Gastrointestinal (GI) System ORGAN SYSTEMS


Inflammation of the stomach lining.

Inflammation of the stomach lining.


Gastritis is a condition involving inflammation of the gastric (stomach) mucosa. A wide variety of factors can cause acute gastritis including some bacterial infections, consumption of certain beverages and some medications. This inflammation of the stomach lining leads to a variety of symptoms.


The current classification of gastritis centers on time course (acute versus chronic), histological features, anatomic distribution, and underlying pathological mechanisms.

  • Acute gastritis
  • Chronic gastritis


Infectious etiology:

  • H. pylori-associated gastritis (M/C cause worldwide)
  • H. pylori-negative gastritis: Tobacco smoking, alcohol, and/or NSAIDs/steroids
    • The patients should fulfill all four of these criteria:
      • Negative triple staining of gastric mucosal biopsies (H&E, the Alcian blue stain and a modified silver stain)
      • Negative H. pylori culture
      • Negative IgG H. pylori serology
      • No self-reported history of H. pylori treatment
  • Infection by organisms other than H. pylori: Mycobacterium avium-intracellulare, enterococcal infection, Herpes simplex, and cytomegalovirus.
  • Parasitic gastritis: Cryptosporidium, Strongyloides stercoralis, or anisakiasis infection
Scheme on natural course and progression of Helicobacter pylori gastritis from a non-atrophic form to gastric malignancy (sc. “Correa cascade”). Several potentially pathogenetic factors and mechanisms, linked with carcinogenesis, play a role and are triggered stepwise on during the course and progression of the cascade. | Sipponen, P., & Maaroos, H. I. (2015). Chronic gastritis. Scandinavian journal of gastroenterology, 50(6), 657–667.

Autoimmune gastritis:

Chronic inflammatory disease characterized by chronic atrophic gastritis and associated with raised serum anti-parietal and anti-intrinsic factor antibodies.
  • The loss of parietal cells results in a reduction of gastric acid secretion, which is necessary for the absorption of inorganic iron. Therefore, iron deficiency is commonly a finding in patients with autoimmune gastritis. Iron deficiency in these patients usually precedes vitamin B12 deficiency. The disease is common in young women.

Other causes:

  • Bile acid reflux
  • Radiation gastritis
  • Crohn disease-associated gastritis (uncommon)
  • Collagenous gastritis (rare): Characteristically presents with marked subepithelial collagen deposition accompanying with mucosal inflammatory infiltrate. The exact etiology and pathogenesis of collagenous gastritis are still unclear.
  • Eosinophilic gastritis (rare): Part of eosinophilic gastrointestinal disorders characterized by the absence of known causes of eosinophilia (not secondary to an infection, systematic inflammatory disease, or any other causes to explain the eosinophilia).
  • Sarcoidosis-associated gastritis
  • Lymphocytic gastritis (rare): Unclear etiology but an association with H. pylori infection or celiac disease has been suggested
  • Ischemic gastritis (rare and associated with high mortality)
  • Vasculitis-associated gastritis: Diseases causing systemic vasculitis can cause granulomatous infiltration of the stomach (eg. Granulomatosis with polyangiitis, aka Wegner granulomatosis)

Ménétrier disease:

Characterized by:
  • (i) Presence of large gastric mucosal folds in the body and fundus of the stomach
  • (ii) Massive foveolar hyperplasia of surface and glandular mucous cells
  • (iii) Protein-losing gastropathy, hypoalbuminemia, and edema (20-100% cases)
  • (iv) Reduced gastric acid secretion because of loss of parietal cells

Clinical Features

There are no typical clinical manifestations of gastritis.

Acute gastritis:

Many people are asymptomatic or develop minimal dyspeptic symptoms. If not treated the picture may evolve to chronic gastritis.

Sudden onset of epigastric pain, nausea, and vomiting

Chronic and autoimmune gastritis:

These are associated with some common intial findings
  • Hematological disorders: Iron-deficiency anemia (based on blood film showing microscopic hypochromic changes as well as iron studies) commonly presents in the early stages of autoimmune gastritis. Achlorhydria causing impairment of iron absorption in the duodenum and early jejunum is the main cause.[20] Iron-deficiency anemia could also occur in other types of chronic gastritis
  • Positive histological examination of gastric biopsies

Associated conditions:

Presence of other autoimmune disorders, neurological symptoms (related to vitamin B12 deficiency) or positive family history:
  • Autoimmune gastritis is associated with other autoimmune disorders (mainly thyroid diseases) including Hashimoto thyroiditis but also with Addison disease, chronic spontaneous urticaria, myasthenia gravis, Diabetes type 1, vitiligo, and perioral cutaneous autoimmune disorders especially erosive oral lichen planus.


History of smoking, consumption of alcohol, intake of NSAIDs or steroids, allergies, radiotherapy or gall bladder disorders should all be considerations. A history of treatment for inflammatory bowel disease, vasculitic disorders, or eosinophilic gastrointestinal disorders might require exploration if no cause of gastritis is apparent.

Invasive methods (requiring gastroscopy and biopsies):

The diagnosis of gastritis has its basis in histopathological examination of gastric biopsy tissues. While medical history and laboratory tests are helpful, endoscopy and biopsy is the gold standard in making the diagnosis, identifying its distribution, severity, and cause. The methods include histological staining (H&E, the Alcian blue stain and a modified silver stain), cultures, rapid urease test, and molecular detection (PCR DNA)
  • Staining of gastric mucosal biopsies by immunohistochemistry is recommended to detect H. pylori.
Serial sections of formalin fixed paraffin embedded biopsy tissue from two patients with gastric intestinal metaplasia without carcinoma. Haematoxylin-eosin staining (A, D), alcian blue/high iron diamine staining (B, E), and immunoperoxidase assay with the monoclonal antibody mAb Das-1 (C, F); (A-C) is from the same patient and (D-F) from the second patient. mAb Das-1 stained both goblet cells (shorter arrow) and metaplastic non-goblet cells (longer arrow) in the glands (C), suggesting colonic phenotype (incomplete type); While GIM is clearly evident with the presence of goblet cells (D, E) in the second patient, but mAb Das-1 did not stain the glands including goblet cells (F). The arrow shows the unstained goblet cells suggesting complete phenotype or small intestinal phenotype (original magnification × 160 for each part) | Mirza ZK, Das KK, Slate J, Mapitigama RN, Amenta PS, Griffel LH, Ramsundar L, Watari J, Yokota K, Tanabe H, et al. Gastric intestinal metaplasia as detected by a monoclonal antibody is highly associated with gastric adenocarcinoma. Gut. 2003;52:807–812.

Non-invasive methods (not requiring gastroscopy and biopsies):

Serological tests for detection of antibodies against H. pylori cannot differentiate between active and past infection.
  • Urease breath test (13C-UBT)
  • Fecal antigen test
  • Serology

Autoimmune gastritis:

The diagnosis of autoimmune gastritis centers on laboratory and histological examination. These include:
  • Atrophic gastritis of gastric corpus (body) and fundus of the stomach
  • Autoantibodies against the intrinsic factor and the parietal cells (M/sensitive serum biomarker)
  • Raised serum gastrin levels
  • Serum pepsinogen 1 level and pepsinogen 1 to pepsinogen 2 ratios
  • Other tests: Gastrin-17, IgG, and anti-H. pylori antibodies, cytokines (such as IL-8), and ghrelin (a growth-hormone-releasing peptide that is produced mainly by the gastric fundus mucosa).

Risk of gastric cancer in autoimmune gastritis:

In these patients, the risk of cancer is high irrespective of whether they have or do not have on-going H. pylori infection.
  • (1) Low levels of pepsinogen 1
  • (2) Low pepsinogen 1/pepsinogen 2 ratios
  • (3) High fasting serum gastrin
  • (4) Atrophic gastritis of the corpus and fundus

OLGA/OLGIM staging (Operative Link on Gastritis/IM Assessment) of atrophic gastritis:

This classification delineates the patients into five subgroups (0–IV) with markedly dissimilar likelihood to have or get a gastric cancer. The classification and sorting may objectively advice which one of the patients would need and benefit most of endoscopic surveillances and follow-ups.
OLGA staging for risk of stomach cancer: The staging is a practical tool for the delineation of patients to high (stages III–IV) and low (stages 0–II) risk groups for cancer, for gastric cancer of the intestinal type in particular. The staging requires endoscopy and proper biopsy practice but can also be done non-invasively by a blood test with applying specific biomarkers (pepsinogen I and II, gastrin-17 and Helicobacter pylori serology) that reflect the function (acid secretion) and the structure of both antral and corpus mucosa in the blood plasma/serum. | Rugge M, Meggio A, Pennelli G, Piscioli F, Giacomelli L, De Pretis G, et al. Gastritis staging in clinical practice: the OLGA staging system. Gut. 2007;56:631–6.

Simultaneous treatment with proton-pump inhibitors leads to false-negative results in both invasive and non-invasive tests. Also, patients treated with proton-pump inhibitors usually have negative histological staining for H. pylori.


Treatment regimens differ from antibiotics (in H. pylori gastritis) to vitamin supplementation (in autoimmune metaplastic atrophic gastritis) to immunomodulatory therapy (in autoimmune enteropathy) to dietary modifications (in eosinophilic gastritis).

H. pylori-associated gastritis:

After two eradication failures, H. pylori culture and tests for antibiotic resistance should be a consideration.
  • 1st line | Triple-therapy: Clarithromycin/PPI/amoxicillin for 14 to 21 days
  • 2nd line | Quadruple bismuth containing therapy

Autoimmune gastritis:

Monitor Iron and folate levels, and eradicate any co-infection with H. pylori. Endoscopic surveillance for cancer risk and gastric neuroendocrine tumors (NET) is required.
  • Substitution of deficient iron and vitamin B12 (parenteral 1000 micrograms or oral 1000 to 2000 micrograms)

Other forms of treatment:

  • Cessation of alcohol, smoking, anti-inflammatory drugs, spicy food, as well as managing stress
  • Immunomodulatory therapy in autoimmune enteropathy
  • Dietary modification in eosinophilic gastritis

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