Chronic Gastritis A long-standing condition in which the gastric mucosa, is inflamed or irritated over an extended period of time.
Etiology
• The most common (90%) cause of chronic gastritis is infection with the bacillus Helicobacter pylori.
• Autoimmune gastritis, the most common cause of atrophic gastritis represents less than 10% of cases of chronic gastritis
• Less common causes include radiation injury and chronic bile reflux.
Symptoms:
The symptoms and signs associated with chronic gastritis typically are less severe but more persistent than those of acute gastritis.
Nausea
Upper abdominal discomfort
Sometimes with vomiting
But hematemesis is uncommon.
Causes:
The most common cause of chronic gastritis is infection with the bacillus Helicobacter pylori.
Autoimmune gastritis, the most common cause of atrophic gastritis, represents less than 10% of cases of chronic gastritis and is the most common form of chronic gastritis in patients without H. pylori infection.
Less common causes include radiation injury and chronic bile reflux.
Helicobacter pylori Gastritis:
These spiral-shaped or curved bacilli are present in gastric biopsy specimens from almost all patients with duodenal ulcers and a majority of those with gastric ulcers or chronic gastritis.
Predominantly antral gastritis with high acid production, despite hypogastrinemia.
Epidemiology
In the United States, H. pylori infection is associated with
Poverty
Household crowding,
Limited education,
African-American
Mexican American ethnicity
Dwelling in areas with poor hygiene
Birth outside of the United States.
Colonization rates exceed 70% in some groups and range from less than 10% to more than 80% worldwide. In high-prevalence areas, infection often is acquired in childhood and then persists for decades. Thus, the incidence of H. Pylori infection correlates most closely with sanitation and hygiene during an individual childhood.
Pathogenesis:
• Four features are linked to H. pylori virulence
• Flagella, which allow the bacteria to be motile in viscous mucus
• Urease, which generates ammonia from endogenous urea, thereby elevating local gastric pH around the organisms and protecting the bacteria from the acidic pH of the stomach.
• Adhesins, which enhance bacterial adherence to surface foveolar cells
• Toxins, such as that encoded by cytotoxin-associated gene A (CagA), may be involved in ulcer or cancer development by poorly defined mechanisms.
Morphology
Gastric biopsy specimens generally demonstrate H. pylori in infected persons.
Organisms are abundant within surface mucus. Tropism for Foveolar epithelium in the antrum.
Intraepithelial and lamina propria neutrophils are prominent.
The superficial lamina propria includes large numbers of plasma cells, often in clusters or sheets, as well as increased numbers of lymphocytes and macrophages.
Pit abscesses may form.
Lymphoid aggregates with germinal centers within the superficial lamina propria. Progression to (mucosa-associated lymphoid tissue) MALT lymphoma.
Intestinal metaplasia, the presence of goblet cells admixed with gastric foveolar epithelium, is a risk factor for the development of gastric adenocarcinoma.
Diagnostic test
In addition to histologic identification of the organism, several diagnostic tests have been developed including
A noninvasive serologic test for anti–H. pylori antibodies,
Fecal bacterial detection
Urea breath test based on the generation of ammonia by bacterial urease.
Gastric biopsy specimens also can be analyzed by
– Rapid urease test
– Bacterial culture
– Polymerase chain reaction (PCR) assay for bacterial DNA.
Treatment:
Effective treatments include combinations of antibiotics and proton pump inhibitors.
Patients with H. pylori gastritis usually improve after treatment, although relapses can follow incomplete eradication or reinfection
Late complications
Persistence of the disease causes
• Pan gastritis
• Multifocal atrophic gastritis, reduced acid secretion
• Intestinal metaplasia
• Increased risk of gastric adenocarcinoma
• Hyperplasia of lymphoid aggregates has the potential to transform into lymphoma.
Autoimmune Gastritis:
Autoimmune gastritis accounts for less than 10% of cases of chronic gastritis.
Autoimmune gastritis typically spares the antrum and induces hypergastrinemia.
Pathogenesis:
• Antibodies to parietal cells and intrinsic factors that can be detected in serum and gastric secretions
• Loss of parietal cells, which secrete acid and intrinsic factors.
• Deficient acid production stimulates gastrin release, resulting in hypergastrinemia and hyperplasia of antral gastrin-producing G cells.
• Lack of intrinsic factor disables ileal vitamin B1 absorption, leading to B12 deficiency and megaloblastic anemia (pernicious anemia);
• The Reduced serum concentration of pepsinogen I reflect chief cell loss.
Morphology:
• Diffuse damage of the oxyntic (acid-producing) mucosa within the body and fundus.
• Diffuse atrophy, mucosa of the body and fundus is markedly thinned, and rugal folds are lost.
• The inflammatory infiltrate is composed of lymphocytes, macrophages, and plasma cells; in contrast with H. pylori gastritis, the inflammatory reaction most often is deep and centered on the gastric glands.
• Parietal and chief cell loss can be extensive
• Intestinal metaplasia may develop.
Clinical Features
• Antibodies to parietal cells and intrinsic factors are present early in the disease, but pernicious anemia develops in only a minority of patients.
• The median age at diagnosis is 60 years
• There is a slight female predominance.
• Autoimmune gastritis often is associated with other autoimmune diseases but is not linked to specific human leukocyte antigen (HLA) alleles.
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