A histological term for inflammation of the gastric mucosa.
Helicobacter pylori infection and use of non-steroidal anti-inflammatory drugs (NSAIDs) or alcohol are the most common causes. Other causes include stress (secondary to mucosal ischaemia) and autoimmune gastritis. Rare forms include phlegmonous gastritis (a rare bacterial infection).
Diagnosis is based on clinical history and characteristic histological findings. A variety of methods may be used to diagnose H pylori infection.
Presence of suspicious features suggestive of upper GI malignancy requires urgent endoscopy. These include GI bleeding, anaemia, early satiety, unexplained weight loss (>10% body weight), progressive dysphagia, odynophagia, or persistent vomiting.
Treatment depends on the aetiology. Options include H pylori -eradication therapy, reduction of NSAIDs or alcohol exposure, and symptomatic therapy with histamine-2 antagonists and/or proton-pump inhibitors.
If untreated, progression to peptic ulcer disease may occur. Other complications of some forms of gastritis include gastric carcinoma and gastric lymphoma.
Helicobacter pylori infection may cause both an acute and chronic gastritis.  Erosive gastritis may occur in response to NSAID/alcohol use or misuse    and to bile reflux into the stomach that may follow previous gastric surgery or cholecystectomy.     Stress gastritis, most commonly related to mucosal ischaemia seen in critically ill patients, represents a continuum of disease ranging from superficial (erosions) to deep mucosal damage known as stress ulceration.  Autoimmune gastritis is a diffuse form of mucosal atrophy characterised by auto-antibodies to parietal cells and intrinsic factor resulting in inflammatory infiltration and atrophy of the corpus mucosa.   Phlegmonous gastritis is a rare but life-threatening infection of the gastric submucosa and muscularis propria seen in immunocompromised patients.    
Clinical Associate Professor of Medicine
University of Chicago Pritzker School of Medicine
Center for the Study of Complex Diseases
NorthShore University HealthSystem
EDE declares that he has no competing interests.
Dr Eli D. Ehrenpreis would like to gratefully acknowledge Dr Nicole Marie Gentile, Dr Parakkal Deepak, and Dr Elad Eichenwald, previous contributors to this monograph. NMG, PD, and EE declare that they have no competing interests.
Professor and Consultant Gastroenterologist
Department of Gastroenterology
Leeds General Infirmary
AA is the author of studies referenced in this monograph.
Assistant Professor of Medicine
Section of Gastroenterology and Nutrition
Rush University Medical Center
GS declares that he has no competing interests.
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