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What is gastritis?
Patients typically refer to the symptom of dyspepsia as gastritis. Gastroenterologists use the term gastritis to describe endoscopic observations. Pathologists refer to a histologic finding. Most would agree that gastritis requires a mucosal biopsy as it is a histopathologic diagnosis. Inflammation of the gastric mucosa can be classified into two types: gastritis or gastropathy. The gastric mucosa can have injury to its epithelium and regeneration without having significant inflammation. When this happens, it is referred to as gastropathy. Gastritis, however, refers to inflammation of the gastric mucosa with an associated inflammatory infiltrate. Although gastritis can be either acute or chronic, most cases of gastritis are truly chronic as acute gastritis is infrequently diagnosed soon after initiation of the inflammatory process.
What are the endoscopic findings associated with gastritis?
There is not one particular endoscopic entity that defines gastritis. Both gastroenterologists and pathologists have come to realize that endoscopic appearance frequently does not predict changes in histology (i.e., the presence of inflammation). Endoscopists use the word gastritis to describe an array of findings, including erythema, edema, enlarged gastric folds, polyps, the presence of erosions or ulcers, mucosal bleeding, or atrophy. The most common endoscopic finding associated with histologically diagnosed gastritis is a normal endoscopic appearance.
What is the Sydney system for diagnosis of gastritis?
The Sydney system is a gastric biopsy protocol indicating where gastric mucosal biopsies should be obtained to optimize diagnosis of gastritis including Helicobacter pylori. Five biopsy specimens are taken: two from the antrum within 2 to 3 cm from the pylorus (one from the distal lesser curvature and one from the distal greater curvature), two from the corpus approximately 8 cm from the cardia (one from the lesser and the other from the greater curvature), and one from the incisura angularis. Samples from the antrum, corpus, and incisura angularis should be separately identified. Duodenal biopsies may be useful in certain settings (e.g., suspected celiac disease and lymphocytic gastritis, or duodenal Crohn’s disease and granulomatous gastritis).
What are common causes of chronic gastritis?
The most common cause of chronic gastritis is H. pylori infection. Autoimmune gastritis (atrophic gastritis) accounts for the most common cause of H. pylori– negative chronic gastritis (roughly 5%); less common causes include infections, eosinophilic gastritis, lymphocytic gastritis, granulomatous gastritis, graft-versus-host disease, and inflammatory bowel disease ( Table 9-1 ). As mentioned previously, most cases of gastritis are “chronic” because patients with acute gastritis are rarely diagnosed.
Pathologic Diagnosis | Histologic Findings | Etiologic Factors | Endoscopic Findings | Clinical Associations |
---|---|---|---|---|
Acute suppurative gastritis | Neutrophilic inflammation | Acute H. pylori and Streptococcal gastritis or other bacteria | May be normal or have mucosal fold swelling; dark red, distended stomach; pus | Acute gastroenteritis-like illness, perforation, gangrene |
Chronic and chronic active gastritis | Mixed inflammatory infiltrates (neutrophils, plasma cells, eosinophils) with or without foveolar hyperplasia, lymphoid aggregates, erosions, ulcers, intestinal metaplasia, atrophy (late stages) | Chronic H. pylori gastritis | Typically normal; may present with erythema, friability, nodularity, or in some cases erosions or ulcerations | Varies; most may be asymptomatic; can present with duodenal ulcer, gastric ulcer, gastric adenocarcinoma; some association with functional dyspepsia |
Lymphocytic gastritis | Chronic active inflammation with increased intraepithelial lymphocytes with or without foveolar hyperplasia, erosions, ulcers | Hypersensitivity to gliadin, hypersensitivity to unknown agents, autoimmune | Varioliform or chronic erosive gastritis (nodules with central ulceration); picture of Ménétrier’s disease | Celiac sprue; Ménétrier’s disease |
Granulomatous gastritis | Multifocal (frequently necrotizing) active chronic inflammation with epithelioid granulomas | Idiopathic isolated granulomatous gastritis; Crohn’s disease; fungal, mycobacterial, and spirochetal infections; sarcoidosis; vasculitis; drug reactions | Variable, including thickened folds and ulcerations | Depends on underlying disease |
Eosinophilic gastritis | Sheets of eosinophils | Idiopathic food allergy, drug allergy, parasitic disease | Prominent folds, hyperemia, nodularity, ulcer, or may be normal | Pain; nausea, vomiting; early satiety; weight loss, anemia |
Hypertrophic lymphocytic gastritis | Lymphocytic gastritis with extreme foveolar hyperplasia | Clinical syndrome identical to Ménétrier’s gastropathy; etiologic factors presumed different | Same as hypertrophic gastropathy | Same as hypertrophic gastropathy |
What are common etiologic factors of reactive gastropathy?
Medications (particularly nonsteroidal antiinflammatory drugs [NSAIDs]), toxins, tobacco, alcohol, portal hypertensive gastropathy, cocaine, stress, radiation, bile reflux, ischemia, mechanical injury from gastric cardia prolapsing to the esophageal lumen during retching or vomiting, aging, and certain infections are commonly associated with reactive gastropathy.
What medications are frequently associated with gastropathy?
Acetylsalicylic acid (even low-dose) and NSAIDs
Oral iron
Potassium chloride
Bisphosphonate
Fluoride
Systemic chemotherapy
Hepatic arterial infusion of chemotherapy
Toxic ingestion of heavy metals
How does the gastric mucosa normally protect itself from injury given its acidic environment?
The stomach has epithelial defense mechanisms that serve to maintain its mucosal integrity. These protective mechanisms are often characterized into three components: preepithelial, epithelial, and postepithelial, all of which are prostaglandin dependent. See Box 9-1 and Figure 9-1 .
Mucus barrier forms a continuous gel into which bicarbonate-rich fluid is secreted, forming a protective pH gradient by maintaining a neutral pH.
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