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Types of Gastritis
Types of Gastritis
Types of Gastritis
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Chapter 13: Types of Gastritis
Gastric atrophy can be assessed non-invasively by measur- (GI) bleeding. On endoscopy, there are multiple 2–15 mm
ing serum pepsinogen I (PgI), which is produced and secreted diameter superficial round gastric erosions, mucosal oedema,
by chief cells, and pepsinogen II (PgII), which is produced by and petechial haemorrhages, typically in the gastric body.
oxyntic and antral mucosa. Patients with gastric atrophy have a Biopsies of acute gastritis are not common. Histology may
lower PgI/PgII ratio.2 Assessment of serum pepsinogen, gas- show acute congestion, superficial fibrin thrombi, superficial
trin, and antibodies against Helicobacter, parietal cells, and lamina propria haemorrhage, and mucosal necrosis (Figure
intrinsic factor can be combined with endoscopy and histology 13.1). Neutrophils are rare unless there is erosion. Iron pill
(of separately identified antral and corpus biopsies) in evaluat- gastritis is accompanied by grey/brown iron deposition in the
ing the distribution and aetiology of atrophic gastritis. When superficial lamina propria, which can be confirmed on Perls
corpus atrophy is associated with normal antral biopsies, a stain.
diagnosis of autoimmune gastritis is suggested and can be
confirmed clinically by the detection of antibodies to parietal Collagenous Gastritis
cells and intrinsic factor. In contrast, if the antral biopsies also
Collagenous gastritis is an extremely rare condition that may
show atrophy, then Helicobacter gastritis is the likely cause of
affect children or adults, with a female preponderance reported
the corpus atrophy, unless there is concurrent autoimmune
in adults. Patients may be asymptomatic or may present with
gastritis and Helicobacter gastritis. Intense inflammation
epigastric or abdominal pain, diarrhoea, and anaemia. The
accompanying the atrophy in the antrum and corpus suggests
atrophic autoimmune pangastritis.
Hypertrophic Gastritis
Florid foveolar hyperplasia and gastritis may be apparent in a
lymphocytic gastritis, H. pylori gastritis, or cytomegalovirus
gastritis (see later discussion). This should be distinguished
from the non-inflamed hypertrophic gastric mucosa resulting
from diffuse hyperplasia of oxyntic mucosa in Zollinger–
Ellison syndrome, florid foveolar hyperplasia without gastritis
in Ménétrier disease, and mucosal infiltration by adenocarci-
noma or lymphoma.
(A) (B)
Figure 13.2 Collagenous gastritis with (A) a thickened collagen plate highlighted on (B) Masson trichrome.
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disease may be restricted to the stomach, but patients may also Focally Enhanced Gastritis (Focally Active Gastritis)
have coeliac disease, collagenous sprue, and/or collagenous
Focally enhanced gastritis (also known as focally active gastri-
colitis.5 It may also occur following olmesartan therapy.6
tis) is characterised by discrete foci of lymphocytes, plasma
According to some reports, corpus involvement is more com-
cells, and macrophages around and within gastric foveolae and
mon in children and antrum involvement more common in
glands, particularly in the deep mucosa, in a background of
adults,7 but this is not a consistent finding.6
normal mucosa.13,14 Occasional eosinophils and neutrophils
On histology, there is surface epithelial damage, thickening
may also be present. It is more frequently present in the
of the subepithelial collagen plate (to >10 μm) with entrapped
antrum and has been described in patients with Crohn’s dis-
capillaries and inflammatory cells in the collagen plate, and an
ease or ulcerative colitis15–17 as well as in patients without
associated lymphoplasmacytic inflammatory cell infiltrate in
idiopathic inflammatory bowel disease (e.g. Helicobacter gas-
the lamina propria (Figure 13.2A). There may be prominent
tritis and following bone marrow transplantation).15,18 When
eosinophils, increased intraepithelial lymphocytes, occasional
focally enhanced gastritis is accompanied by granulomas that
neutrophils, and, uncommonly, corpus mucosal atrophy.
are not associated with disrupted glands, the possibility of
Masson trichrome stain or tenascin immunohistochemistry7
Crohn’s disease can be suggested. In children, focally enhanced
can be used to highlight the thickened collagen plate (Figure
gastritis may predict inflammatory bowel disease. However,
13.2B) and, along with Congo red, distinguishes this from gastric
focally enhanced gastritis alone should not be interpreted as a
amyloid. Lamina propria fibrosis may be seen in radiation gas-
specific marker of idiopathic inflammatory bowel disease.15
tritis or ischaemic gastritis, but in these conditions the fibrosis
diffusely involves the lamina propria and is not confined to the
subepithelial zone. Patients may respond to gluten-free diet, Granulomatous Gastritis
steroids, or withdrawal of triggering drugs (e.g. olmesartan), but Granulomas may occur in the stomach in a wide variety of
the success of current treatment options appears to be limited. diseases (Figure 13.3) (Fact Sheet 13.2). Crohn’s disease is the
most common cause in the Western world.19,20 Other causes
Eosinophilic (Allergic) Gastritis include sarcoidosis, infection (tuberculosis, syphilis,
Mycobacterium avium intracellulare, histoplasmosis, mucor-
This is a rare entity characterised by a prominent eosinophil
mycosis, anisakiasis, schistosomiasis, Whipple’s disease), reac-
infiltrate in the wall of the stomach. It may be isolated to the
tion to foreign or endogenous materials, vasculitis, chronic
stomach, but often occurs as part of an eosinophilic
granulomatous disease, Langerhans cell histiocytosis, and
gastroenterocolitis.8 Patients may have a history of allergic
malignancy. A proposed association with Helicobacter
disease such as asthma, food intolerance or atopic eczema, a
infection21,22 is questioned by many authors.19,23,24
peripheral eosinophilia, and raised serum IgE.
In Crohn’s disease, the granulomas may be associated with
The eosinophil infiltrate is maximal and diffuse in the
focally enhanced gastritis (see above). In sarcoidosis, the com-
antrum, whereas corpus involvement is less frequent and
pact epithelioid granulomas may be present in the absence of
tends to be patchy if present.9 The eosinophil infiltrate is
any other inflammation. Central necrosis may be seen in the
typically predominantly submucosal but may involve any
granulomas of mycobacterial or fungal infection, eosinophils
layer of the stomach wall. Patients present with nausea and
may be prominent with parasitic infection, and food debris
vomiting, abdominal pain, diarrhoea, failure to thrive, or
(when there is involvement of the muscularis propria) gastric
outlet obstruction. Fact Sheet 13.1 Some Causes of Gastric Eosinophil
When there is gastric mucosal involvement, there is a Infiltrates
marked eosinophil infiltrate (20–30 eosinophils per high-
• Eosinophilic/allergic gastroenterocolitis
power field) in the lamina propria with intraepithelial eosino-
• Parasitic infection
phils and eosinophil gland abscesses.10 There may be epithelial
damage and erosions, but there are few, if any, other inflamma- • Helicobacter gastritis
tory cells. • Other infections
Eosinophils may be present in the gastric mucosa in other • Drug reactions
conditions (Fact Sheet 13.1) such as parasitic infection, • Autoimmune gastritis
Helicobacter gastritis, autoimmune gastritis, Crohn’s disease, • Collagenous gastritis
connective tissue disorders, drug reactions, inflammatory • Crohn’s disease
fibroid polyp, and malignancy (e.g. adenocarcinoma, lym- • Connective tissue disorders
phoma, Langerhans cell histiocytosis, systemic mastocytosis).11 • Inflammatory fibroid polyp
In these entities, the eosinophils are a component of a mixed • Neoplasia
inflammatory cell infiltrate, rather than a ‘pure’ infiltrate as seen
• Adenocarcinoma
in eosinophilic gastritis. However, it is always prudent to con-
• Lymphoma
sider and exclude these other possibilities before making a
diagnosis of eosinophilic gastritis. Therapeutic options for eosi- • Langerhans cell histiocytosis
nophilic gastritis include dietary restriction, antihistamines, • Systemic mastocytosis
steroids, and (for persistent gastric outlet obstruction) surgery.12
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Chapter 13: Types of Gastritis
(A) (B)
Figure 13.3 Granulomatous gastritis with (A) antral mucosal and (B) corpus mucosal granulomas.
Crohn’s disease
Sarcoidosis
Infection
• Tuberculosis
• Syphilis
• Mycobacterium avium intracellulare
• Histoplasmosis
• Mucormycosis
• Anisakiasis
• Schistosomiasis
• Whipple’s disease
• Helicobacter infection (controversial)
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Ischaemic features can be seen in mucosal biopsies taken from and up to 30% of patients with coeliac disease will have lym-
the vertical linear erosions (so-called Cameron lesions) that occur phocytic gastritis that is antral predominant.34,36 The associa-
in large sliding hiatus hernias and result from vascular compres- tion between H. pylori and lymphocytic gastritis seems to be
sion of the hiatus hernia by the diaphragm.30 Clinicopathological restricted to those cases in which there is a significant neutro-
correlation is required to distinguish these erosions from other phil infiltrate.37 Whenever there is a lymphocytic gastritis, the
potentially life-threatening causes of ischaemic gastritis. pathologist should look for H. pylori (with special stains or
immunohistochemistry, if necessary) and when the lymphocy-
Lymphocytic Gastritis tic gastritis is antral-predominant, it is prudent to suggest that
a duodenal biopsy should be performed to exclude coeliac
Lymphocytic gastritis, characterised by increased intraepithe-
disease.
lial lymphocytes (IELs), is not a distinct entity but a type of
Lymphocytic gastritis may also be associated with a lym-
gastritis that has numerous aetiologies (Fact Sheet 13.3).31 It is
phocytic enterocolitis,38 Crohn’s disease, Ménétrier disease,
uncommon and occurs more frequently in women.32 Patients
HIV, common variable immunodeficiency, medication (e.g.
may be asymptomatic or may present with anorexia, epigastric
toclopidine or olmesartan),39,40 and gastric malignancy (lym-
pain, and sometimes weight loss and a protein-losing gastro-
phoma or adenocarcinoma).26 However, many cases are idio-
enteropathy. The stomach may be endoscopically normal,
pathic, with no known association.
hypertrophic with thickened folds, or show numerous ‘vol-
Lymphocytic gastritis may resolve spontaneously but can
cano-like’ erosions (given the term varioliform gastritis), par-
persist for many years. Some patients may respond to a gluten-
ticularly in the corpus. On histology, there are more than 25
free diet41 or H. pylori eradication, while those with medica-
IELs/100 epithelial cells in the surface and foveolar epithelium
tion-induced lymphocytic gastritis may respond to withdrawal
(Figure 13.5A), while the deeper epithelium is spared.33,34
of the medication.
These intraepithelial lymphocytes express CD3 and CD8 on
immunohistochemistry (Figure 13.5B). There is accompanying
chronic inflammation (lymphocytes, plasma cells, eosinophils, Reactive Gastritis
and mast cells) in the lamina propria, which can be minimal or The terms reactive gastritis or gastropathy, chemical gastritis
quite marked, and there may be neutrophils, particularly when or gastropathy, and reflux gastritis or gastropathy have typi-
erosions are present. Lymphocytic gastritis commonly involves cally been used interchangeably to describe the appearance
the whole stomach but may be restricted to the corpus or seen when the gastric mucosa is subjected to a range of insults,
antrum. Patients with evidence of protein loss may have hyper- most usually reflux of alkaline duodenal contents / bile or
trophic lymphocytic gastritis, characterised by hypertrophic drugs in the form of NSAIDs. Other rarer associations, includ-
gastric folds and florid foveolar hyperplasia resembling ing with ischaemia, have been noted.42
Ménétrier disease. The histological features of reactive gastritis are foveolar
Lymphocytic gastritis is associated with Helicobacter pylori hyperplasia (with or without reactive epithelial changes), vas-
infection in 20% of cases and coeliac disease in up to 40% of cular congestion, oedema, smooth muscle fibres in the super-
cases.32,34,35 Conversely, 4% of patients with H. pylori infection ficial lamina propria between the foveolae, and little or no
will have a lymphocytic gastritis that is corpus predominant, accompanying inflammation (Figure 13.6).43 In some cases,
(A) (B)
Figure 13.5 Lymphocytic gastritis with chronic inflammation in the lamina propria and (A) increased intraepithelial lymphocytes confirmed on (B) CD3
immunohistochemistry.
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Chapter 13: Types of Gastritis
General
• Uncommon; female > male
• Characterised by increased intraepithelial lymphocytes
(IELs)
• Not a distinct entity; has numerous aetiologies
Endoscopy
• Normal/hypertrophic with thickened folds/numerous
‘volcano-like’ erosions (varioliform gastritis), particularly in
the corpus
Histology
• Often involves whole stomach; may be restricted to corpus
or antrum
• 25 IELs/100 epithelial cells in surface and foveolar
epithelium; deeper epithelium is spared
• IELs: CD3+ CD8+
• Lamina propria chronic inflammation (lymphocytes, plasma Figure 13.6 Reactive gastritis with typical corkscrew foveolar hyperplasia.
cells, eosinophils, mast cells)
• Neutrophils, particularly when erosions are present
• Hypertrophic lymphocytic gastritis (LG) may occur: erosion with associated inflammation, infection with H. pylori,
hypertrophic gastric folds and florid foveolar hyperplasia or intestinal metaplasia.45
resembling Ménétrier disease; protein loss common
The diagnosis of reactive gastritis should not usually present
Associations a significant challenge histologically. However, pathologists
• Helicobacter pylori infection in 20% of LG have different thresholds for calling a biopsy ‘mild reactive
• Coeliac disease in up to 40% of LG gastritis’ rather than normal. Different mucin immunohisto-
• 4% of patients with Helicobacter pylori infection have LG chemical profiles have been demonstrated between reactive
(corpus-predominant) gastritis and H. pylori gastritis, but the clinical utility of this
• 30% of patients with coeliac disease have LG (antral- investigation is uncertain.46 Distinguishing reactive gastritis
predominant) from a hyperplastic polyp may be difficult if endoscopic findings
• Lymphocytic enterocolitis are not available. Up to 20% of hyperplastic polyps may show a
• Crohn’s disease reactive gastritis in the background stomach.47 Ménétrier dis-
• Ménétrier disease ease may also be included in the differential diagnosis. Florid
• HIV foveolar hyperplasia may resemble dysplasia.
• Common variable immunodeficiency
• Medication (e.g. toclopidine or olmesartan) Russell Body / Mott Cell Gastritis
• Gastric malignancy (lymphoma or adenocarcinoma) Russell body gastritis was first described by Tazawa and
• No demonstrable association in many cases Tsutsumi in 1998.48 The lamina propria of the gastric mucosa
is infiltrated by abundant Mott cells, i.e. plasma cells containing
Russell bodies (spherical eosinophilic intracytoplasmic inclu-
sions resulting from the accumulation of immunoglobulins
Practice Points 13.1 Lymphocytic Gastritis within the rough endoplasmic reticulum) (Figure 13.7). The
plasma cells do not show cellular atypia or mitotic figures, and
• If LG is observed, Helicobacter pylori should be sought by
do not show Ki67-immunopositivity. Most cases have H. pylori
the pathologist (with special stains or
immunohistochemistry, if necessary).
gastritis with accompanying lymphocytes, eosinophils, neutro-
phils, and organisms in the surface mucus. In other cases, the
• When LG is antral predominant, a duodenal biopsy to
exclude coeliac disease is advisable.
Mott cells are the only inflammatory cells in the lamina propria.
In initial reports, the Mott cells were shown to be polyclonal.
However, several more recent reports describe monoclonal Mott
cells (typically kappa light chain restricted) while the plasma
tablet debris or bile entrapped adjacent to the surface may cells that lack Russell bodies are polyclonal.49,50
identify the aetiology. The diagnostic criteria have not changed Patients may present with dyspepsia and epigastric pain,
significantly since their initial description, and a more recent and, on endoscopy, have erosive or nodular gastritis or a
study using a visual analogue scale scoring system has again discrete lesion (the latter due to a localised accumulation of
revalidated them.44 Reactive gastritis may be complicated by Russell body-containing plasma cells). The antrum is the most
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(A) (B)
Figure 13.7 Russell body gastritis with (A) abundant Mott cells in the lamina propria (B) more readily visible at higher power.
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Chapter 13: Types of Gastritis
(A) (B)
Figure 13.8 Autoimmune gastritis with (A) chronic inflammation, loss of parietal cells, and mucosal atrophy and (B) pseudopyloric metaplasia and intestinal
metaplasia.
micronodular ECL-cell hyperplasia (Figure 13.10), adenomatoid The differential diagnosis for autoimmune gastritis
ECL-cell hyperplasia (when there are clusters of five or more includes H. pylori gastritis and atrophic autoimmune pan-
micronodules), ECL-cell dysplasia (when micronodules fuse gastritis (Table 13.1). The inflammation in Helicobacter
together), and type 1 neuroendocrine (carcinoid) tumours gastritis is typically predominantly antral, in a superficial
when these fused nodules form a lesion >5 mm in diameter. location in the mucosa, includes neutrophils, and not
As well as neuroendocrine tumours, patients with autoim- accompanied by ECL-cell hyperplasia. However, H. pylori
mune gastritis can develop other types of polyp.60 The inflam- may lead to autoantibodies against parietal cells.66 Atrophic
matory changes and atrophy can be patchy, resulting in islands autoimmune pangastritis involves the antrum as well as the
of residual normal oxyntic mucosa (Figure 13.11) that may give corpus, and is also characterised by transmucosal inflam-
the impression of polyps.61 Hyperplastic polyps, intestinal type mation, but may have abundant neutrophils as well as
adenomas, and pyloric gland adenomas may also occur.62 increased intraepithelial lymphocytes. The inflammation in
Patients with pernicious anaemia have an increased risk of autoimmune atrophic pangastritis persists even when there
gastric (intestinal type) adenocarcinoma,63,64 but the increase is severe atrophy, in contrast to autoimmune gastritis and
may be related to coexistent H. pylori infection.65 Helicobacter gastritis. Lymphoplasmacytic infiltration of the
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deep lamina propria of the stomach may also be a manifes- lymphocytes, prominent apoptotic bodies, and loss of parietal
tation of IgG4-related disease, according to recent reports.67 cells (Figure 13.12). There may be ulceration, but there is no
evidence of H. pylori. In contrast to autoimmune gastritis, the
Atrophic Autoimmune Pangastritis intense inflammation persists even when there is severe atrophy
and there is no ECL-cell hyperplasia. Treatment comprises
In contrast to autoimmune gastritis, atrophic autoimmune pan-
immunosuppressive therapy.
gastritis (first described by Jevremovic et al. in 2006)68 involves
the antrum as well as the corpus. Patients present with nausea and
vomiting, abdominal pain, diarrhoea, and protein loss. Patients Infectious Gastritis
may have other systemic autoimmune diseases (e.g. systemic Helicobacter pylori infection is the most common cause of
lupus erythematosus, coeliac disease, or autoimmune haemolytic bacterial gastritis. However, bacterial infection may also lead
anaemia) and/or autoimmune enteropathy with anti-goblet cell to the rare entities of emphysematous gastritis and phlegmo-
and anti-enterocyte antibodies.69 It is characterised by intense nous gastritis. Gastric viral, fungal, or parasitic infections, as
lymphoplasmacytic inflammation that involves the superficial well as tuberculosis and syphilis, are also uncommon and are
and deep lamina propria and is accompanied by neutrophils, usually a manifestation of disseminated infection.
including gland microabscesses, increased intraepithelial
Helicobacter pylori Gastritis
Helicobacter pylori infection typically causes a superficial
chronic active gastritis (Figure 13.13) that may be complicated
by atrophic gastritis and also by gastric adenocarcinoma and
MALT lymphoma (hence the designation of H. pylori as a
carcinogen).70,71 The prevalence of H. pylori infection, which
is transmitted through the faeco-oral and oro-oral routes,
varies widely throughout the world, with a high prevalence in
developing countries.72,73 With the emergence of antibiotic-
resistant H. pylori strains and the knowledge that eradication of
infection does not always prevent the progression of gastric
pathology, current research is using in vivo and ex vivo models
to investigate the mechanisms underlying H. pylori–induced
gastric pathology and to evaluate new therapeutic strategies.73
Acute H. pylori infection is usually self-limited and, conse-
quently, endoscopy and biopsy are not usually performed.
Endoscopy in chronic infection may detect antral predominant
erythema, nodules, erosions, or ulceration.
Figure 13.11 Autoimmune gastritis with residual normal oxyntic mucosa On histology, chronic H. pylori gastritis is characterised by
which may give the endoscopic impression of a polyp. a superficial, chronic active gastritis in the antrum with a
(A) (B)
Figure 13.12 Atrophic autoimmune pangastritis with (A) transmucosal chronic inflammation, loss of parietal cells and (B) gland microabscesses and increased
intraepithelial lymphocytes.
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Figure 13.14 Helicobacter pylori demonstrated by immunohistochemistry. Figure 13.15 Helicobacter heilmannii are much larger organisms than
Helicobacter pylori and do not adhere to the epithelial cells.
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Chapter 13: Types of Gastritis
Practice Points 13.2 Helicobacter pylori the vomitus, which may be pathognomonic.91 Imaging reveals
diffuse thickening of the gastric wall. On endoscopy, there is
• Avoid overdiagnosing prominent lymphoid tissue as enlargement or flattening of the rugal folds with marked sub-
lymphoma mucosal oedema.
• Assess all biopsies that show Helicobacter pylori gastritis for Histologically, the mucosa is usually intact and there is
intestinal metaplasia, atrophy, dysplasia, adenocarcinoma, florid oedema and neutrophil infiltration of the submucosa
and MALT lymphoma. with microabscesses. A Gram stain will demonstrate the bac-
teria in the submucosa. Thrombosis in the mural vessels can
lead to secondary ischaemic necrosis with transmural inflam-
mation, necrosis of the muscularis propria, and sometimes
H. pylori and non–H. pylori gastritis are common in such perforation.93 The recommended treatment is either conserva-
specimens.86,87 There are no specific special recommendations tive (with antibiotics) and/or localised or total resection.
for dealing with preoperative biopsies or the resected speci- Phlegmonous gastritis can be distinguished from emphy-
mens other than establishing if H. pylori are present or not. sematous gastritis by the lack of gas bubbles in the wall of the
stomach.
Emphysematous Gastritis
Emphysematous gastritis is a rare and commonly fatal disease Viral Gastritis
caused by invasion of the gastric wall by gas-producing organ- Cytomegalovirus (CMV) is the most common viral infection
isms such as Clostridium, Escherichia coli, Streptococcus, of the stomach and occurs in young children and immuno-
Enterobacter, and Pseudomonas aeruginosa.88 Patients present compromised adults (e.g. those with HIV or post-transplant)
with an acute abdomen and systemic toxicity and may have (see also Chapter 4). It may coexist with graft-versus-host
haematemesis and melaena. Imaging reveals intramural gas disease (GvHD) and may also occur in immunocompetent
bubbles. Emphysematous gastritis may result from a septic patients. Patients may be asymptomatic or present with epi-
focus in the gastric wall as a consequence of alcohol abuse, gastric pain, nausea and vomiting, or haematemesis. On endo-
ingestion of NSAIDs or corrosive agents, recent abdominal scopy, the mucosa may be normal or there may be nodules,
surgery, or pancreatitis, and is more common in immunocom- erosive gastritis, and ulcers. Gastric outlet obstruction, per-
promised patients. Whether the bacteria enter the stomach foration, and gastrocolic fistula formation have also been
wall through mucosal ulceration and/or by haematogenous described.94,95 Children may have a hypertrophic gastropathy
spread to the stomach is uncertain. and protein-losing enteropathy resembling Ménétrier disease.96
Macroscopically, the gastric wall feels crepitant because of On histology, the gastric mucosa may be normal but contain
the presence of the intramural gas bubbles. On histology, there occasional CMV inclusions, or there may be marked inflamma-
may be ulceration, mucosal necrosis, transmural oedema, tion and ulceration with abundant CMV inclusions (Figure
transmural neutrophils, and numerous gas-filled spaces with 13.16A). CMV inclusions may be intranuclear (with classical
or without a giant cell reaction. In advanced disease, the entire ‘owls’ eye’ appearance) or intracytoplasmic (eosinophilic and
stomach wall may be gangrenous and necrotic. Treatment is granular) and can be found in epithelial, endothelial (Figure
either conservative or by surgical resection.89 13.16B or stromal cells either on routine H&E staining or
The differential diagnosis includes gastric emphysema, when immunohistochemistry.
gas enters the stomach wall following gastric mucosal trauma Herpes simplex virus gastritis is rare97 and occurs in
(e.g. vomiting, endoscopy, or nasogastric tube insertion) or immunocompromised individuals. On endoscopy, there may
ruptured pulmonary emphysematous blebs, and phlegmonous be oedematous nodules or ulcers. On histology, there is acute
gastritis (see the section that follows). Patients with gastric and chronic inflammation with ulceration. Herpes simplex viral
emphysema are not septic, do not have transmural oedema inclusions are found in the gastric epithelial cells and are
and neutrophils, and have a good prognosis.90 Although phleg- demonstrable on H&E staining or with immunohistochemistry.
monous gastritis is characterised by predominantly submucosal Herpes varicella zoster viral infection may occur in the
oedema and neutrophilic inflammation, there is no intramural stomach and may be detected by immunohistochemistry or
gas. molecular testing.98
Epstein–Barr virus (EBV) infection rarely affects the sto-
Phlegmonous Gastritis mach, where it may be misdiagnosed as lymphoma. Patients
This is an extremely rare form of gastritis, is often fatal, and is with acute EBV infection may not have GI symptoms or may
caused by suppurative bacterial infection of the submucosa of present with epigastric pain and nausea. Gastric ulcers are
the stomach. The most common organism is haemolytic strep- apparent on endoscopy.99,100 On histology, there is ulceration
tococcus. Predisposing factors include mucosal injury (e.g. and expansion of the lamina propria by a diffuse atypical
following endoscopy), diabetes mellitus, chronic alcoholism, lymphoid infiltrate composed of small, intermediate-sized,
and immunocompromise, but phlegmonous gastritis may also and large lymphocytes with immunoblast-like cells.
occur in previously healthy individuals.91,92 Patients present Neutrophils are scanty, even when ulceration is present, and
with acute epigastric pain, nausea and vomiting, fever, and there are no lymphoid follicles or H. pylori. On immunohisto-
signs of sepsis. Occasional patients may present with pus in chemistry, this lymphoid infiltrate is composed of a mixture of
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(A) (B)
Figure 13.16 Cytomegalovirus gastritis with (A) abundant viral inclusions in granulation tissue and (B) occasional inclusions in mucosal endothelial cells.
Fungal Gastritis
Fungal infection of the stomach is rare and may be localised to
the stomach or occur as part of a disseminated infection.
Candida is the most common cause of fungal gastritis and
occurs as an opportunistic infection in immunocompromised
individuals and in patients with chronic alcoholism, malnutri-
tion, malignancy, or severe atrophic gastritis and
achlorhydria.101,102 Candida may also colonise chronic peptic
ulcers in immunocompetent individuals.103 On endoscopy,
there may be pale yellow/white mucosal membranes, warty
nodules, or ulceration. On histology, fungal hyphae and spores
are present within ulcer slough and hyphae are seen infiltrating
the ulcer base. Hyphae may invade vessel walls leading to Figure 13.17 Gastric giardia seen on the surface of the antral mucosa.
thrombosis or rupture and haemorrhage. Other gastric fungal
infections include mucormycosis (see Figure 18.17), where the
broad, non-septate branching hyphae may infiltrate the ulcer immunocompromised patients. In the stomach the organisms
base and vessel walls;104 Histoplasma capsulatum (see Figure are apparent on the luminal border, with accompanying
18.19), where the organisms are present in macrophages;105,106 inflammation in the lamina propria. Involvement of the
Cryptococcus neoformans (see Figure 4.2);107,108 and antrum is more common than in the corpus.110 Gastric tox-
Pneumocystis jiroveci (see Figure 4.3).109 Fungal gastritis may oplasmosis has been described in immunocompromised
occasionally be associated with granulomas. Special histo- patients with disseminated disease111 and as isolated gastric
chemistry may highlight the fungal elements, e.g. periodic infection.112 Infected patients may have a normal endoscopy or
acid–Schiff diastase (PASD) and Grocott–Gomori methena- thickening of the gastric folds. The trophozoites can be identi-
mine silver for histoplasmosis, and Masson–Fontana for fied in epithelial, endothelial, or stromal cells. Anisakiasis
Cryptococcus. (which may be associated with granulomatous inflammation),
Strongyloides (Figure 18.26), Schistosoma (Figures 18.27 and
22.8), and Ascaris lumbricoides (Figure 18.24) infections have
Parasitic Gastritis all been described in the stomach. Giardia can occasionally be
Patients with parasitic infections of the stomach may have a present in the surface mucus of gastric antrum (Figure 13.17),
non-specific active chronic gastritis or abundant mucosal eosi- which may be normal or have intestinal metaplasia, in patients
nophils. Cryptosporidiosis (Figure 18.22) occurs in with duodenal infection.113
198
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Tim Andrews and Fiona Campbell
(A) (B)
Figure 13.18 Iron pill gastritis with (A) grey-brown crystalline material on the surface that is (B) Perls positive.
has been described in association with fatal upper GI haemor- undergone renal transplant. In the stomach, it may cause a
rhage. However, the histological changes are non-specific.123 florid reactive gastritis with associated granuloma formation.
There is debate about the most effective way to administer The GvHD-like changes reported at other sites have not been
NSAIDs (including whether they should be taken with food, identified in the gastric mucosa.128–130
the need for additional gastro-protective medications, and the Infliximab is a tumour necrosis factor-α inhibitor used in
most appropriate drug and formulation to use), and whether the treatment of inflammatory conditions, including rheuma-
there is an association (positive or negative) between NSAIDs toid arthritis and Crohn’s disease. It may cause lymphocytic
and coexisting H. pylori infection.124 There is also interest in gastritis and eosinophilic gastritis.131
the evolving field of pharmacogenomics where the presence or
absence of a certain polymorphism in a metabolising enzyme
may be associated with the side-effect profile of a given drug Gastritis Associated with Novel
such as NSAIDs.125 These are all clinically important consid- Immunomodulatory Agents
erations but do not influence the histological picture, and the Several ‘novel’ agents which target a range of immune func-
reader is directed to the relevant literature. tions, including specific T-cell surface molecules, are now used
commonly to treat a range of solid tumours such as malignant
Other Drugs Associated with Specific Inflammatory melanoma and non–small-cell lung cancer. These agents seem
Changes in the Gastric Mucosa to be responsible for a range of deleterious effects on the GI
tract mucosa, and commonly cause diarrhoea. While much of
Doxycycline is a tetracycline antibiotic that has been asso-
the literature focuses on changes in the lower GI tract, small
ciated with ulceration in the upper GI tract. Several studies
studies and case reports have described changes in the gastric
have described a characteristic pattern of injury, including
mucosa. These include inflammation with prominent neutro-
vascular degeneration in superficial capillaries with associated
phils and, in some cases, gland abscesses (associated with
perivascular oedema, endotheliitis, and fibrin microthrombi.
Ipilimumab, Pembrolizumab, and Nivolumab),132 lymphocy-
These findings have not been reported in patients with other
tic gastritis (Pembrolizumab and Durvalumab),133 and acute
forms of ulceration.126,127
haemorrhagic/erosive gastritis (Nivolumab).134 Increased
Olmesartan is an angiotensin II inhibitor used in the treat-
apoptotic debris may be seen in some cases.134a The possibility
ment of hypertension and appears to cause significant GI side
that gastric mucosal changes could be therapy-related should
effects more often than other agents in this class. The effects are
always be considered when there is such a drug history.
typically duodenal (mimicking collagenous sprue / coeliac dis-
ease) or ileocolonic, but rare associations with lymphocytic/
collagenous gastritis have been reported.6,40 Radiotherapy- and Chemotherapy-Associated
Gastritis Associated with Immunosuppressive Gastric Mucosal Injury
Radiation for upper abdominal neoplasia such as oesophageal
Agents cancer or pancreatic cancer135,136 may lead to gastric injury,
Mycophenolate mofetil is an immunomodulatory drug used which can take the form of acute gastritis, deep acute ulcers, or
in several conditions including in patients who have chronic ulceration (see also Chapter 3).137–140
200
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Chapter 13: Types of Gastritis
Acute radiation gastritis may occur a few days to a few Ectopic radioembolic 90Y microspheres in the gastric mucosal
months after radiation exposure and is characterised by degen- and submucosal vessels produce ulceration as a consequence of
erative changes in the gastric epithelium, oedematous and localised chronic ischaemic injury.
hyalinised lamina propria, telangiectasia, and submucosal ‘Conventional’ chemotherapy agents such as 5-flurouracil
oedema. There is swelling of endothelial cells, a reduction in (5-FU) are also associated with a range of mucosal changes
the size of the vessel lumina, coagulative mucosal necrosis, and including florid ulceration. The appearances are drug and dose
superficial ulceration. This usually resolves within 2–3 months dependent and there may be degenerative and regenerative
with regeneration of the mucosa, but there may be residual changes that are florid enough to create a diagnostic dilemma
atrophy, fibrosis, atypical radiation fibroblasts, and with relationship to dysplasia/malignancy.142 So-called ‘radia-
endarteritis. tion recall’ gastritis describes the situation where previous
Deep acute ulcers may develop 1–2 months after radiation radiation therapy results in more severe damage than would
exposure as a consequence of vascular damage ischaemia with otherwise have been expected when chemotherapy is subse-
endothelial proliferation, fibrinoid necrosis, and radiation quently administered.
fibroblasts. Chronic ulceration may occur a few months to
several years after radiation exposure and is a result of ischae- Recreational Drugs
mia caused by fibrous obliteration of blood vessels. The
The literature related to illicit and recreational drugs is extre-
chronic ulcers resemble peptic ulcers, are usually solitary,
mely sparse, perhaps because their effects do not come to
and occur more frequently in the antrum. There is fibrosis,
medical attention or because there are effects more cata-
which may be glassy/hyalinised, bizarre radiation fibroblasts,
strophic than those on the stomach. ‘Gastritis’ not otherwise
telangiectasia, atypical endothelial cells in capillaries, and hya-
specified may occur in association with inhalational ketamine
linised arterial walls.
use (with symptoms resolving on drug cessation).143 Gastric
Intra-arterial radiation therapy (where yttrium-90–contain-
perforation associated with crack cocaine use is also well
ing microspheres are implanted permanently into primary or
described.144
secondary malignant tumours in the liver, via the hepatic artery)
may lead to gastric ulceration in up to 30% of patients.141
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