❖ Definition:  

 Atrophic gastritis is a histopathologic entity characterized by: 

✓ Chronic inflammation of the gastric mucosa. 

✓ With loss of the gastric glandular cells and replacement by intestinal-type epithelium, 

pyloric-type glands, and fibrous tissue. 

❖ Causes:  

 Two main causes of atrophic gastritis can be distinguished histologically:   

1) H pylori–associated atrophic gastritis: 

➢ Usually, a multifocal process that involves both the antrum and the oxyntic mucosa of 

the gastric corpus and fundus.  

➢ Frequently asymptomatic, but individuals with this disease are at increased risk of 

developing gastric carcinoma, which may decrease following H pylori eradication. 

2) Autoimmune gastritis: 

➢ Essentially is restricted to the gastric corpus and fundus. 

➢ Individuals with autoimmune gastritis may develop pernicious anemia because of 

extensive loss of parietal cell mass and anti-intrinsic factor antibodies. 

➢ Patients with chronic atrophic gastritis develop low gastric acid output and 

hypergastrinemia, which may lead to enterochromaffin-like (ECL) cell hyperplasia and 

carcinoid tumors.  

❖ Pathophysiology:  

1) H pylori–associated atrophic gastritis: 

➢ H pylori lodge within the mucous layer of the stomach along the gastric surface 

epithelium and rarely are present in the deeper glands. 

➢ The infection is usually acquired during childhood and progresses over the lifespan of 

the individual if left untreated. 

➢ Significant damage associated with the release of bacterial and inflammatory toxic 

products is inflicted on the gastric epithelial cells, resulting in gastric atrophy over time.  

 

➢ During the process of gastric mucosal atrophy, some glandular units develop an 

intestinal type of epithelium, and intestinal metaplasia throughout the gastric mucosa 

when atrophic gastritis is fully established. 

➢ Other glands are simply replaced by fibrous tissue, resulting in corpus atrophy, which 

results in hypochloridia or achloridia raises serum gastrin levels, thereby increasing the 

risk for the development of neuroendocrine tumors. 

2) Autoimmune gastritis: 

➢ The development of chronic atrophic gastritis limited to corpus-fundus mucosa and 

marked diffuse atrophy of parietal and chief cells. 

➢ Associated with serum antiparietal and anti-intrinsic factor antibodies that cause 

intrinsic factor (IF) deficiency, which, in turn, causes decreased availability of cobalamin 

(vitamin B-12) and, eventually, Pernicious anemia in some patients.  

❖ Prognosis:  

➢ Atrophic gastritis is a progressive condition with increasing loss of gastric glands and 

replacement by foci of intestinal metaplasia over years. 

➢ Results from studies evaluating the evolution of atrophic gastritis after eradication of H 

pylori have been conflicting. 

➢ Follow-up for up to several years after H pylori eradication has not shown regression of 

gastric atrophy in most studies, 

whereas other studies report improvement in the extent of atrophy. 

➢ H pylori eradication in patients with endoscopically-resected early gastric cancer resulted 

in decreased appearance of new early cancers, while intestinal-type gastric cancers 

developed in the control group without H pylori eradication. 

➢ Also, eradication of H pylori if the organisms are detected in patients with atrophic 

gastritis, help in prevention of development of gastric cancer. 

❖ Complications: increased risk of:  

 Gastric ulcers, Gastric adenocarcinoma, Gastric polyps. 

 Pernicious anemia  

 Malabsorption associated with megaloblastic changes in the epithelium of the small intestine. 

 Neurologic manifestations: 

➢ These result from demyelination, followed by axonal degeneration and neuronal death. 

➢ The affected sites include peripheral nerves, posterior and lateral columns of the 

spinal cord, and the cerebrum. 

❖ Physical Examination: 

➢ Physical examination is of little contributory value in atrophic gastritis; however, some 

findings are associated specifically with the complications. 

➢ In uncomplicated H pylori–associated atrophic gastritis: 

✓ Clinical findings are few and nonspecific. 

✓ Epigastric tenderness may be present. 

✓ If gastric ulcers coexist, guaiac-positive stool may result from occult blood loss. 

➢ In a patient with autoimmune atrophic gastritis: 

✓ Findings result from the development of pernicious anemia and neurologic complications.  

✓ With severe cobalamin deficiency, the patient is pale and has slightly icteric skin and eyes. 

✓ The pulse is rapid, and the heart may be enlarged. 

✓ Auscultation usually reveals a systolic flow murmur. 

❖ Diagnostic Considerations: 

➢ Chronic atrophic gastritis with intestinal metaplasia is recognized to be a precancerous 

lesion that can evolve toward low- and high-grade intraepithelial lesions and gastric cancer, 

particularly those involving H pylori infection. 

➢ Autoimmune atrophic gastritis has been associated with thyroid diseases, type 1 DM, 

Addison disease, chronic spontaneous urticaria, myasthenia gravis and vitiligo.  

❖ Laboratory Studies: 

 Endoscopic multiple gastric biopsies, 2 biopsy samples from the gastric antrum, 2 from the 

corpus and 1 from the incisura, and submit to pathology in separate vials. 

 Decreased serum pepsinogen I levels 

and the ratio of pepsinogen I to pepsinogen II in the serum can assess gastric atrophy. 

 Combination of pepsinogen, gastrin-17 and anti- H pylori antibodies a reliable tool for 

diagnosis of atrophic gastritis. 

 Other laboratory findings may include the following:-  

1) Elevated serum gastrin levels  

2) Microcytic, hypochromic anemia (which may precede the development of megaloblastic, 

vitamin B12-associated anemia)  

3) Vitamin B12 deficiency (which may elevated homocysteine levels)  

4) Rapid urease test from gastric biopsy tissue  

5) Bacterial culture of gastric biopsy to assess antibiotic susceptibility in patients in whom 

first-line eradication therapy fails.  

6) Serologic detection of anti-H pylori antibodies.  

 

❖ Diagnosis of autoimmune gastritis is made as follows:  

 Antiparietal and anti-IF antibodies in the serum. 

 Achlorhydria, both basal and stimulated, and hypergastrinemia. 

 Low serum cobalamin (B-12) levels (< 100>

 Shilling test: Results may be abnormal and can be corrected by IF. 

❖ Treatment of atrophic gastritis:-  

 Once atrophic gastritis is diagnosed, treatment can be directed: 

1) Eradication of HB pylori–associated atrophic gastritis. 

2) Correct complications as Pernicious anemia by vitamin B-12.   

3) Attempt to reverse the atrophic process. 

❖ Prevention: 

 Epidemiologic studies of H pylori–associated chronic gastritis show that acquisition of the 

infection is associated with large, crowded households and lower socioeconomic status. 

 Follow-up care may be individualized depending on the findings during endoscopy. 

For example, if dysplasia is found at endoscopy, increased surveillance is necessary.