Pathophysiology

The pathophysiology of chronic gastritis complicating a systemic disease, such as hepatic

cirrhosis, uremia, or an infection, is described in the articles specifically dealing with these
diseases. The pathogenesis of the most common forms of gastritis is described below.

H pyloriassociated chronic gastritis

Helicobacter pylori is the leading cause of chronic gastritis, peptic ulcer disease, gastric
adenocarcinoma and primary gastric lymphoma. First described by Marshall and Warren in 1983,
H pylori is a spiral gram-negative rod that has the ability to colonize and infect the stomach. The
bacteria survive within the mucous layer that covers the gastric surface epithelium and the upper
portions of the gastric foveolae. The infection is usually acquired during childhood. Once present
in the stomach, the bacteria passes through the mucous layer and becomes established at the
luminal surface of the stomach causing an intense inflammatory response in the underlying
tissue.[2, 7, 8, 9]

The presence of H pylori is associated with tissue damage and the histologic finding of both an
active and a chronic gastritis. The host response to H pylori and bacterial products is composed
of T and B lymphocytes, denoting chronic gastritis, followed by infiltration of the lamina propria
and gastric epithelium by polymorphonuclear leukocytes (PMNs) that eventually phagocytize the
bacteria. The presence of PMNs in the gastric mucosa is diagnostic of active gastritis.[10, 11]

Interaction of H pylori with the surface mucosa results in the release of interleukin (IL)-8, which
leads to recruitment of PMNs and may begin the entire inflammatory process. Gastric epithelial
cells express class II molecules, which may increase the inflammatory response by presenting H
pylori antigens, leading to the activation of numerous transcription factors, including NF-kB,
AP-1 and CREB-1. This in turn leads to further cytokine release and more inflammation. High
levels of cytokines, particularly tumor necrosis factor- (TNF-)[12] and multiple interleukins (eg,
IL-1, IL-6, IL-8, IL-10, IL-12, IL-17 and IL-18), are detected in the gastric mucosa of patients
with H pylori gastritis.[10, 11]

Leukotriene levels are also quite elevated, especially the level of leukotriene B4, which is
synthesized by host neutrophils and is cytotoxic to gastric epithelium.[13] This inflammatory
response leads to functional changes in the stomach, depending on the areas of the stomach
involved. When inflammation affects the gastric corpus, parietal cells are inhibited, leading to
reduced acid secretion. Continued inflammation results in loss of parietal cells, and the reduction
in acid secretion becomes permanent.

Antral inflammation alters the interplay between gastrin and somatostatin secretion, affecting G
cells (gastrin-secreting cells) and D cells (somatostatin-secreting cells), respectively. Specifically,
gastrin secretion is abnormal in individuals who are infected with H pylori, with an exaggerated
meal-stimulated release of gastrin being the most prominent abnormality.[14]
When the infection is cured, neutrophil infiltration of the tissue quickly resolves, with slower
resolution of the chronic inflammatory cells. Paralleling the slow resolution of the monocytic
infiltrates, meal-stimulated gastrin secretion returns to normal.[15]

Various strains of H pylori exhibit differences in virulence factors, and these differences
influence the clinical outcome of H pylori infection. People infected with H pylori strains that
secrete the vacuolating toxin A (vacA) are more likely to develop peptic ulcers than people
infected with strains that do not secrete this toxin.[16]

Another set of virulence factors is encoded by the H pylori pathogenicity island (PAI). The PAI
contains the sequence for several genes and encodes the CAGA gene. Strains that produce CagA
protein (CagA+) are associated with a greater risk of development of gastric carcinoma and
peptic ulcers. However, infection with CagA- strains also predisposes the person to these
diseases.[17, 18, 19, 20]

H pylori- associated chronic gastritis progresses according to the following 2 main topographic
patterns, which have different clinical consequences:

Antral predominant gastritis This is characterized by inflammation and is mostly

limited to the antrum; individuals with peptic ulcers usually demonstrate this pattern

Multifocal atrophic gastritis This is characterized by the involvement of the corpus and
gastric antrum with progressive development of gastric atrophy (loss of the gastric
glands) and partial replacement of gastric glands by an intestinal-type epithelium
(intestinal metaplasia); individuals who develop gastric carcinoma and gastric ulcers
usually demonstrate this pattern.

As previously mentioned, 50% of the world's population is infected with H pylori. The
overwhelming majority of those infected do not develop significant clinical complications and
remain carriers with asymptomatic chronic gastritis. Some individuals who carry additional risk
factors may develop peptic ulcers, gastric mucosaassociated lymphoid tissue (MALT)
lymphomas, or gastric adenocarcinomas.

An increased duodenal acid load may precipitate and wash out bile salts, which normally inhibit
the growth of H pylori. Progressive damage to the duodenum promotes gastric foveolar
metaplasia, resulting in sites for H pylori growth and more inflammation. This cycle renders the
duodenal bulb increasingly unable to neutralize acid entering from the stomach until changes in
the bulb structure and function are sufficient for an ulcer to develop. H pylori can survive in
areas of gastric metaplasia in the duodenum, contributing to the development of peptic ulcers.[8]

MALT lymphomas may develop in association with chronic gastritis secondary to H pylori
infection. The stomach usually lacks organized lymphoid tissue, but after infection with H
pylori, lymphoid tissue is universally present. Acquisition of gastric lymphoid tissue is thought to
be due to persistent antigen stimulation from byproducts of chronic infection with H pylori.[21]
The continuous presence of H pylori results in the persistence of MALT in the gastric mucosa,
which eventually may progress to form low- and high-grade MALT lymphomas. MALT
lymphomas are monoclonal proliferations of neoplastic B cells that have the ability to infiltrate
gastric glands. Gastric MALT lymphomas typically are low-grade T-celldependent B-cell
lymphomas, and the antigenic stimulus of gastric MALT lymphomas is thought to be H pylori.

Another complication of H pylori gastritis is the development of gastric carcinomas, especially in

individuals who develop extensive atrophy and intestinal metaplasia of the gastric mucosa. It is
well accepted that a multistep process initiated by H pylori related chronic inflammation of the
gastric mucosa progresses to chronic atrophic gastritis, intestinal metaplasia, dysplasia, and
finally leading to the development adenocarcinoma. Although the relationship between H pylori
and gastritis is constant, only a small proportion of individuals infected with H pylori develop
gastric cancer. The incidence of gastric cancer usually parallels the incidence of H pylori
infection in countries with a high incidence of gastric cancer and is consistent with H pylori
being the cause of the precursor lesion, chronic atrophic gastritis.[21, 22]

Persistence of the organisms and associated inflammation during long-standing infection is likely
to permit the accumulation of mutations in the gastric epithelial cells genome, leading to an
increased risk of malignant transformation and progression to adenocarcinoma. Studies have
provided evidence of the accumulation of mutations in the gastric epithelium secondary to
oxidative DNA damage associated with chronic inflammatory byproducts and secondary to
deficiency of DNA repair induced by chronic bacterial infection.

Although the role of H pylori in peptic ulcer disease is well established, the role of the infection
in non-ulcer or functional dyspepsia remains highly controversial. A recent meta-analysis
demonstrates that H pylori eradication therapy is associated with improvement of dyspeptic
symptoms in patients with functional dyspepsia in Asian, European, and American populations.
[23]
Although this study illustrates that H pylori eradication may be beneficial for symptom relief
in some populations, routine H pylori testing and treatment in nonulcer dyspepsia are not
currently widely accepted. Therefore, H pylori eradication strategies in patients with nonulcer
dyspepsia must be considered on a patient-by-patient basis.

Infectious granulomatous gastritis

Granulomatous gastritis (see the image below) is a rare entity. Tuberculosis may affect the
stomach and cause caseating granulomas. Fungi, including cryptococcus, can also cause
caseating granulomas and necrosis, a finding that is usually observed in patients who are
immunosuppressed. Granulomatous gastritis has also been associated with H pylori infection.[24]
 Granulomatous chronic gastritis.
Noncaseating granulomas in the lamina propria. Image courtesy of Sydney Finkelstein, MD,
PhD, University of Pittsburgh.

Gastritis in patients who are immunosuppressed

Cytomegalovirus (CMV) infection of the stomach is observed in patients with underlying

immunosuppression. Histologically, a patchy, mild inflammatory infiltrate is observed in the
lamina propria. Typical intranuclear eosinophilic inclusions and, occasionally, smaller
intracytoplasmic inclusions are present in the gastric epithelial cells and in the endothelial or
mesenchymal cells in the lamina propria. Severe necrosis may result in ulceration.

Other infectious causes of chronic gastritis in immunosuppressed patients, include the Herpes
simplex virus (HSV), which causes basophilic intranuclear inclusions in epithelial cells.
Mycobacterial infections involving Mycobacterium avium-intracellulare are characterized by
diffuse infiltration of the lamina propria by histiocytes, which rarely form granulomas.

Autoimmune atrophic gastritis

Autoimmune atrophic gastritis is associated with serum anti-parietal and antiintrinsic factor (IF)
antibodies. The gastric corpus undergoes progressive atrophy, IF deficiency occurs, and patients
may develop pernicious anemia.[25]

The development of chronic atrophic gastritis (sometimes called type A gastritis) limited to
corpus-fundus mucosa and marked diffuse atrophy of parietal and chief cells characterizes
autoimmune atrophic gastritis. In addition to hypochlorhydria, autoimmune gastritis is associated
with serum anti-parietal and anti-IF antibodies that cause IF deficiency, which, in turn, causes
decreased availability of cobalamin, eventually leading to pernicious anemia in some patients.
Hypochlorhydria induces G-Cell (Gastrin producing) hyperplasia, leading to hypergastrinemia.
Gastrin exerts a trophic effect on enterochromaffin-like (ECL) cells and is hypothesized to be
one of the mechanisms leading to the development of gastric carcinoid tumors (ECL tumors).[26,
27]

In autoimmune gastritis, autoantibodies are directed against at least 3 antigens, including IF,
cytoplasmic (microsomal-canalicular), and plasma membrane antigens. There are two types of IF
antibodies, types I and II. Type 1 antibody prevents the attachment of B12 to IF and Type II
antibody prevents attachment of the vitamin B12-intrinsic factor complex to ileal receptors.[28]

Cell-mediated immunity also contributes to the disease. T-cell lymphocytes infiltrate the gastric
mucosa and contribute to the epithelial cell destruction and resulting gastric atrophy.

Chronic reactive chemical gastropathy

Chronic reactive chemical gastritis is associated with long-term intake of aspirin or NSAIDs. It
also develops when bile-containing intestinal contents reflux into the stomach. Although bile
reflux may occur in the intact stomach, most of the features associated with bile reflux are
typically found in patients with partial gastrectomy, in whom the lesions develop near the
surgical stoma.

The mechanisms through which bile alters the gastric epithelium involve the effects of several
bile constituents. Both lysolecithin and bile acids can disrupt the gastric mucous barrier, allowing
the back diffusion of positive hydrogen ions and resulting in cellular injury. Pancreatic juice
enhances epithelial injury in addition to bile acids. In contrast to other chronic gastropathies,
minimal inflammation of the gastric mucosa typically occurs in chemical gastropathy.

Chronic noninfectious granulomatous gastritis

Noninfectious diseases are the usual cause of gastric granulomas; these include Crohn disease,
sarcoidosis, and isolated granulomatous gastritis. Crohn disease demonstrates gastric
involvement in approximately 33% of the cases. Granulomas have also been described in
association with gastric malignancies, including carcinoma and malignant lymphoma.
Sarcoidlike granulomas may be observed in people who use cocaine, and foreign material is
occasionally observed in the granuloma. An underlying cause of chronic granulomatous gastritis
cannot be identified in up to 25% of cases. These patients are considered to have idiopathic
granulomatous gastritis (IGG).[29]

Lymphocytic gastritis

Lymphocytic gastritis is a type of chronic gastritis characterized by dense infiltration of the

surface and foveolar epithelium by T lymphocytes and associated chronic infiltrates in the lamina
propria. Because its histopathology is similar to that of celiac disease, lymphocytic gastritis has
been proposed to result from intraluminal antigens.[30, 31, 32, 33, 34]

High antiH pylori antibody titers have been found in patients with lymphocytic gastritis, and in
limited studies, the inflammation disappeared after H pylori was eradicated.[35] However, many
patients with lymphocytic gastritis are serologically negative for H pylori. A number of cases
may develop secondary to intolerance to gluten and drugs such as ticlopidine.[32, 36]

Eosinophilic gastritis

Large numbers of eosinophils may be observed with parasitic infections such as those caused by
Eustoma rotundatum and Anisakis marina. Eosinophilic gastritis can be part of the spectrum of
eosinophilic gastroenteritis. Although the gastric antrum is commonly affected and can cause
gastric outlet obstruction, this condition can affect any segment of the GI tract and can be
segmental.[37] Patients frequently have peripheral blood eosinophilia.

In some cases, especially in children, eosinophilic gastroenteritis can result from food allergy,
usually to milk or soy protein. Eosinophilic gastroenteritis can also be found in some patients
with connective tissue disorders, including scleroderma, polymyositis, and dermatomyositis.

Radiation gastritis

Radiation gastritis usually occurs 2-9 mo after initial radiotherapy. The dose at which 5 percent
of patients develop complications at five years, when the entire stomach is irradiated, is
estimated to be 50 Gy. Small doses of radiation (up to 15 Gy) cause reversible mucosal damage,
whereas higher doses cause irreversible damage with atrophy and ischemic-related ulceration.
Reversible changes consist of degenerative changes in the epithelial cells and nonspecific
chronic inflammatory infiltrate in the lamina propria. Higher amounts of radiation cause
permanent mucosal damage, with atrophy of fundic glands, mucosal erosions, and capillary
hemorrhage. Associated submucosal endarteritis results in mucosal ischemia and secondary ulcer
development.[38, 39]

Ischemic gastritis

Ischemic gastritis is believed to result from atherosclerotic thrombi arising from the celiac and
superior mesenteric arteries.[40, 41]

Prognosis

The prognosis of chronic gastritis is strongly related to the underlying cause. Chronic gastritis as
a primary disease, such as H pylori-associated chronic gastritis, may progress as an
asymptomatic disease in some patients, whereas other patients may report dyspeptic symptoms.
The clinical course may be worsened when patients develop any of the possible complications of
H pylori infection, such as peptic ulcer or gastric malignancy.[21]

H pylori gastritis is the most frequent cause of MALT lymphoma- occurring in 0.1% of those
infected. Patients with chronic atrophic gastritis may have a 12- to 16-fold increased risk of
developing gastric carcinoma, compared with the general population. Approximately 10% of
infected persons develop peptic ulcer and the lifetime risk of gastric cancer is in the range of 1-
3%.[75]
Eradication of H pylori results in rapid cure of the infection with disappearance of the
neutrophilic infiltration of the gastric mucosa. Disappearance of the lymphoid component of
gastritis might take several months after treatment. Data on the evolution of atrophic gastritis
after eradication of H pylori have been conflicting. Follow-up for as long as several years after H
pylori eradication has not demonstrated regression of gastric atrophy in most studies, whereas
others report improvement in the extent of atrophy and intestinal metaplasia.[76, 77]

Another important question is whether H pylori eradication in a patient with atrophic gastritis
reduces the risk of gastric cancer development. Unfortunately the data up to now has been
mixed. A prospective study in a Japanese population reported that H pylori eradication in patients
with endoscopically resected early gastric cancer resulted in the decreased appearance of new
early cancers, whereas intestinal-type gastric cancers developed in the control group without H
pylori eradication. This finding supports an intervention approach with eradication of H pylori if
the organisms are detected in patients with atrophic gastritis; the goal is to prevent the
development of gastric cancer.[78, 79, 80] However, recent reports have shown that gastric cancers
can still arise after adequate H pylori therapy.[81, 82]

In patients with autoimmune gastritis, the major effects are consequent to the loss of parietal and
chief cells and include achlorhydria, hypergastrinemia, loss of pepsin and pepsinogen, anemia,
and an increased risk of gastric neoplasms. The prevalence of gastric neoplasia in patients with
pernicious anemia, is reported to be about 1-3% for adenocarcinoma and 1- 7% for gastric
carcinoid.[83, 84]

Etiology
Chronic gastritis may be caused by either infectious or noninfectious conditions. Infectious
forms of gastritis include the following:

Chronic gastritis caused by H pylori infection This is the most common cause of
chronic gastritis.

Gastritis caused by Helicobacter heilmannii infection [42]

Granulomatous gastritis associated with gastric infections in mycobacteriosis, syphilis,

histoplasmosis, mucormycosis, South American blastomycosis, anisakiasis, or
anisakidosis
 Chronic gastritis associated with parasitic infections - Strongyloides species,
schistosomiasis, or Diphyllobothrium latum

Gastritis caused by viral (eg, CMV or herpesvirus) infection [43]

Noninfectious forms of gastritis include the following:

Autoimmune gastritis

Chemical gastropathy- usually related to chronic bile reflux, NSAID and aspirin intake [44]

Uremic gastropathy

Chronic noninfectious granulomatous gastritis [29, 45, 46] This may be associated with
Crohn disease, sarcoidosis, Wegener granulomatosis, foreign bodies, cocaine use, isolated
granulomatous gastritis, chronic granulomatous disease of childhood, eosinophilic
granuloma, allergic granulomatosis and vasculitis, plasma cell granulomas, rheumatoid
nodules, tumoral amyloidosis and granulomas associated with gastric carcinoma, gastric
lymphoma, or Langerhans cell histiocytosis

Lymphocytic gastritis, including gastritis associated with celiac disease (also called
collagenous gastritis) [30, 31, 32, 33, 47]

Eosinophilic gastritis

Radiation injury to the stomach

Graft-versus-host disease (GVHD)

Ischemic gastritis [40]

Gastritis secondary to drug therapy (NSAIDs and aspirin)

Some patients have chronic gastritis of undetermined etiology or gastritis of undetermined type
(eg, autistic gastritis[48] ).

Previous

http://emedicine.medscape.com/article/176156-overview#a5
Chronic Gastritis

Author: Akiva J Marcus, MD, PhD; Chief Editor: BS Anand, M

Pathophysiology

Acute gastritis has a number of causes, including certain drugs; alcohol; bile; ischemia; bacterial,
viral, and fungal infections; acute stress (shock); radiation; allergy and food poisoning; and direct
trauma. The common mechanism of injury is an imbalance between the aggressive and the
defensive factors that maintain the integrity of the gastric lining (mucosa).

Acute erosive gastritis can result from an exposure to a variety of agents or factors. This is
referred to as reactive gastritis. These agents/factors include nonsteroidal anti-inflammatory
medications (NSAIDs), alcohol, cocaine, stress, radiation, bile reflux, and ischemia. The gastric
mucosa exhibits hemorrhages, erosions, and ulcers. NSAIDs, such as aspirin, ibuprofen, and
naproxen, are the most common agents associated with acute erosive gastritis. This results from
both oral and systemic administration of these agents, either in therapeutic doses or in
supratherapeutic doses.

Because of gravity, the inciting agents lie on the greater curvature of the stomach. This partly
explains the development of acute gastritis distally on or near the greater curvature of the
stomach in the case of orally administered NSAIDs. However, the major mechanism of injury is
the reduction in prostaglandin synthesis. Prostaglandins are chemicals responsible for
maintaining mechanisms that result in the protection of the mucosa from the injurious effects of
the gastric acid. Long-term effects of such ingestions can include fibrosis and stricture formation.

Bacterial infection is another cause of acute gastritis. The corkscrew-shaped bacterium called H
pylori is the most common cause of gastritis. Complications result from a chronic infection
rather than from an acute infection. The prevalence of H pylori in otherwise healthy individuals
varies depending on age, socioeconomic class, and country of origin. The infection is usually
acquired in childhood. In the Western world, the number of people infected with H pylori
increases with age.

Evidence of H pylori infection can be found in 20% of individuals younger than 40 years and in
50% of individuals older than 60 years. How the bacterium is transmitted is not entirely clear.
Transmission is likely from person to person through the oral-fecal route or through the ingestion
of contaminated water or food. This is why the prevalence is higher in lower socioeconomic
classes and in developing countries. H pylori is associated with 60% of gastric ulcers and 80% of
duodenal ulcers.
H pylori gastritis typically starts as an acute gastritis in the antrum, causing intense
inflammation, and over time, it may extend to involve the entire gastric mucosa resulting in
chronic gastritis.

The acute gastritis encountered with H pylori is usually asymptomatic. The bacterium imbeds
itself in the mucous layer, a protective layer that coats the gastric mucosa. It protects itself from
the acidity of the stomach through the production of large amounts of urease, an enzyme that
catalyzes the breakdown of urea to the alkaline ammonia and carbon dioxide. The alkaline
ammonia neutralizes the gastric acid in the immediate vicinity of the bacterium conferring
protection.

H pylori also has flagella that enable it to move and help it to penetrate the mucous layer so that
it comes into contact with gastric epithelial cells. It also has several adhesion molecules that help
it to adhere to these cells. It produces inflammation by activating a number of toxins and
enzymes that activate IL-8, which eventually attracts polymorphs and monocytes that cause
acute gastritis.

Antigen-presenting cells activate lymphocytes and other mononuclear cells that lead to chronic
superficial gastritis. The infection is established within a few weeks after the primary exposure to
H pylori. It produces inflammation via the production of a number of toxins and enzymes. The
intense inflammation can result in the loss of gastric glands responsible for the production of
acid. This is referred to as atrophic gastritis. Consequently, gastric acid production drops. The
virulence genotype of the microbe is an important determinant for the severity of the gastritis and
the formation of intestinal metaplasia, the transformation of gastric epithelium. This
transformation can lead to gastric cancer.

Reactive gastropathy is the second most common diagnosis made on gastric biopsy specimens
after H pylori gastritis. This entity is believed to be secondary to bile reflux and was originally
reported after partial gastrectomy (Billroth I or II). It is now considered to represent a
nonspecific response to a variety of other gastric irritants.

Helicobacter heilmanii is a gram-negative, tightly spiraled, helical-shaped organism with 5-7

turns. The prevalence of H heilmanii is extremely low (0.25-1.5%). The source of H heilmanii
infection is unclear, but animal contact is thought to be the means of transmission.

Tuberculosis is a rare cause of gastritis, but an increasing number of cases have developed in
patients who are immunocompromised. Gastritis caused by tuberculosis is generally associated
with pulmonary or disseminated disease.

Secondary syphilis of the stomach is a rare cause of gastritis.

Phlegmonous gastritis is an uncommon form of gastritis caused by numerous bacterial agents,
including streptococci, staphylococci, Proteus species, Clostridium species, and Escherichia coli.
Phlegmonous gastritis usually occurs in individuals who are debilitated. It is associated with a
recent large intake of alcohol, a concomitant upper respiratory tract infection, and AIDS.
Phlegmonous means a diffuse spreading inflammation of or within the connective tissue. In the
stomach, it implies infection of the deeper layers of the stomach (submucosa and muscularis). As
a result, purulent bacterial infection may lead to gangrene.

Phlegmonous gastritis is rare. The clinical diagnosis is usually established in the operating room,
as these patients present with an acute abdominal emergency requiring immediate surgical
exploration. Without appropriate therapy, it can progress to peritonitis and death.

Viral infections can cause gastritis. Cytomegalovirus (CMV) is a common viral cause of gastritis.
It is usually encountered in individuals who are immunocompromised, including those with
cancer, immunosuppression, transplants, and AIDS. Gastric involvement can be localized or
diffuse.

Fungal infections that cause gastritis include Candida albicans and histoplasmosis. Gastric
phycomycosis is another rare lethal fungal infection. The common predisposing factor is
immunosuppression. C albicans rarely involves the gastric mucosa. When isolated in the
stomach, the most common locations tend to be within a gastric ulcer or an erosion bed. It is
generally of little consequence. Disseminated histoplasmosis can involve the stomach. The usual
presenting clinical feature is bleeding from gastric ulcers or erosions on giant gastric folds.

Parasitic infections are rare causes of gastritis. Anisakidosis is caused by a nematode that embeds
itself in the gastric mucosa along the greater curvature. Anisakidosis is acquired by eating
contaminated sushi and other types of contaminated raw fish. It often causes severe abdominal
pain that subsides within a few days. This nematode infection is associated with gastric fold
swelling, erosions, and ulcers.

Ulcero-hemorrhagic gastritis is most commonly seen in patients who are critically ill. Ulcero-
hemorrhagic gastritis is believed to be secondary to ischemia related to hypotension and shock or
to the release of vasoconstrictive substances, but the etiology is often unknown. The gastric
mucosa reveals multiple petechiae, mostly in the fundus and body, or exhibits a diffusely
hemorrhagic pattern. The gross pathology may resemble that of NSAID- or other ingestion-
induced gastritis, except that the location of injury is different. This form of gastritis can be life-
threatening if the patient experiences hemorrhaging and may even require emergency
gastrectomy.

Inflammatory bowel disease and microscopic colitis appear to be inversely associated with H
pylori infection.[1] Microscopic evidence of acute gastritis can be seen in patients with Crohn
disease, though clinical manifestations are rare (occurring in only about 2-7% of patients with
Crohn disease). Focally enhancing gastritis is now recognized as a condition seen in both Crohn
disease and ulcerative colitis.

Eosinophilic gastritis is often seen in conjunction with eosinophilic gastroenteritis but can be
associated with various disorders, including food allergies (eg, cow milk, soy protein), collagen
vascular diseases, parasitic infections, gastric cancer, lymphoma, Crohn disease, vasculitis, drug
allergies, and H pylori infections. An eosinophilic infiltrate is seen involving the gastric wall or
epithelium.

Etiology
Acute gastritis has a number of causes, including certain drugs; alcohol; bacterial, viral, and
fungal infections; acute stress (shock); radiation; allergy and food poisoning; bile; ischemia; and
direct trauma.

Note the following:

Drugs - NSAIDs, such as aspirin, ibuprofen, and naproxen; cocaine; iron; colchicine,
when at toxic levels, as in patients with failing renal or hepatic function; kayexalate;
chemotherapeutic agents, such as mitomycin C, 5-fluoro-2-deoxyuridine, and floxuridine

Potent alcoholic beverages, such as whisky, vodka, and gin

Bacterial infections - H pylori (most frequent), H heilmanii (rare), streptococci (rare),

staphylococci (rare), Proteus species (rare), Clostridium species (rare), E coli (rare),
tuberculosis (rare), secondary syphilis (rare)

Viral infections (eg, CMV)

Fungal infections - Candidiasis, histoplasmosis, phycomycosis

Parasitic infection (eg, anisakidosis)

Acute stress (shock)

Radiation

Allergy and food poisoning

Bile: The reflux of bile (an alkaline medium is important for the activation of digestive
enzymes in the small intestine) from the small intestine to the stomach can induce
gastritis.
 Ischemia: This term is used to refer to damage induced by decreased blood supply to the
stomach. This rare etiology is due to the rich blood supply to the stomach.

Direct trauma

Prognosis
Gastritis generally clears spontaneously. With treatment, the mortality rate of phlegmonous
gastritis is 65%.

Mortality/morbidity

The mortality/morbidity is dependent on the etiology of the gastritis. Generally, most cases of
gastritis are treatable once the etiology is determined. The exception to this is phlegmonous
gastritis, which has a mortality rate of 65%, even with treatment.

Complications

Complications of acute gastritis include the following:

Bleeding from an erosion or ulcer

Gastric outlet obstruction due to edema limiting the adequate transfer of food from the
stomach to the small intestine

Dehydration from vomiting

Renal insufficiency as a result of dehydration

http://emedicine.medscape.com/article/175909-overview#a2

Acute Gastritis

Author: Mohammad Wehbi, MD; Chief Editor: BS Anand, MD