Atrophic gastritis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:

Digestive System


Atrophic gastritis is a process of chronic inflammation of the stomach mucosa, leading to loss of gastric glandular cells and their eventual replacement by intestinal and fibrous tissues. As a result, the stomach's secretion of essential substances such as hydrochloric acid, pepsin, and intrinsic factor is impaired, leading to digestive problems, vitamin B12 deficiency, and megaloblastic anemia. It can be caused by persistent infection with Helicobacter pylori, or can be autoimmune in origin.

Autoimmune Metaplastic Atrophic Gastritis (AMAG) is an inherited form of atrophic gastritis characterized by an immune response directed toward parietal cells and intrinsic factor. The presence of serum antibodies to parietal cells and to intrinsic factor are characteristic findings. The autoimmune response subsequently leads to the destruction of parietal cell mass which then results in profound hypochlorhydria (and elevated gastrin levels). The inadequate production of intrinsic factor also leads to vitamin B12 malabsorption and pernicious anemia. AMAG is typically confined to the gastric body and fundus

Hypochlorhydria induces G Cell (Gastrin producing) hyperplasia which leads to hypergastrinemia. Gastrin exerts a trophic effect on enterochromaffin-like cells (ECL cells are responsible for histamine secretion) and is hypothesized to be one mechanism to explain the malignant transformation of ECL cells into carcinoid tumors in AMAG.

Patients with AMAG and pernicious anemia are also at increased risk for the development of gastric adenocarcinoma. The optimal endoscopic surveillance strategy is not known but all nodules and polyps should be removed in these patients.

Environmental metaplastic atrophic gastritis (EMAG) is due to environmental factors, such as diet and H. pylori infection. EMAG is typically confined to the body of the stomach. Patients with EMAG are also at increased risk of gastric carcinoma.

Recent research has shown that AMAG is a result of the immune system attacking the parietal cells,the attack is being triggered by H. pylori through a mechanism called molecular mimicry.

Historical Perspective




Drug Side Effect


Differentiating Atrophic gastritis from Other Diseases

Epidemiology and Demographics

Risk Factors


Natural History, Complications, and Prognosis

Natural History




Diagnostic Criteria

History and Symptoms

Physical Examination

Laboratory Findings

Imaging Findings

Other Diagnostic Studies

Differential diagnosis

Differential Diagnosis

Atrophic gastritis must be differentiated from:[1][2][3][4][5][6][7][8][9]

Disease Cause Symptoms Diagnosis Other findings
Pain Nausea



Heartburn Belching or


Weight loss Loss of


Stools Endoscopy findings
Location Aggravating Factors Alleviating Factors
Acute gastritis Food Antacids ? ? ? - ? Black stools -
Chronic gastritis Food Antacids ? ? ? ? ? - H. pylori gastritis

Lymphocytic gastritis

  • Enlarged folds
  • Aphthoid erosions
Atrophic gastritis Epigastric pain - - ? - ? ? - H. pylori


Autoimmune gastritis diagnosis include:

Crohn's disease - - - - - ? ?
  • Mucosal nodularity with cobblestoning
  • Multiple aphthous ulcers
  • Linier or serpiginous ulcerations
  • Thickened antral folds
  • Antral narrowing
  • Hypoperistalsis
  • Duodenal strictures
  • Lower esophageal sphincter abnormalities
  • Spicy food
  • Tight fitting clothing

(Suspect delayed gastric emptying)

? - - - - Other symptoms:


Peptic ulcer disease
Duodenal ulcer
  • Pain aggravates with empty stomach

Gastric ulcer

  • Pain aggravates with food
  • Pain alleviates with food
? ? - - - Gastric ulcers
  • Discrete mucosal lesions with a punched-out smooth ulcer base with whitish fibrinoid base
  • Most ulcers are at the junction of fundus and antrum
  • 0.5-2.5cm

Duodenal ulcers

Other diagnostic tests
Gastrinoma - - ?

(suspect gastric outlet obstruction)

? - - - Useful in collecting the tissue for biopsy

Diagnostic tests

Gastric Adenocarcinoma - - ? ? ? ? ? Esophagogastroduodenoscopy
  • Multiple biopsies are taken to establish the diagnosis
Other symptoms
Primary gastric lymphoma - - - - - ? - - Useful in collecting the tissue for biopsy Other symptoms


Medical Therapy




  1. Sugimachi K, Inokuchi K, Kuwano H, Ooiwa T (1984). "Acute gastritis clinically classified in accordance with data from both upper GI series and endoscopy". Scand J Gastroenterol. 19 (1): 31–7. PMID 6710074.
  2. Sipponen P, Maaroos HI (2015). "Chronic gastritis". Scand J Gastroenterol. 50 (6): 657–67. doi:10.3109/00365521.2015.1019918. PMC 4673514. PMID 25901896.
  3. Sartor RB (2006). "Mechanisms of disease: pathogenesis of Crohn's disease and ulcerative colitis". Nat Clin Pract Gastroenterol Hepatol. 3 (7): 390–407. doi:10.1038/ncpgasthep0528. PMID 16819502.
  4. Sipponen P (1989). "Atrophic gastritis as a premalignant condition". Ann Med. 21 (4): 287–90. PMID 2789799.
  5. Badillo R, Francis D (2014). "Diagnosis and treatment of gastroesophageal reflux disease". World J Gastrointest Pharmacol Ther. 5 (3): 105–12. doi:10.4292/wjgpt.v5.i3.105. PMC 4133436. PMID 25133039.
  6. Ramakrishnan K, Salinas RC (2007). "Peptic ulcer disease". Am Fam Physician. 76 (7): 1005–12. PMID 17956071.
  7. Banasch M, Schmitz F (2007). "Diagnosis and treatment of gastrinoma in the era of proton pump inhibitors". Wien Klin Wochenschr. 119 (19–20): 573–8. doi:10.1007/s00508-007-0884-2. PMID 17985090.
  8. Dicken BJ, Bigam DL, Cass C, Mackey JR, Joy AA, Hamilton SM (2005). "Gastric adenocarcinoma: review and considerations for future directions". Ann Surg. 241 (1): 27–39. PMC 1356843. PMID 15621988.
  9. Ghimire P, Wu GY, Zhu L (2011). "Primary gastrointestinal lymphoma". World J Gastroenterol. 17 (6): 697–707. doi:10.3748/wjg.v17.i6.697. PMC 3042647. PMID 21390139.

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