Clarithromycin is preferred over metronidazole because the
recurrence rates with clarithromycin are far less compared to a
triple-therapy using metronidazole
• However, in areas where clarithromycin resistance is known,
metronidazole is the option of choice
• Quadruple bismuth containing therapy would be of benefit,
particularly if using metronidazole
 Treatment of Autoimmune gastritis

• Substitution of deficient iron and vitamin B12 (parenteral 1000

micrograms or oral 1000 to 2000 micrograms) is needed.
• Monitor Iron and folate levels
• Eradicate any co-infection with H. pylori.
• Endoscopic surveillance for cancer risk and gastric neuroendocrine
tumors (NET) is required
 ATROPHIC GASTRITIS AND
MULTIFOCAL GASTRIC CANCER
 Treatment of Autoimmune gastritis
• cessation of alcohol, smoking, anti-inflammatory drugs, spicy food
• managing stress
• immunomodulatory therapy in autoimmune enteropathy
• dietary modification in eosinophilic gastritis
 Differential Diagnosis of chronic gastritis
• Peptic ulcer disease
• Gastric cancer
• Cholecystitis
• Zollinger-Ellison syndrome
• Dyspepsia
• Gallstone disease
 Differential Diagnosis of chronic gastritis
• Pancreatitis
• Myocardial ischemia
• Crohn disease
• Menetrier disease
• Lymphoma
• Celiac disease
• Multiple endocrine neoplasias
Menetrier disease
 Complications of gastritis
• Peptic ulcer
• Chronic atrophic gastritis (in autoimmune or long-standing H. pylori
gastritis)
• Gastric metaplasia/dysplasia
• Gastric cancer (adenocarcinoma)
• Iron-deficiency anemia (chronic gastritis and early stages of gastric
autoimmunity)
• Vitamin B12 deficiency (autoimmune gastritis)
• Gastric bleeding
Iron-deficiency anemia
 Complications of gastritis
• Achlorhydria (autoimmune gastritis, chronic H. pylori gastritis)
• Gastric perforation
• Mucosa-associated lymphoid tissue (MALT) lymphoma
• Neuroendocrine tumors (NET) (previously referred to as gastric
carcinoid; complicates autoimmune gastritis)
• Vitamin C, vitamin D, folic acid, zinc, magnesium, and calcium
deficiency (atrophic autoimmune gastritis)
THE END