Gastritis

CHAPTER
52
Gastritis
MARK FELDMAN AND EDWARD L. LEE
CHAPTER OUTLINE
Definition...................................................................................868
Acute Gastritis...........................................................................868
Chronic Gastritis........................................................................869
Gastritis in IBD..........................................................................878
Gastritis due to Hp.................................................................... 869

Chronic Atrophic Gastritis
(Gastric Atrophy)................................................................... 870
Gastritis Cystica Profunda..........................................................879

Gastric Graft-versus-Host Disease.............................................879
Allergic Gastritis........................................................................879
Reactive Gastropathies (Acute Erosive Gastritis)........................879
Carditis......................................................................................872
Infectious Gastritis.....................................................................872
Viral.......................................................................................... 872
Bacterial................................................................................... 873
Fungal...................................................................................... 875
Parasitic................................................................................... 875
Granulomatous Gastritis............................................................876
Sarcoid Gastritis........................................................................ 876
Xanthogranulomatous Gastritis................................................... 876
Distinctive Gastritides................................................................876
Collagenous.............................................................................. 876
Lymphocytic.............................................................................. 877
Eosinophilic............................................................................... 877
DEFINITION
Patients, clinicians, endoscopists, and pathologists define gastritis differently. Some define it as a symptom complex, others
as an abnormal endoscopic appearance of the stomach, and
still others use the term to connote microscopic inflammation
of the stomach, usually the mucosa. This third definition of
gastritis is used in this chapter.
There is a weak relationship between the presence of histologic gastritis and gastric symptoms (epigastric pain, nausea,
vomiting, bleeding). In fact, most patients with gastritis are
asymptomatic. In a study of patients with Huntingtons
disease, there was a high prevalence of gastritis despite
minimal if any symptoms.1
The relationship between microscopic and gastroscopic
abnormalities is also weak. In 1 study of 400 patients, histologic gastritis was present despite a normal gastroscopic
examination in 14%, whereas 20% had an abnormal gastroscopic examination with normal histology.2 The latter patients
(abnormal gastroscopy without gastritis) often have reactive
gastropathy (acute erosive gastritis, discussed later).
By definition, gastric biopsies must be obtained to be
able to diagnose gastritis. Indications for gastroscopic biopsies
may include gastric symptoms, gastric erosion or ulcer, thick
gastric fold(s), gastric polyp(s) or mass(es), and for diagnosis
of Hp infection. A set of 5 biopsies should be taken; preferred
Crohns Disease........................................................................ 878

UC............................................................................................ 879
Medications and Toxins............................................................. 880

Bile Reflux................................................................................ 880
Cocaine.................................................................................... 881
Stress....................................................................................... 881
Radiation.................................................................................. 881
Ischemia................................................................................... 881
Prolapse................................................................................... 881
Portal Hypertensive Gastropathy................................................881

Linear Erosions within a Hiatal Hernia.......................................881
Hyperplastic Gastropathies, Including Mntriers Disease........881
Differential Diagnosis.................................................................883
Treatment..................................................................................883
sites are shown in eFigure 52-1. The location of the biopsy

sites should be identified for the pathologist on an accessioning form.
Every biopsy represents an excellent opportunity for
the clinician and pathologist to communicate to correlate clinical data, endoscopic findings, and pathology. Errors may
occur when the pathologist attempts to interpret biopsies
without clinical input. It is important for the pathologist
to become familiar with the range of normal gastric biopsy
findings.
The Sydney classification system was an attempt to unify
terminology for endoscopic and histologic gastritis and gastropathy.3 However, the complexity of the Sydney system and
failure to obtain adequate numbers of biopsies from the specific regions of the stomach required to use the classification
precluded widespread clinical use outside of clinical research
studies. This chapter use provides an etiology-based classification of gastritis and reactive gastropathies.
ACUTE GASTRITIS
Acute gastritis, characterized by dense infiltration of the
stomach with neutrophilic leukocytes, is rare. This rarity is in
distinction to the much more common active gastritis,
where neutrophils can be present along with chronic inflammatory cells (lymphocytes, plasma cells), as in Hp gastritis
868
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Chapter 52 Gastritis 868.e1
eFIGURE 52-1.

Chapter 52 Gastritis 869

(see Chapter 51). Most forms of acute neutrophilic gastritis are
due to gastric infections with invasive organisms.
Phlegmonous (suppurative) gastritis is an infection of the
gastric submucosa and muscularis propria, often sparing the
mucosa.4-9 Many types of invasive microorganisms have
been identified, including Gram-negative bacteria, anaerobes,
Gram-positive organisms including group A streptococci,5
and fungi (e.g., mucormycosis; see later). The gastric phlegmon may simulate a mass.4 Infection may spread from the
stomach to the liver and spleen, with abscess formation.9 The
esophagus may also be involved in or even be the apparent
source of the infection.6 Acute phlegmonous/necrotizing gastritis has been associated with a variety of conditions including recent large intake of alcohol, upper respiratory tract
infection, and AIDS and other immunocompromised states,
including liver transplantation.
An especially severe form of phlegmonous gastritis is
emphysematous gastritis, due to infections with gas-producing
organisms.10-20 Gas in the wall of the stomach and in the portal
venous system is often present (Fig. 52-1). Radiographic studies
(plain films, CT) show gas bubbles conforming to the contour
of the stomach, often in the form of cystic gas pockets. Although
full recovery from phlegmonous or emphysematous gastritis

may occur, the condition may progress to gastric (and esophageal) gas gangrene and be fatal.20 Risk factors for emphysematous gastritis include gastroduodenal surgery, ingestion of
corrosive materials, gastroenteritis, or GI infarction.
Patients with phlegmonous or emphysematous gastritis
typically present with acute upper abdominal pain, peritonitis, purulent ascitic fluid, fever, and hypotension. Preoperative
diagnosis is possible with plain film, US, or CT. Gastroscopy
with or without biopsy and culture of gastric contents may
establish the diagnosis.
Grossly, the stomach wall appears thick and edematous
with multiple perforations, and the mucosa may demonstrate
a granular, green-black exudate. Microscopically, the edematous submucosa reveals an intense polymorphonuclear infiltrate and numerous Gram-positive and/or Gram-negative
organisms, as well as vascular thrombosis. The mucosa may
demonstrate extensive areas of necrosis.
The mortality rate of phlegmonous gastritis is close to 70%,
probably because it is so often misdiagnosed and because
treatment is initiated too late. The definitive treatment is either
resection or drainage of the stomach, combined initially with
large doses of systemic broad-spectrum antibiotics directed
against the most common organisms (Escherichia coli and other
Gram-negative bacilli, anaerobic and group A streptococci,
and Staphylococcus aureus).
Acute phlegmonous gastritis can also paradoxically be
associated with both granulocytic leukemia7 and with neutropenia.8,17 Although not as common as neutropenic cecitis
(typhlitis) or enterocolitis, neutropenic gastritis can be an isolated finding.17
Other forms of acute gastritis are discussed later (see Infectious Gastritis).
CHRONIC GASTRITIS
FIGURE 52-1. CT of Emphysematous gastritis. Abdominal CT image
in a 67-year old male diabetic with coronary artery disease
and prior stroke who was admitted from his nursing home with
sudden onset of nausea, vomiting and abdominal pain. Physical
examination showed diffuse tenderness throughout the abdomen. CT shows curvilinear air in the posterior wall of the fluidfilled stomach, as well as portal venous gas. He was treated
successfully with broad-spectrum antibiotics, with resolution
of the emphysema documented on a repeat scan 2 weeks later.
(Courtesy T. Ynosencio, MD, Baylor University Medical Center,
Dallas, Tex.)
Diffuse antral gastritis
Chronic gastritis is much more common than acute gastritis,

although most forms of chronic gastritis are clinically silent.
Their importance relates to the fact that these gastritides are
risk factors for other conditions such as PUD, gastric hyperplastic polyps, and benign and malignant gastric neoplasms.
Three types of chronic gastritis are recognized (Fig. 52-2
and 52-3).
Gastritis due to Hp
Hp infection is the most common cause of gastritis (Fig. 52-3C;
see Chapter 51). For example, in a Veterans Affairs population
Environmental metaplastic
atrophic gastritis
Autoimmune metaplastic
atrophic gastritis
FIGURE 52-2. Topographic patterns of chronic gastritis. The darker areas in the schematic of environmental metaplastic atrophic gastritis
and autoimmune metaplastic atrophic gastritis represent areas of focal atrophy and intestinal metaplasia.

870 Section VI Stomach and Duodenum
E
FIGURE 52-3. Histopathology of chronic gastritides. A and B, Normal mucosal biopsy from the gastric body and antrum, respectively.
C, Diffuse antral gastritis. The glands show an infiltrate of neutrophils, in addition to an increase in chronic inflammatory cells in the
lamina propria. This lesion is typically associated with Hp infection. D, Environmental metaplastic atrophic gastritis. Note several glands
lined by goblet cells (arrow). The biopsy is from the gastric body, and similar changes were present in the antrum. E, Autoimmune
metaplastic atrophic gastritis in a man with pernicious anemia. The gland in the lower left is lined by goblet cells. Nests of enterochromaffinlike cells are also visible (arrows).
undergoing diagnostic upper endoscopy with gastric biopsy,

nearly 80% of patients with gastritis had Hp infection.21
A form of Hp gastritis characterized by mucosal infiltration by plasma cells that contain Russell bodies (Russell body
gastritis) has been described.22-24 Another form of Hp gastritis
that can be recognized endoscopically is nodular gastritis,
which can be reversible following eradication of the organism
from the stomach.25-27 Nodular gastritis/gastropathy can also
be seen in other conditions, however, such as Crohns disease,
syphilitic gastritis, lymphocytic (varioliform) gastritis, collagenous gastritis (all discussed later), and secondary (AA)
amyloidosis.28
Chronic Atrophic Gastritis (Gastric Atrophy)

As discussed in Chapter 48, the gastric mucosa has a rapid
rate of turnover, with new cells derived from progenitor
(stem) cells replacing the cells that are shed into the lumen or
destroyed. This process maintains the thickness and the varied
cell population of glands comprising the oxyntic and antral
mucosa. During chronic inflammation of the stomach, the rate
of cell loss may exceed the ability of the stomach to replace
lost cells, and the mucosa thins. Metaplasia of this epithelium
into an intestinal-type epithelium also occurs. This thinning
of the mucosa and intestinal metaplasia, if associated with


TABLE 52-1 Operative Link Gastritis Assessment (OLGA)
Classification of Cancer Risk in Chronic Gastritis Based
on the Degree of Gastric Atrophy
CORPUS (BODY, FUNDUS)
ATROPHY
None (0)
None
(0)
Mild
(1)
Moderate Severe
(2)
(3)
STAGE 0
STAGE I
STAGE II
A
N
Mild (1)
STAGE I STAGE I STAGE II
T
R
Moderate (2) STAGE II STAGE II STAGE III
U
M* Severe (3)
STAGE III STAGE III STAGE IV
STAGE II
STAGE III
STAGE IV
STAGE IV
*Antrum includes the biopsy result from the incisura angularis (see Fig. 52-1).
Modified from Rugge M, Correa P, Di Mario F, etal. OLGA staging for gastritis:
A tutorial. Dig Liver Dis 2008; 40:650-8.
TABLE 52-2 The Spectrum of Autoimmune (AMAG) and

Environmental (EMAG) Metaplastic Atrophic Gastritis
AMAG
AMAG/EMAG Overlap
EMAG
Antibodies to intrinsic factor,

parietal cell
Hp gastritis (current, past)
Other autoimmune disorders
Potentially reversible (Hp Rx)
Antral sparing
Antral involvement
Serum PGI and PGI/PGII

ratio
Serum PG levels more

variable
Hypergastrinemia (can be
marked)
Normal or slight increase in

serum gastrin
Gastric carcinoid tumors

PG, Pepsinogen
chronic inflammation, is termed chronic atrophic gastritis, or

gastric atrophy.29-51 Chronic atrophic gastritis may be regional
or diffuse and is often patchy (see Fig. 52-2).
The importance of chronic atrophic gastritis (gastric
atrophy) is 2-fold. First, loss of specialized cells within gastric
glands, such as parietal cells, leads to a reduction or absence
of their secreted products, such as intrinsic factor and gastric
acid (hypochlorhydria or achlorhydria), with adverse consequences (e.g., vitamin B12 malabsorption, bacterial overgrowth,
and enteric infections). Second, patients with chronic atrophic
gastritis with intestinal metaplasia are at increased risk of
developing gastric dysplasia and cancer (see Chapter 54).
In 2005, an international group of gastroenterologists and
pathologists (the Operative Link for Gastritis Assessment
[OLGA]) attempted to stage the risk of progression from
chronic atrophic gastritis to gastric cancer.52 OLGA stages 0
through IV are recognized (Table 52-1). The OLGA system is
based on the assumption that gastric cancer risk is related to
the degree of gastric atrophy.53 Recent studies have suggested
that the OLGA stage in fact does correlate with increasing
cancer risk and also with endoscopic evidence of gastric
atrophy.54-56 Others have proposed that intestinal metaplasia,
easier to recognize by pathologists than gastric atrophy,
should be used in place of gastric atrophy (OLGIM).57,58
However, focusing on intestinal metaplasia rather than degree
of gastric atrophy may be less sensitive in identifying patients
at high gastric cancer risk.59
Two types of chronic atrophic gastritis are recognized (Fig.
52-2 and Fig. 52-3 D and E): an environmental metaplastic
atrophic gastritis (EMAG), also called multifocal atrophic gastritis, and an autoimmune metaplastic atrophic gastritis (AMAG),
also called diffuse corporal atrophic gastritis. At the extreme ends
of the spectrum, these 2 types can be distinguished using clinical, laboratory, endoscopic, and histologic features (Table
52-2). However, in many cases the distinction between EMAG
(usually due to Hp infection) and AMAG (usually due to
autoreactive T and B/plasma cells against various antigens of
the parietal cell) is blurred because of overlapping features.
For example, in EMAG the Hp may disappear from the
stomach over time as the gastric epithelium is replaced by
metaplastic intestinal epithelium, although immunoglobulin
(Ig)G antibodies to Hp may persist. Likewise, it has been proposed that, through molecular mimicry, antibodies to Hp can
cross react with parietal cell antigens such as H+,K+-ATPase
(the proton pump) to result in a form of AMAG.60-62
Environmental Metaplastic Atrophic Gastritis

EMAG is characterized by the involvement of both the
gastric antrum and corpus with mucosal atrophy and intestinal metaplasia (Fig. 52-3D). It is important for the endoscopists to obtain the recommended set of 5 biopsies from the
antrum, incisura, and body in order for the pathologist to
render a diagnosis of EMAG (see Fig. 52-2). Atrophic gastritis
involving the corpus may be associated with pseudopyloric
metaplasia, in which the mucosa resembles antral mucosa but
stains for pepsinogen I (PGI), a proenzyme expressed in
corpus mucosa.
Gastroscopy may show a pale mucosa, shiny surface, and
prominent submucosal vessels. However, endoscopy is neither
sensitive nor specific in diagnosing chronic atrophic gastritis,
especially in patients younger than age 50.31 Magnifying
endoscopy and auto fluorescence imaging video endoscopy
may be more sensitive in detecting atrophy.29,30
The pathogenesis of EMAG is multifactorial, but Hp infection plays the most important role and has been incriminated
in about 85% of patients. EMAG can occur early in life in
Hp-infected individuals. Genetic and environmental factors,
especially diet, are also important. Certain population groups
are predisposed to EMAG, including African Americans,
Scandinavians, Asians, Hispanics, Central and South Americans, Japanese, and Chinese. In China, a model has been
developed based on gender, general health, family history of
cancer, and diet/alcohol use to stratify the risk of gastric
cancer in EMAG and the need for screening gastroscopy.32
Intestinal metaplasia is a risk factor for dysplasia and gastric
cancer, usually the intestinal type (see Chapter 54). The incidence of gastric neoplasia in intestinal metaplastic lesions of
the stomach has been estimated to be 1% per year, although
most of these incident lesions were dysplastic ones and not
cancers.34
Intestinal metaplasia of the gastric mucosa can be classified
into 3 types, as described in Chapter 54, where their possible
associations with the intestinal type of gastric cancer are discussed. In some cases, especially in patients living in the
Pacific basin, metaplastic gastric cells are ciliated, probably
due to environmental factors that are more prominent in the
Pacific than the Atlantic Ocean basins.63
Whether long-term therapy with PPIs in patients with Hp
gastritis hastens the development of EMAG is controversial;
recent studies in patients who were treated with lansoprazole


for 6 years suggest that this outcome should not be a significant concern.64
Autoimmune Metaplastic Atrophic Gastritis

AMAG, also called diffuse corporal atrophic gastritis, is an autoimmune destruction of glands in the corpus of the stomach.
AMAG is the pathologic process in patients with pernicious
anemia, an autoimmune disorder often occurring in patients
of northern European or Scandinavian background and in
African Americans.
Patients with AMAG exhibit achlorhydria or hypochlorhydria, hypergastrinemia secondary to low or absent gastric acid
with antral G-cell hyperplasia, and low serum PGI concentrations and low ratios of serum PGI/PGII. They often have
circulating antibodies to parietal cell antigens and to intrinsic
factor (IF). Antibodies to IF are less sensitive but more specific
for AMAG, whereas antibodies to parietal cells are more sensitive but less specific. These antibodies can apparently cross
from the maternal circulation to the fetus to cause neonatal
vitamin B12 deficiency with methylmalonic aciduria.65 Autoreactive T cells against the H+,K+-ATPase are also thought to
play a role in the pathogenesis of AMAG.
Incomplete (colonic) intestinal metaplasia (type III) may
occur in AMAG and be a risk factor for gastric carcinoma in
areas of the world that experience a higher incidence of gastric
carcinoma than in the United States. Metaplastic intestinal
Paneth cells in AMAG appear to secrete an antibacterial
peptide of the alpha-defensin family, human defensin 5
(HD-5), a peptide not produced in the normal stomach.66 HD-5
could prevent invasion by indigenous, bacterial flora that
overgrow in the atrophic, anacidic stomach. Metaplastic pancreatic acinar cells are also a feature of AMAG.67
Histologically, atrophic glands with extensive intestinal
metaplasia are confined to the corpus mucosa (Fig. 52-3E).
Early in the course of this disease, atrophy may be focal and
the preserved islands of relatively normal oxyntic mucosa
may appear polypoid endoscopically or radiologically. Rarely,
AMAG progresses to diffuse (complete) atrophy. Hypergastrinemia, a consequence of achlorhydria, is associated with
enterochromaffin-like cell hyperplasia and gastric carcinoid
tumors,35 discussed in more detail in Chapter 33. AMAG was
associated with non-tumoral hypergastrinemia in a patient
with lymphocytic colitis and no evidence of enterochromaffinlike cell hyperplasia or gastric carcinoid tumor.68
Antibodies to parietal cell antigens, most notably the
proton pump (H+,K+-ATPase) are frequently present in patients
with AMAG. These antibodies are frequently detected in
patients with various other autoimmune diseases, including
type 1 diabetes mellitus37-39 and autoimmune thyroid diseases
(Graves and Hashimotos),40,41 explaining the association of
these conditions with pernicious anemia. The risk of AMAG
is increased 3- to 5-fold in type 1 diabetic individuals, and
some authors have suggested screening type 1 diabetics with
gastroscopy and mucosal biopsy. AMAG has also been associated with autoimmune pancreatitis, as well as celiac disease/
dermatitis herpetiformis.45,69
A proportion of the CD4+ lymphocytes present in the
chronic inflammatory infiltrate within the gastric mucosa in
patients with AMAG proliferate in response to H+,K+-ATPase.
Most CD4+ cells secrete Th1 cytokines such as TNF-, provide
help for B cell immunoglobulin production, and enhance
perforin-mediated cytotoxicity, as well as Fas ligandmediated
apoptosis. These factors in combination may contribute to
gland destruction in AMAG.
Many patients with AMAG have antibodies to Hp and/or
Hp in their oxyntic mucosa. Thus, Hp may play a role in the
early pathogenesis of AMAG.70 It appears that cagA+/vacA+

Hp are most likely to cause AMAG. These Hp are often the
s1m1 vacA subtype that also express Lewis blood group antigens X and Y.71 Lewis antigens may help camouflage Hp
because these antigens are also present on human gastric
epithelial cells. It has been suggested that when antibodies
to Lewis antigens X and Y from Hp develop, they cross-react
with antigens on epithelial cells, such as the H+,K+-ATPase
on parietal cells, resulting in AMAG (molecular mimicry).
If chronic atrophic gastritis with intestinal metaplasia
develops in such patients over time, the incidence of Hp
infection will then decrease. Based on uncontrolled studies
from Japan,72 eradication of Hp often leads to a decrease in
the amount of gastric atrophy and intestinal metaplasia,
whereas failed eradication attempts accomplish neither of
these endpoints.
CARDITIS
There is often a small rim of gastric glands in the cardia of the
stomach just below the squamocolumnar junction of the
esophageal and gastric mucosa (see Chapter 48). In an endoscopic study of normal volunteers, the majority had a cardiactype mucosa in this region; the remainder had oxyntic mucosa
with parietal and chief cells.73 Inflammation of this cardiactype mucosa (carditis) has been attributed to Hp and to
GERD. Carditis occurring in healthy volunteers is mainly due
to infection with Hp.73 However, in patients found to have
carditis during a diagnostic endoscopy, Hp carditis (usually
active) was present in only 11%. The severity of carditis in
this population was more related to 24-hour acid exposure of
the lower esophagus.74 Atrophic carditis, often accompanied
by intestinal metaplasia, has been proposed to be a precursor
of adenocarcinoma of the gastroesophageal junction (see
Chapters 45, 47, and 54).
INFECTIOUS GASTRITIS
Viral
Cytomegalovirus
Cytomegalovirus (CMV) is a human herpesvirus (HHV5)
that may infect the stomach. Although gastric CMV infection
may occur in an immunocompetent host, infection usually
occurs in the immunocompromised.75 Patients with transplants (see Chapter 35), AIDS (see Chapter 34), or cancer, or
who are taking immunosuppressive drugs (especially glucocorticoids) are at increased risk.
Patients with CMV infection of the stomach may experience epigastric pain that may be postural,76 with fever and
atypical lymphocytosis. Upper GI (UGI) tract radiographic
studies, if performed, may reveal a rigid and narrowed gastric
antrum suggestive of an infiltrating antral neoplasm. Gastroscopy may reveal a congested and edematous antral mucosa,
covered with multiple ulcerations, suggestive of gastric malignancy, submucosal antral mass, or gastric ulcer. A hypertrophic and/or polypoid type of gastritis resembling Mntriers
disease with a similar type of protein-losing gastropathy has
been described, especially in children, including 1 case with
CMV/Hp coinfection.77
Examination of mucosal biopsy specimens shows inflammatory debris, chronic active gastritis, and enlarged cells
with CMV inclusion bodies indicative of an active infection

FIGURE 52-4. Histopathology of cytomegalovirus (CMV) gastritis. A, Low-power view of CMV gastritis. An acute inflammatory infiltrate
is present in the lamina propria. Glandular destruction and reactive glands are present. Cystic glands are also evident. B, High-power
view of the cystic area deep in the mucosa shown in A. Several cytomegalic cells with the typical intranuclear and intracytoplasmic
inclusions of CMV are present.
(Fig. 52-4). Owl-eye intranuclear inclusions are the hallmark

of CMV infection in routine H&E histologic preparations and
may be found in vascular endothelial cells, mucosal epithelial
cells, and connective tissue stromal cells. Multiple granular,
basophilic, cytoplasmic inclusions may also be present. Usual
treatment is with IV ganciclovir or foscarnet.
Other Herpesviruses
Gastritis from HSV-1 (HHV1) or varicella-zoster virus (VZV;
HHV3) is rare.78,79 Infected individuals typically experience
the initial infection at an early age, and the virus then remains
dormant until reactivation. Reactivation has been related to
radiation therapy, cancer chemotherapy, lymphoma, and
cancer. The typical immunocompromised patient with these
viral gastritides may experience nausea, vomiting, abdominal
pain, fever, chills, fatigue, and weight loss. Barium-air doublecontrast radiographs show a cobblestone pattern, shallow
ulcerations with a ragged contour, and an interlacing network
of crevices filled with barium that corresponds to areas of
ulceration. Gastroscopy reveals multiple, small, raised, ulcerated plaques or linear, superficial ulcers in a crisscrossing
pattern, giving the stomach a cobblestone appearance. Brush
cytology and biopsies should be performed at the time of
endoscopy. Brush cytology has the advantage of sampling a
wider area of mucosa. Grossly, the ulcers are multiple, small,
and of uniform size. Microscopically, cytologic smears and
biopsy specimens show numerous single cells and clumps of
cells, with ground-glass nuclei and eosinophilic intranuclear
inclusion bodies surrounded by halos. Treatment with acyclovir is reasonable but of unproved value.
EBV (HHV4) is not present in normal gastric mucosa, but
can be present in the stomach in almost half of the patients
with gastritis.80 Whether EBV is a cause of the gastritis is
uncertain, however. Recently, EBV infection has been linked
to gastritis cystica profunda (discussed later) and with gastric
cancer.81 Infectious mononucleosis due to acute EBV infection
may lead to gastric lymphoid hyperplasia with atypical
lymphocytes.82
Measles
Rarely, morbilliform gastritis with giant cells of the WarthinFinkeldey type may occur.83
Bacterial
Mycobacterial
Gastric infection with Mycobacterium tuberculosis is a rare
entity.84 Patients typically present with abdominal pain,
nausea and vomiting, GI bleeding, anemia, fever, and weight
loss. Gastric TB may be associated with gastric outlet obstruction or with hemorrhage from a tuberculous gastric ulcer.
Radiographic studies reveal an enlarged stomach with a narrowed, deformed antrum and prepyloric ulcerations. Upper
endoscopy demonstrates ulcers, masses, or gastric outlet
obstruction. Grossly, the stomach may demonstrate multiple
small mucosal erosions, ulcers, an infiltrating mass (hyper
trophic form), sclerosing inflammatory disease, or pyloric
obstruction either by extension from peripyloric nodes or
by invasion from other neighboring organs. Biopsies show
necrotizing granulomas with the presence of acid-fast bacilli,
best demonstrated with Kinyoun acid-fast stain. Treatment is
discussed in Chapter 84.
Although Mycobacterium avium is a common opportunistic
bacterial infection among patients with AIDS, the stomach is
rarely involved. Microscopically, the gastric mucosa demonstrates numerous foamy histiocytes containing many acid-fast
bacilli. Treatment is discussed in Chapter 34.
Actinomycosis
Primary gastric actinomycosis is a rare, chronic, progressive,
suppurative disease characterized by formation of multiple
abscesses, draining sinuses, abundant granulation, and dense
fibrous tissue.85 Intestinal actinomycosis is more common than
gastric and has a predilection for the terminal ileum, cecum,
and appendix. The presenting symptoms of gastric actinomycosis include fever, epigastric pain, epigastric swelling,
abdominal wall abscess with fistula, and UGI bleeding. Radiographic studies frequently suggest a malignant tumor or a
gastric ulcer. Endoscopy is suggestive of a circumscribed and
ulcerated gastric carcinoma, and the diagnosis can be made
with endoscopic biopsy.
Grossly, the resected stomach demonstrates a large, illdefined, ulcerated mass in the wall of the stomach. Microscopically, multiple abscesses show the infective agent,
Actinomyces israelii, a Gram-positive filamentous anaerobic


bacterium that normally resides in the mouth. A biopsy of a
mass containing pus or a biopsy of a draining sinus may reveal
actinomycosis. If the disease is recognized only by histologic
examination, the prognosis is good. Prolonged (6- to 12-month)
high-dose antibiotic treatment with amoxicillin or penicillin is
recommended.
Syphilis
Case reports and small series of cases emphasize the importance of the gastroenterologist and pathologist remaining alert
to the protean manifestations of syphilis and being familiar
with the histopathologic pattern of the disease.86-88 Gastric
involvement in secondary or tertiary syphilis is rarely recognized clinically, and its diagnosis by examination of endoscopic biopsy specimens has been reported infrequently. The
features of syphilis in the stomach should be recognized
because they can provide a window of opportunity for effective antibiotic therapy before the disease progresses and
causes permanent disability. Syphilitic gastritis can occur in
conjunction with hepatitis and proctitis.87 Gastric syphilis can
occur in the setting of infection with HIV.
Patients typically present with symptoms of PUD, often
with UGI bleeding. Diseases that may mimic gastric syphilis
include PUD, gastric carcinoma, gastric lymphoma, gastric TB,
and gastric Crohns disease. The acute gastritis of early secondary syphilis produces the earliest radiologically detectable
sign of the disease. Radiographs show a nonspecific gastritis
with diffusely thickened folds that may become nodular
with or without detectable ulcers. Strictures in the midstomach (hourglass stomach) may be present (Fig. 52-5A).
Endoscopy shows numerous shallow, irregular ulcers with

overlying white exudate and surrounding erythema (see
Fig. 52-5B). The surrounding mucosa may also demonstrate a
nodular appearance. Gastroscopy may also demonstrate
prominent, edematous gastric folds.
Grossly, the stomach may be thickened and contracted and
may show multiple serpiginous ulcers. Partial gastrectomy
specimens may show compact, thick, mucosal rugae and
numerous small mucosal ulcers. Microscopically, biopsies
show severe gastritis with dense plasma cell infiltrate in the
lamina propria, varying numbers of neutrophils and lymphocytes, gland destruction, vasculitis, and granulomas. WarthinStarry silver stain or modified Steiner silver impregnation
stain reveals numerous spirochetes. Serum Venereal Disease
Research Laboratory (VDRL) and Treponema immunofluorescence studies may be positive, and the Treponema pallidum
gene may be detected by PCR. Treatment with penicillin is
highly effective (see Fig. 52-5C).
Other Bacteria
Helicobacter heilmannii spiral bacteria are an infrequent
cause of chronic active gastritis, and may be a risk factor
for gastric MALT lymphoma.89 These organisms, originally
known as Gastrospirillum hominis, are longer than Hp and
have multiple spirals. One of these H. heilmannii species,
Helicobacter bizzozeronii, has been isolated from human gastric
mucosa.90 Another organism that, like Hp, can stain with
the Giemsa reagent is Campylobacter hypointestinalis.91 The
clinical significance of these non-Hp curved bacilli remains to
be established.
FIGURE 52-5. Gastric syphilis (syphilitic gastritis). Film from an upper GI series (A) showing a stricture in the mid-stomach (hourglass
stomach), with antral deformity. Endoscopic appearance before (B) and 4 weeks after (C) penicillin therapy in another patient with
gastric syphilis.


blood vessel walls. Treatment is resection of the affected
necrotic portion of the stomach. Invasive gastric mucormycosis is almost always fatal.
Fungal
Candidiasis
Fungal contamination of gastric ulcers with Candida species
is not uncommon.92 There is debate whether fungal colonization in patients with gastric ulcers and chronic gastritis has
any clinical significance or whether the organisms aggravate
and perpetuate gastric ulceration. Endoscopically, gastric
ulcers associated with Candida albicans tend to be larger in
diameter and are more often suspected to be malignant than
typical gastric ulcers. Diffuse superficial erosions may also
be noted.
Fungal colonization of the GI tract is frequent in patients
with underlying malignancy and in immunocompromised
patients who have been treated with antibiotics or glucocorticoids but may occur also in immunocompetent patients.
Massive growth of yeast organisms in the gastric lumen (yeast
bezoar) is a potential complication of gastric surgical procedures, usually for PUD. Candida infection of the stomach
may occur in alcoholic patients. Radiologic studies show tiny
aphthoid erosions, which represent the earliest detectable
radiographic change in gastric candidiasis. Aphthoid ulcers
progress to deep linear ulcers.
Grossly, the gastric mucosa demonstrates tiny aphthous
erosions, widespread punctate, linear ulcerations, or gastric
ulcers. Microscopically, the layer of necrotic fibrinoid debris
demonstrates yeasts or pseudohyphae. The organisms can be
seen in the H&E stain; however, special stains such as periodic
acidSchiff-diastase stain or Gomori methenamine silver stain
may be required. Treatment is usually not necessary, but if
symptomatic candidiasis is suspected, fluconazole is reasonable but of unproved efficacy.
Aspergillosis
Histoplasmosis
The stomach is rarely affected by Strongyloides stercoralis.101

The organism may colonize the intact gastric mucosa and may
be associated with a bleeding peptic ulcer. Most patients are
immune compromised. Diagnosis can be made by endoscopic
biopsy, examination of stools, examination of duodenal aspirate, and examination of peripheral smear with elevated eosinophil count. Disseminated strongyloidiasis (hyperinfection)
can be rapidly fatal. Treatment is discussed in Chapter 114.
Progressive disseminated histoplasmosis is rare, occurring

most frequently in the very young or the older adult or in
those with immunodeficiency. Disseminated histoplasmosis
can involve any portion of the GI tract, although gastric
involvement is uncommon.93 Hypertrophic gastric folds, a
mass that mimics a gastric carcinoma, or gastric ulceration
may be associated with gastric histoplasmosis. Radiographic
studies may demonstrate an annular infiltrating lesion of the
stomach, and endoscopy may demonstrate enlarged and reddened gastric folds. Biopsy specimens show an intensive infiltration of macrophages containing Histoplasma capsulatum.
Treatment with IV liposomal amphotericin B or itraconazole
is appropriate.
Mucormycosis
Gastric mucormycosis (also called zygomycosis or phycomycosis) is a rare and highly lethal fungal infection.94 Risk factors
include malnutrition, immunosuppression, antibiotic therapy,
and metabolic acidosis, usually diabetic ketoacidosis. Most
patients present with UGI bleeding or gastric ulcers.95 Gastric
mucormycosis can be classified as invasive or noninvasive
(colonization). The former is characterized by deep invasion
of the stomach wall and by blood vessel involvement with
the fungus. Abdominal pain is the most frequent presenting
complaint. In the noninvasive type, the fungus colonizes
the superficial mucosa without causing an inflammatory
response.
Grossly, surgical specimens from affected patients reveal
hemorrhagic necrosis involving the mucosa and gastric wall.
Microscopically, non-septate 10- to 20-m hyphae branched at
right angles are present in the tissue and they infiltrate into
Acute Aspergillus gastritis is rare and can be highly

invasive.96
Cryptococcosis
The stomach and duodenum may be involved in immunocompromised hosts in conjunction with cryptococcal
meningitis.97
Other Fungi
Monascus ruber gastritis, acquired by eating dried, salted fish,
can result in invasive infection.98
Parasitic (see also Chapters 113 and 114)

Cryptosporidiosis
Cryptosporidiosis may rarely involve the stomach.99
Giardiasis
Giardia lamblia can rarely infect the stomach. A patient on a
PPI with small, cotton-like antral lesions has been described.100
Strongyloidiasis
Anisakidosis
Invasive anisakidosais (formerly, anisakiasis) may occur after
the ingestion of raw marine fish containing nematode larvae
of the genus Anisakis. Most cases of anisakidosis have been
diagnosed in Japan. The parasite may migrate into the wall of
the stomach, small intestine, or colon. Typically, patients
present with sporadic epigastric pain or have no symptoms at
all. Gastric perforation due to chronic gastric anisakidosis may
occur. Some patients exhibit a mild peripheral eosinophilia.
Endoscopy may show firm, yellowish submucosal masses
with erosions. Radiographic studies may reveal notchedshadow defects suggestive of a gastric tumor.
Grossly, the stomach demonstrates multiple erosive foci
with hemorrhage and small 5- to 10-mm gastric lesions in the
stomach wall. Microscopically, sections of the stomach show
a marked eosinophilic granulomatous inflammatory process
with intramural abscesses and granulation tissue. The eosinophilic abscess may contain a small worm measuring 0.3mm
in diameter, which can be identified as the larval form. The
diagnosis may be confirmed serologically if the larvae are not
detectable by endoscopy. Treatment is endoscopic removal of
the nematode. Successful relief of acute dyspeptic symptoms,
which can be quite severe, has been reported with an overthe-counter medicine containing wood cresolate.102

Ascariasis
Although gastric ascariasis is rare, chronic, intermittent gastric
outlet obstruction caused by Ascaris lumbricoides may occur.103
Gastric ascariasis has also been associated with UGI hemorrhage, with endoscopic examination showing several Ascaris
worms in the stomach and duodenum. Treatment is endoscopic removal, followed by mebendazole or albendazole (see
Chapter 114).
Necatoriasis
Endoscopic discovery, capture, and removal from the stomach
of the hookworm Necator americanus has been reported.104
Capillariasis
Eosinophilic gastritis from capillariasis has been reported,
perhaps linked to ingestion of raw fish.105
GRANULOMATOUS GASTRITIS
A variety of granulomatous diseases can affect the stomach.106,107
Crohns disease (Fig. 52-6), discussed later and also in Chapter
115, is the most common of them in children. Sarcoidosis and
Crohns are the most common in adults. Infection with spirochetes, mycobacteria, fungi, parasites, and the Whipples
bacillus (see Chapter 109) can also cause granulomatous
gastritis, as can xanthogranulomatous gastritis (discussed
later), foreign bodies, lymphoma, Langerhans cell histio
cytosis (gastric eosinophilic granuloma), eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome), and
chronic granulomatous disease of childhood.
An isolated idiopathic granulomatous gastritis also occurs.
Some of these idiopathic cases may eventually evolve into
Crohns disease or sarcoidosis. Other cases of idiopathic
granulomatous gastritis appear to be due to Hp infection and
may slowly resolve following appropriate antibiotic therapy,
sometimes leaving a curious mucosal discoloration.108
tract affected in sarcoidosis, being involved in approximately

10% of cases.109 A diagnosis of sarcoid gastritis of the stomach
cannot be made with confidence in the absence of granulomatous disease in other organs.
Affected patients, usually in the third to fifth decades of
life, typically present with epigastric pain, nausea, vomiting,
and weight loss. Occasionally they present with massive GI
hemorrhage. Gastric sarcoidosis may result in pyloric outlet
obstruction, achlorhydria, and pernicious anemia. Radiographically, gastric sarcoidosis may mimic the diffuse form of
gastric carcinoma (linitis plastica) or Mntriers disease.
Endoscopy may reveal a narrow distal stomach with multiple prepyloric ulcers or erosions, atrophy, thick gastric folds
with a diffuse cobblestone appearance, or normal mucosa
associated with microscopic granulomas. Surgical specimens
from patients with gastric sarcoidosis show a thickened
stomach wall with foci of erosions and ulcers. Microscopically,
mucosal biopsies show multiple non-caseating granulomas,
although granulomas may be necrotizing.110 The presence of
granulomas in GI tissue is a nonspecific finding, and special
stains should be performed to rule out granulomatous infections, particularly TB. In some cases it may be difficult to
differentiate gastric sarcoidosis from gastric Crohns disease
or from isolated idiopathic granulomatous gastritis. Glucocorticoid therapy is the cornerstone of treatment for gastric sarcoidosis (see Chapter 36). Subtotal gastric resection is reserved
for patients with obstruction and severe hemorrhage.
Xanthogranulomatous Gastritis
Xanthogranulomatous gastritis (XGG) is a rare form of gastritis, with only 11 reported cases worldwide. XGG is characterized by marked proliferation of foamy histiocytes mixed with
acute and chronic inflammatory cells, multinucleated giant
cells, and fibrosis. The destructive inflammatory and fibrotic
process may extend into adjacent organs and simulate, or
coexist with, a gastric neoplasm.111-113
DISTINCTIVE GASTRITIDES
Sarcoid Gastritis
Collagenous
Sarcoidosis is a systemic granulomatous disease, sometimes

involving the GI tract and liver (see Chapter 36). The stomach
(usually the antrum) is the most common portion of the GI
Collagenous gastritis is rare, and can be associated with collagenous duodenitis, collagenous colitis, lymphocytic colitis,
celiac disease, and/or autoimmune disorders.114-120 In one
series, 2 clinical patterns were identified. In the children and
young adults, the presenting symptoms, anemia and epigastric pain, were attributed to the gastritis per se, whereas in the
older adults (ages 35 to 77), the presenting symptom was often
diarrhea due to coexisting celiac disease or collagenous
colitis.120
UGI barium radiography may demonstrate an abnormal
mucosal surface with a mosaic-like pattern in the body of the
stomach, corresponding to mucosal nodularity. Endoscopy
may reveal multiple diffusely scattered, discrete submucosal
hemorrhages, gastric erosions, and nodularity of the body of
the stomach along the greater curvature.
Biopsy specimens from the body and antrum of the
stomach reveal a patchy, chronic, superficial gastritis, focal
atrophy, and focal deposition of collagen 20 to 75 m thick in
the subepithelial region of the lamina propria (Fig. 52-7). Tiny
erosions of the surface epithelium are present, and the inflammatory infiltrate consists of mainly plasma cells, intraepithelial lymphocytes and eosinophils, together with marked
hypertrophy of the muscularis mucosa. Little is known about
the etiology, natural history, and proper treatment of this
condition.
FIGURE 52-6. Histopathology of granulomatous gastritis in a patient

with Crohns disease. A noncaseating granuloma is present
within the lamina propria. (H&E, 200.)


gastritis in adults is typically seen in patients with Hp infection (see Chapter 51). Hp eradication treatment in patients
with lymphocytic gastritis causes significant improvement
in the gastric intraepithelial lymphocytic infiltrate, corpus
inflammation, and dyspeptic symptoms. The relationship
between lymphocytic gastritis and gastric lymphoid hyperplasia, which also is associated with Hp infection, is not clear.
Patients with gastric MALT lymphoma have a significantly
increased prevalence of lymphocytic gastritis due to Hp
infection. Thus, lymphocytic gastritis may be a precursor of
gastric MALT lymphoma in patients with Hp infection (see
Chapters 31 and 54).
Other etiologic associations of lymphocytic gastritis in
clude celiac disease, HIV infection, Crohns disease, common
variable immunodeficiency, and medication.121 Recent findings provide compelling evidence that lymphocytic gastritis
may only occur as a manifestation of celiac disease, and also
be a marker of a more severe and earlier-onset form of celiac
disease123,124 (see Chapter 107). Following institution of a
gluten-free diet, the lymphocytic gastritis slowly resolves in
these patients.
Endoscopy in lymphocytic gastritis shows thick mucosal
folds, nodularity, and aphthous erosion (varioliform gastritis).125 Gastric biopsies show expansion of the lamina propria
by an infiltrate of plasma cells, lymphocytes, and rare neutrophils. These findings may be seen in the antral mucosa only,
body mucosa only, or in antral as well as body mucosa. The
surface and superficial pit epithelium shows a marked intraepithelial infiltrate with T lymphocytes, with flattening of the
epithelium and loss of apical mucin secretion.
Lymphomatoid gastropathy126,127 is a recently described entity
in which natural killer (NK) lymphocytes that are CD56+ infiltrate the stomach, simulating a gastric lymphoma. Cases are
being reported from Japan, where endoscopic screening
of healthy individuals for cancer is common. In a series with
10 men and women ages 46 to 75, the lesions appeared as
approximately 1-cm elevated nodules; gastric symptoms
were absent. Most lymphomatoid lesions resolved without
therapy, although the lesions sometimes recurred. Deaths
have not been reported. Chronic active gastritis can also occur
in X-linked lymphoproliferative disease.128
Lymphocytic
Lymphocytic gastritis121 is characterized by a dense lymphocytic infiltration of surface and pit gastric epithelium (Fig.
52-8A). Lymphocytic gastritis is related to an endoscopic form
of gastritis known as varioliform gastritis, characterized by
nodules, thickened rugal folds, and erosions.122 Lymphocytic
B
FIGURE 52-7. Histopathology of collagenous gastritis. (A, H&E,
200; B, Masson trichrome, 400.) The subepithelial thickening
of the collagen band is apparent. (From Wang HL, Shah AG,
Yerian LM, etal. Collagenous gastritis: An unusual association
with profound weight loss. Arch Pathol Lab Med 2004;
128:229-32.)
Eosinophilic
Eosinophilic gastroenteritis129,130 is a rare condition of unknown
etiology characterized by eosinophilic infiltration of the GI
FIGURE 52-8. Histopathology of lymphocytic gastritis (A) and eosinophilic gastritis (B). A, High-power view of the antral mucosa shows
numerous dark-staining mononuclear cells with striking intraepithelial lymphocytosis. B, Numerous eosinophils are noted within
the lamina propria and within the walls and lumens of the gastric glands. The patient also had peripheral blood eosinophilia. (H&E.)
(Courtesy Pamela Jensen, MD, Dallas, Tex.)


tract, peripheral blood eosinophilia, and GI symptomatology
in the absence of known causes for eosinophilia (e.g., parasitic
infection) or another GI disorder (e.g., IBD). As discussed
in Chapter 29, the stomach is frequently involved as one of the
manifestations of eosinophilic gastroenteritis (eosinophilic
gastritis).
Eosinophilic gastroenteritis is classified according to the
layer(s) of GI tract involved (i.e., mucosal layer disease, muscle
layer disease, and subserosal disease). In the stomach, mucosal
involvement may result in abdominal pain, nausea, vomiting,
weight loss, anemia, and protein-losing gastropathy. Patients
with muscular layer disease generally have gastric outlet
obstructive symptoms,130 and rare patients with subserosal
eosinophilic infiltration may develop eosinophilic ascites.
Radiographic studies may demonstrate thickened mucosal
folds, nodularity, or ulcerations. Endoscopy may reveal
normal-appearing mucosa or hyperemic edematous mucosa
with surface erosions or prominent gastric folds. Eosinophilic
gastritis may simulate gastric cancer.
Gastric mucosal biopsies are critical to the diagnosis
and show marked eosinophilic infiltration, eosinophilic pit
abscesses, necrosis with numerous neutrophils, and epithelial
regeneration (see Fig. 52-8B). Abnormal eosinophilic infiltration, defined as at least 20 eosinophils per high-power field,
can be either diffuse or multifocal. A diagnosis of eosinophilic
gastritis has been proposed for cases in which eosinophils
infiltrate the surface, foveolar epithelium, the mucosa, or submucosa or are associated with other features of mucosal
damage (e.g., foveolar hyperplasia or architectural distortion
with significant chronic or active inflammation).129 A fullthickness biopsy of the stomach is necessary for the diagnosis
of muscle layer disease.
As discussed in Chapter 29, patients with disabling
symptoms can be effectively treated with glucocorticoids after
other systemic disorders associated with peripheral eosinophilia have been excluded. Therapeutic endoscopic or surgical
intervention may be required in patients with obstructive
complications.
GASTRITIS IN IBD
Gastritis not due to Hp is becoming increasingly recognized in adult and, especially, pediatric patients with
Crohns disease and UC.131-133 The most common histologic
abnormalities in IBD-associated gastritis are chronic inactive

and chronic active non-Hp gastritis. Focally enhanced gastritis
and Hp gastritis are less common. Focally enhanced gastritis
is characterized by tiny collections of lymphocytes and macrophages (histiocytes) surrounding gastric pits and glands,
often with infiltrates of neutrophils as well (Fig. 52-9). Focally
enhanced gastritis can be seen in Crohns disease (including
in Crohns patients with isolated terminal ileitis without
colitis), but not commonly in UC.131-133
Crohns Disease
Crohns disease involving the stomach is uncommon, and
usually occurs together with lower intestinal disease (see
Chapter 115). Although rare cases may be isolated to the
stomach or the stomach and duodenum, a diagnosis of isolated Crohns disease of the stomach should be made with
caution,134 and close follow-up is indicated for the subsequent
development of Crohns disease elsewhere in the GI tract or
of other granulomatous diseases such as sarcoidosis.
Symptoms of gastric Crohns are nonspecific and include
nausea and vomiting, epigastric pain, anorexia, and weight
loss. Radiologic studies show antral fold thickening, antral
narrowing, shallow ulcers (aphthae), or deeper ulcers. Involvement of the stomach from adjacent ileal or colonic disease
segments is best visualized by radiologic examination. Endoscopy allows better visualization of mucosal defects and is
characterized by reddened mucosa, irregularly shaped ulcers,
and erosions in a disrupted mucosal pattern. Nodular lesions
occur and often reveal the presence of erosions on the top of
nodules. An atypical cobblestone pattern may be associated
with the nodules surrounded by fissure-like ulceration. The
swollen folds, traversed by linear furrows or erosive fissures,
have been referred to as bamboo-joint like.135 Ulcerations or
erosions associated with Crohns disease of the stomach typically are most commonly located in the antrum and the prepyloric region. In contrast to PUD where the ulcers tend to be
round or oval, the ulcerations and erosions of Crohns disease
are frequently serpiginous or longitudinal.
The microscopic features of biopsy or surgical specimens
of gastric Crohns disease can be, but are not always, similar
to those in the ileum or colon (see Chapter 115). They include
granulomatous gastritis (see earlier section), transmural
chronic inflammation, ulcers, and marked submucosal fibrosis
(see Fig. 52-6). Granulomas may be present in endoscopically
FIGURE 52-9. Histopathology of focally enhanced gastritis. A, Low-power view of gastric mucosa showing ill-defined nodules of inflammatory cells. (H&E, 10.) B, Higher-power view shows a mixed infiltrate of lymphocytes, eosinophils, and neutrophils focally impinging
on the glandular epithelium. (H&E, 40.) (Courtesy Jonathan Baker, MD, and Pamela Jensen, MD, Dallas, Tex.)


normal antral mucosa. Focally advanced gastritis is also
common (Fig. 52-9).
Therapy of gastritis in Crohns disease should be driven
by symptoms and not solely by demonstration of gastritis
on mucosal biopsy. Double-blinded randomized controlled
clinical trials of pharmacologic agents are lacking in gastric
and duodenal Crohns disease. PPIs should be the first therapy
for symptomatic patients. The effectiveness of glucocorticoids, immunosuppressive medications, and antiTNF-
drugs has not yet been demonstrated in controlled clinical
trials, but there are reports of success with infliximab.134
Gastric outlet obstruction refractory to medical therapy can
be treated by gastroenterostomy, ideally laparoscopically.
Treatment of Crohns disease is discussed in more detail in
Chapter 115.
UC (see also Chapter 116)

The prevalence of gastritis is lower in UC than in Crohns
disease, particularly the prevalence of focally enhanced gastritis, but it is greater than in controls without IBD.131,132 In
approximately 5% of cases of UC, the endoscopic appearance
of the stomach is abnormal and similar to the appearance of
the rectum and colon. Such UC patients with ulcerative gastritis were characterized by (1) gastric histopathology similar
to colonic histopathology, (2) little or no response to acidreducing medications (H2RAs or PPIs), and (3) response of the
ulcerative gastritis to standard treatment of UC. All UC
patients with ulcerative gastritis either had pancolitis or had
had a proctocolectomy; many of the latter also had pouchitis.136,137 It has been speculated that anti-inflammatory drugs
such as glucocorticoids, commonly used in UC, may mask the
ulcerative gastritis in some patients.
GASTRITIS CYSTICA PROFUNDA

Gastritis cystica profunda (GCP) is a rare condition138-145
that can occur as a complication of partial gastrectomy with
gastrojejunostomy for PUD, typically occurring at the site
of the gastroenterostomy. GCP may also develop in the unoperated stomach. GCP can be associated with Mntriers
disease138,139 and with gastric cancer.140-143 Targeted deletion of
the subunit of the apical K+ efflux channel of the parietal cell
leads to a GCP-like lesion in mice with invasive gastric
cancer.144 Inverted hyperplastic gastric polyp may be a variant
of GCP. GCP may also be iatrogenic after attempted gastric
polypectomy.145
Gastric symptoms in GCP, if present, are nonspecific. Radiography and endoscopy typically demonstrate multiple exophytic gastric masses that simulate a malignancy. EUS may
assist in the diagnosis by demonstrating the cystic nature of
the lesions. A diagnosis of GCP should lead to a thorough
examination for a gastric cancer. Whether patients without
cancer require endoscopic surveillance for subsequent cancer
development is not clear.
GCP can be removed by snare polypectomy after submucosal injection to elevate the lesion. Endoscopic submucosal
dissection of GCP has also been reported, with removal of
coexistent early gastric cancer.140 In some cases, surgical resection will be required.
Grossly, the gastric mucosal surface demonstrates multiple nodules and exophytic masses. On section, the gastric wall
is thick and multiple cysts are present. Microscopically, the
mucosa is characterized by foveolar hyperplasia, and cystic
glands extend through a disrupted muscularis mucosa
into the submucosa and, rarely, into the muscularis propria
(Fig. 52-10).
FIGURE 52-10. Histopathology of gastritis cystica profunda. Note

the cystic dilatation of numerous gastric glands that extend
through the muscularis mucosae (arrow), simulating a gastric
carcinoma. (H&E stain).
GASTRIC GRAFT-VERSUS-HOST DISEASE

(see also Chapter 35)
Graft-versus-host disease (GVHD) most often occurs after
allogeneic bone marrow transplantation; it is less common
after solid organ transplantation. Acute GVHD occurs between
post-transplant days 21 and 100, whereas chronic GVHD
occurs after day 100. The GI tract (especially the intestine) is
commonly affected in acute GVHD. Gastric GVHD is characterized by nausea, vomiting, and upper abdominal pain
without diarrhea. Gastric mucosal biopsies may be necessary
to diagnose GVHD in patients without diarrhea and with
normal rectosigmoid biopsy specimens, especially if they have
UGI symptoms. In general, however, rectosigmoid biopsies
are more sensitive than gastric (or duodenal) biopsies in diagnosing acute GVHD.146 The basic pathologic lesion of gastric
GVHD consists of necrosis of single cells (apoptotic bodies) in
the neck region of the gastric mucosa. The necrosis consists of
an intraepithelial vacuole filled with karyorrhectic debris and
fragments of cytoplasm.
ALLERGIC GASTRITIS
Children with food allergy as diagnosed by an open elimination challenge test have no higher incidence of gastritis than
children without food allergy.147 An exception may be infants
who are allergic to cows milk protein, in whom hematemesis
and endoscopic signs of gastritis are common.148
REACTIVE GASTROPATHIES
(ACUTE EROSIVE GASTRITIS)
The epithelia cells of the gastric mucosa may be damaged by
a variety of mechanisms that do not produce a significant
inflammatory infiltrate. This injury leads to rapid epithelial
restitution (resurfacing) and also to cell regeneration with
foveolar hyperplasia. Because of the paucity of inflammatory
cells, the mentioned lesions are better referred to as reactive
gastropathy, although the term acute erosive gastritis is still
used. Reactive gastropathy occurs in approximately 15% of
endoscopic biopsies of the gastric mucosa. Its incidence
increases with age and with the presence of inflammation
elsewhere in the GI tract.149

FIGURE 52-11. Histopathology of foveolar hyperplasia, typically

seen in reactive gastropathies. The gastric pits show an elongated, corkscrew appearance. (H&E stain).
The endoscopic appearance of the gastric mucosa of

patients who exhibit reactive gastropathy demonstrates a
spectrum of reddish streaks,150 subepithelial hemorrhages,
erosions, and even acute ulcers. Acute erosions and ulcers are
frequently multiple, and the base of these lesions often stains
dark brown owing to exposure of hemoglobin to gastric acid.
Grossly, most gastric erosions and acute gastric ulcers
appear as well-defined hemorrhagic lesions 1 to 2mm in
diameter. If the insult is severe, the mucosa between the
lesions can be intensely hemorrhagic. Microscopically, an
erosion demonstrates superficial lamina propria necrosis. An
acute ulcer is an area of necrosis that extends to the muscularis
mucosa. Foveolar hyperplasia, a sign of epithelial regeneration (Fig. 52-11), is often associated with glands that have
atypical nuclei that can be misdiagnosed as dysplasia or even
carcinoma. The diagnosis of neoplasia in a background of
mucosal necrosis, cellular debris, and granulation tissue
should be made with utmost caution. The biopsy procedure
itself may induce tissue hemorrhage; thus, subepithelial hemorrhage should involve more than one fourth of a biopsy
specimen to be considered significant. Curiously, in patients
with reactive gastropathy the stomach may light up during
PET scanning.151 The most common causes of reactive gastropathy (acute erosive gastritis) are discussed below.
Medications and Toxins

Ingestion of aspirin and/or nonaspirin NSAIDs, including
COX-2selective inhibitors, are very common causes of reactive gastropathy. The relationship between NSAID gastropathy PUDs is discussed in Chapter 53. Some other medications
that can injure the stomach are listed in Table 52-3.152-155
Numerous toxins can damage the stomach, with ethanol
being the most common. After acute ethanol ingestion, subepithelial hemorrhages are seen frequently at endoscopy, typically without prominent mucosal inflammation on biopsy
specimens (Fig. 52-12). The combined effect of alcohol and an
FIGURE 52-12. Histopathology of alcoholic gastropathy. Hemorrhage is confined to the superficial portion of the mucosa, with a
paucity of inflammatory cells. (H&E stain).
TABLE 52-3 Some Medications and Toxins That May

Cause Reactive Gastropathy
Medications
Toxins
Aspirin and other NSAIDs, and

COX-2 inhibitors
Iron supplements
Fluorides
Bisphosphonates
Cancer chemotherapy drugs
Sodium phosphate (bowel
preps)
Bromazepam
Heavy metals (e.g., mercury

sulfate)
Selenium
Caustic/corrosive agents (see
Chapter 27)
Ethyl alcohol
Inhaled ketamine (recreational
use)
NSAID is associated with more gastric mucosal damage than

either agent alone. Some other causes of toxin-induced reactive gastropathy are listed in Table 52-3.
Bile Reflux
Reflux of bile into the stomach is common after operations for
peptic ulcer (see Chapter 53) or for gastric cancer.156 Bile reflux
gastropathy also may occur after cholecystectomy157 or biliary
sphincterotomy, procedures that allow the continuous exposure of bile to the duodenum with the potential for duodenogastric reflux.
Bile reflux gastropathy can also be observed in adult or
pediatric patients who have not had surgery.150,158 For example,
adult patients with dyspeptic symptoms, gastric reddish
streaks seen at endoscopy, and reactive gastropathy histologically often have bile in their stomachs.150 Children with proved
bile reflux are characterized mainly by having foveolar hyperplasia.158 Bile reflux gastropathy may eventually result in
intestinal metaplasia.157


Diagnosis of bile reflux gastropathy can be challenging
because many patients with bile in their stomach have no
symptoms. Thus, a combination of clinical, endoscopic, and
histologic findings are required, and there are no universally
agreed upon criteria for diagnosis. A bile reflux index has
been proposed based on histology (the presence of intestinal
metaplasia and tissue edema and the absence of Hp and
chronic inflammation). Using this method, patients with
GERD were found to have a higher prevalence of bile reflux
gastropathy than controls.159 A more direct approach has been
to use a gastric probe to assess the bilirubin level in the
stomach (Bilitech 2000),160 but this is a test for reflux and
not gastropathy.
Endoscopy in patients with bile reflux gastropathy shows
swelling, redness, erosions, and bile staining of the gastric
mucosa. It is uncertain whether, in patients with prior gastrectomy, coexisting Hp gastritis worsens or lessens the
endoscopic abnormalities.161,162 Biopsy specimens show foveolar hyperplasia, dilated cystic glands, atypical glands that
may be misdiagnosed as dysplasia or carcinoma, and a
paucity of acute and chronic inflammatory cells. Intestinal
metaplasia157 and gastric atrophy may result and may
increase the risk of carcinoma in the gastric stump (see
Chapter 54). Unfortunately, bile-diverting procedures performed because of severe bile gastropathy do not reverse
gastric atrophy or intestinal metaplasia. It may therefore be
worthwhile, at the time of the original gastric surgery for
gastric cancer or peptic ulcer, to construct a 30-cm Roux-enY limb or perform a 10- to 12-cm isoperistaltic jejunal interposition to try to prevent bile gastropathy and subsequent
metaplastic changes.
Treatment of bile reflux gastropathy in the intact or operated stomach is also challenging and not based on a large
number of controlled clinical trials.163-167 In a randomized trial
of bile reflux gastropathy following cholecystectomy, both the
PPI rabeprazole (20mg daily), the antacid hydrotalcite (1g 3
times daily), and especially their combination improved
symptoms and gastric histopathologic abnormalities, as well
as lessened bile reflux as assessed by Bilitec 2000 monitoring.167 Sucralfate has also been used successfully in some
studies, but not others.164,166 In most clinical trials, placebo
was not given; instead, medications were compared to observation alone. Other medical therapies for bile reflux gastropathy of questionable value include ursodeoxycholic acid and
cholestyramine.163,165 At present, lacking definitive studies,
medical therapy should precede surgical therapy for bile
gastropathy.
In patients who fail medical therapy, surgery is recommended if symptoms are severe. For patients with bile reflux
gastropathy or esophagitis following a truncal vagotomy and
gastrojejunostomy, it has been recommended that the gastrojejunostomy be dismantled. For patients with prior Billroth II
gastrectomy and gastrojejunostomy, a Roux-en-Y diversion
can be performed. Long-term results of Roux-en-Y biliary
diversion in previously unoperated and in unoperated patients
are good.168,169
Cocaine
Hemorrhage, gastric ulceration, and pyloric or pre-pyloric
perforation due to crack cocaine use is well described.170-172
Stress
Erosions of the gastric mucosa may occur rapidly after major
physical or thermal trauma, shock, sepsis, or head injury.
These are often referred to as stress ulcers and are discussed
in Chapter 53.
Radiation (see also Chapter 40)

Injury to the stomach from external ionizing radiation can
be classified as acute (<6 months) or chronic (>1 year). It is
thought that the tolerance level for radiation-induced gastropathy is approximately 4500cGy. After a gastric dose of
5500cGy or above, most patients will develop clinical evidence of gastropathy and/or gastric ulcer formation. Selective
internal radiation therapy (SIRT) with yttrium-90 microspheres infused into the hepatic artery to treat malignant liver
tumors can also lead to reactive gastropathy.173,174 Radiationinduced gastric ulcers are usually solitary, from 0.5 to 2cm in
diameter, and located in the antrum. Massive hemorrhagic
gastropathy requiring endoscopic therapy to control the
bleeding has been reported.175,176
Ischemia
Histologic changes consistent with a reactive gastropathy may
be demonstrated in patients with chronic ischemia.177 Chronic
ischemic gastropathy as well as chronic ischemic gastric ulcers
may occur secondary to chronic mesenteric insufficiency or in
association with atheromatous embolization.178,179 Athletes
involved in intense physical activity, especially long-distance
running, may experience recurrent ischemic gastropathy and
chronic GI bleeding with anemia.180
Prolapse
The mucosa of the gastric cardia may prolapse into the esophageal lumen during retching and vomiting and become
injured.181 Barium studies and esophagoscopy may demonstrate the prolapsed gastric mucosa. The prolapsed, congested
mucosa may show erosions and superficial ulcerations. One
study showed a high incidence of pathologic gastroesophageal acid reflux in patients with prolapse gastropathy.182
PORTAL HYPERTENSIVE GASTROPATHY

(see Chapter 92)
This condition represents an important cause of GI blood
loss in patients with cirrhosis.183 Gastric mucosal biopsies
show vascular ectasia and congestion without a significant
degree of inflammatory infiltrate or reactive gastropathy.
LINEAR EROSIONS WITHIN

A HIATAL HERNIA
These lesions (Camerons lesions) are discussed in Chapters
20 and 26.
HYPERPLASTIC GASTROPATHIES,
INCLUDING MNTRIERS DISEASE
Hyperplastic gastropathy is a rare condition characterized by
giant gastric folds associated with epithelial hyperplasia.184
Two clinical syndromes have been identified: (1) Mntriers
disease and a variant of it referred to as hyperplastic,
hypersecretory gastropathy, and (2) ZE syndrome, which is discussed in Chapter 33. Figure 52-13A and B demonstrates
enlarged gastric folds in these conditions. The enlarged gastric
folds in Mntriers disease are due to foveolar cell hyperplasia, edema, and variable degrees of inflammation.
Mntriers disease is typically but not always associated
with protein-losing gastropathy (see Chapter 30) and with

FIGURE 52-13. Radiologic and histopathologic Examples of hyperplastic gastropathy with giant gastric folds. A, Film from
series in a patient with ZES. B, Film from an upper GI series in a patient with Mntriers disease. C, Total gastrectomy
a patient with Mntriers disease (right: body, revealing hyperplastic mucosa and cerebriform rugal folds; left: antrum,
sparing). D, Histopathology of Mntriers disease showing enlarged folds with foveolar hyperplasia, cystically dilated
minimal gastritis.
hypochlorhydria, whereas its hyperplastic, hypersecretory

variant is associated with increased or normal acid secretion
and parietal and chief cell hyperplasia, with or without
excessive gastric protein loss. Mntriers disease has been
associated with Hp infection,185 CMV gastritis,77 and infection
with HIV.186
Other conditions more common than Mntriers disease
can also cause enlarged gastric folds,184 including gastric neoplasm (lymphoma, carcinoma), granulomatous gastritides,
gastric varices, eosinophilic gastritis, and ZE syndrome. Furthermore, pachydermoperiostosis (primary hypertrophic
osteoarthropathy) has been reported to cause a type of hypertrophic gastropathy akin to Mntriers disease,187,188 as has
primary Sjgrens syndrome.189
Affected patients may present with weight loss, epigastric
pain, vomiting, anorexia, dyspepsia, hematemesis, and positive fecal occult blood tests. Mntriers disease may be selflimited and may completely resolve in patients younger than
10 years of age or when it occurs in the postpartum period.
CMV infections can cause Mntriers disease of childhood.77
an upper GI
specimen in
with relative
glands, and
The risk of gastric cancer appears to be increased in

Mntriers disease190 (see Chapter 54). Moreover, a fibrosing variant of the disease can mimic linitis plastic gastric
cancer.191
The mucosa of patients with Mntriers disease demonstrates irregular hypertrophic folds that involve the entire
gastric corpus. The mucosa also demonstrates a swollen,
spongy appearance subdivided by creases, creating a picture
similar to cerebral convolutions. Mntriers disease can be
suspected when EUS shows thickening in the second layer
of the gastric wall (deep mucosa, normally hypoechoic) and
can be confirmed histologically by endoscopic mucosal
resection.192,193 A polypoid variant of Mntriers disease that
resembles multiple hyperplastic gastric polyps has been
described (see Chapter 54).
Gastric resection specimens from patients with Mntriers
disease typically show large polypoid gastric folds or large
cerebriform gastric folds with antral sparing (see Fig. 51-13C).
In the absence of a gastrectomy, a full-thickness gastric
mucosal biopsy is required to adequately assess the gastric


histology in patients with hyperplastic gastropathy. The predominant microscopic feature of Mntriers disease and
hyperplastic, hypersecretory gastropathy is foveolar hyperplasia with cystic dilation (see Fig. 51-13D). The parietal and
chief cells may be decreased and replaced by mucous glands
in Mntriers disease.
The etiology of Mntriers disease is unknown, although
some cases have undoubtedly been infections with CMV or
Hp. Concurrence of the disorder in identical twin men, who
presented at ages 29 and 35, suggests a genetic component.194
A germline mutation in SMAD4 associated with juvenile
polyposis can lead to a mixed hypertrophic/polypoid gastropathy.195 Hyperplasia of surface mucous cells may be due
to enhanced EGF signaling in the gastric mucosa due to local
overproduction of TGF-.196 A unifying working hypothesis
for juvenile polyposis syndrome and Mntriers disease has
been proposed.195 The authors hypothesized a mechanism
that involves TGF-SMAD4 pathway inactivation and TGF-
overexpression related to Hp infection.197
Ideal treatment of hyperplastic gastropathy is unclear
because the condition is so rare and controlled trials are
lacking. Spontaneous resolution may occur, especially in children. Ganciclovir can be used in children with Mntriers
disease associated with CMV gastritis. Hp infection should be
sought and treated, if present. Symptoms may improve with
antisecretory agents (H2RAs, anticholinergic drugs, or PPIs),198
especially if the patient has ZE syndrome or the normogastrinemic hyperplastic, hypersecretory variant of Mntriers
disease. Gastric antisecretory drugs may reduce gastric protein
loss by strengthening intercellular tight junctions.
Some patients with Mntriers disease have responded
to cetuximab (Erbitux), a monoclonal antibody against the
EGF receptor.199 Others have responded to the somatostatin
analog octreotide.200,201 Partial or total gastric resection is
reserved for severe complications such as refractory or recurrent bleeding, obstruction, severe hypoproteinemia, or cancer
development.
DIFFERENTIAL DIAGNOSIS
The most important disorders that can simulate gastritis and
reactive gastropathy are gastric polyps (neoplastic and nonneoplastic) and gastric malignancy (see Chapters 31 and 54).
Although CT criteria have been useful in distinguishing
gastritis/gastropathy from gastric malignancy,202 endoscopy
and gastric biopsy with review by an expert pathologist are
the most useful diagnostic procedures. Increased FDG uptake
by the stomach, especially the proximal half of the stomach,
is seen occasionally during PET scanning in patients with reactive gastropathy (acute erosive gastritis) and should not be
confused with neoplasia.151 Demonstration of B cell clonality
(e.g., by immunostaining) can also help distinguish gastric
marginal zone lymphomas from chronic lymphocytic gastritis
or lymphomatoid gastropathy.
TREATMENT
The treatment of gastritis and gastropathy depends on the
underlying etiology, if one can be identified. It has been shown
in a case-control study performed in a region of southeastern
China with a very high prevalence of chronic gastritis and
gastric cancer that ingestion of green tea reduced the risk of

gastritis and gastric cancer by close to 50%.203 Other proposed
treatments of patients with non-Hp gastritis and dyspepsia
include gastroprotective agents such as sucralfate, gefarnate,204 and rebamipide.205 None is approved for treatment of
gastritis/gastropathy in the United States.
KEY REFERENCES
Full references for this chapter can be found on
www.expertconsult.com.
2. Carr NJ, Leadbetter H, Marriott A. Correlation between the
endoscopic and histologic diagnosis of gastritis. Ann Diagn
Pathol 2012; 16:13-5.
21. Nordenstedt H, Graham DY, Kramer JR, et al. Helicobacter
pylori-negative gastritis: Prevalence and risk factors. Am J
Gastroenterol 2013; 108:65-71.
53. Rugge M, Correa P, Di Mario F, et al. OLGA staging for
gastritis: A tutorial. Dig Liver Dis 2008; 40:650-8.
73. Petersson F, Franzn LE, Borch K. Characterization of the
gastric cardia in volunteers from the general population.
Dig Dis Sci 2010; 55:46-53.
75. Kakugawa Y, Kami M, Matsuda T, et al. Endoscopic
diagnosis of cytomegalovirus gastritis after allogeneic
hematopoietic stem cell transplantation. World J
86. Kim K, Kim EJ, Kim MJ, et al. Clinicopathological features
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59:884-9.
106. Ranault M, Goodier A, Subramony C, et al. Age-related
differences in granulomatous gastritis: A retrospective,
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109. Dulai PS, Rothstein RI. Disseminated sarcoidosis presenting
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120. Brain O, Rajaguru C, Warren B, et al. Collagenous gastritis:
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123. Bhatti TR, Jatla M, Verma R, et al. Lymphocytic gastritis
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126. Takeuchi K, Yokoyama M, Ishizawa S, et al.
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131. Sonnenberg A, Melton SD, Genta RM. Frequent occurrence
of gastritis and duodenitis in patients with inflammatory
bowel disease. Inflamm Bowel Dis 2011; 17:39-44.
136. Hisabe T, Matsui T, Miyaoka M, et al. Diagnosis and
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167. Chen H, Li X, Ge Z, et al. Rabeprazole combined with
hydrotalcite is effective for patients with bile reflux
gastritis after cholecystectomy. Can J Gastroenterol 2010;
24:197-201.
199. Fiske WH, Tanksley J, Nam KT, et al. Efficacy of cetuximab
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883.e2 Section VI Stomach and Duodenum

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CHAPTER

Gastritis due to Hp.................................................................... 869

Gastritis Cystica Profunda..........................................................879

Crohns Disease........................................................................ 878

Medications and Toxins............................................................. 880

Portal Hypertensive Gastropathy................................................881

sites are shown in eFigure 52-1. The location of the biopsy

Chapter 52 Gastritis 868.e1

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Chapter 52 Gastritis 869

full recovery from phlegmonous or emphysematous gastritis

Diffuse antral gastritis

Chronic gastritis is much more common than acute gastritis,

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870 Section VI Stomach and Duodenum

undergoing diagnostic upper endoscopy with gastric biopsy,

Chronic Atrophic Gastritis (Gastric Atrophy)

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Chapter 52 Gastritis 871

TABLE 52-2 The Spectrum of Autoimmune (AMAG) and

Antibodies to intrinsic factor,

Hp gastritis (current, past)

Other autoimmune disorders

Potentially reversible (Hp Rx)

Serum PGI and PGI/PGII

Serum PG levels more

Normal or slight increase in

Gastric carcinoid tumors

chronic inflammation, is termed chronic atrophic gastritis, or

Environmental Metaplastic Atrophic Gastritis

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872 Section VI Stomach and Duodenum

Autoimmune Metaplastic Atrophic Gastritis

early pathogenesis of AMAG.70 It appears that cagA+/vacA+

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Chapter 52 Gastritis 873

(Fig. 52-4). Owl-eye intranuclear inclusions are the hallmark

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874 Section VI Stomach and Duodenum

Endoscopy shows numerous shallow, irregular ulcers with

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Chapter 52 Gastritis 875

The stomach is rarely affected by Strongyloides stercoralis.101

Progressive disseminated histoplasmosis is rare, occurring

Acute Aspergillus gastritis is rare and can be highly

Parasitic (see also Chapters 113 and 114)

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876 Section VI Stomach and Duodenum

tract affected in sarcoidosis, being involved in approximately

Sarcoidosis is a systemic granulomatous disease, sometimes

FIGURE 52-6. Histopathology of granulomatous gastritis in a patient

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Chapter 52 Gastritis 877

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878 Section VI Stomach and Duodenum

abnormalities in IBD-associated gastritis are chronic inactive

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Chapter 52 Gastritis 879

UC (see also Chapter 116)

GASTRITIS CYSTICA PROFUNDA

FIGURE 52-10. Histopathology of gastritis cystica profunda. Note

GASTRIC GRAFT-VERSUS-HOST DISEASE

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880 Section VI Stomach and Duodenum