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Atrophic Gastritis Clinical Presentation

  • Author: Nafea Zayouna, MD; Chief Editor: BS Anand, MD  more...
Updated: Jul 06, 2016


Atrophic gastritis represents the end stage of chronic gastritis, both infectious and autoimmune. In both cases, the clinical manifestations of atrophic gastritis are those of chronic gastritis, but pernicious anemia is observed specifically in patients with autoimmune gastritis and not in those with H pylori–associated atrophic gastritis.

H pylori-associated atrophic gastritis

Acute H pylori infection usually is not detected clinically, but experimental infection results in a clinical syndrome characterized by epigastric pain, fullness, nausea, vomiting, flatulence, malaise, and, sometimes, fever. The symptoms resolve in approximately a week, regardless of whether or not H pylori organisms are eliminated.

Persistence of the organism causes H pylori chronic gastritis, which usually is asymptomatic or may manifest as gastric pain and, rarely, nausea, vomiting, anorexia, or significant weight loss. Symptoms associated with complications of chronic H pylori–associated atrophic gastritis may develop, including gastric ulcers and gastric adenocarcinoma.

Autoimmune atrophic gastritis

The clinical mainfestations of autoimmune atrophic gastritis primarily are related to deficiency of cobalamin, which is not absorbed adequately because of IF deficiency resulting from severe gastric parietal cell atrophy. The disease has an insidious onset and progresses slowly. Cobalamin deficiency affects the hematological, GI, and neurologic systems.

Hematologic manifestations

The most significant manifestation is megaloblastic anemia, but, rarely, purpura due to thrombocytopenia may develop. Symptoms of anemia include weakness, light-headedness, vertigo and tinnitus, palpitations, angina, and symptoms of congestive heart failure.

GI manifestations

The lack of cobalamin is associated with megaloblastosis of the GI tract epithelium. Patients sometimes complain of a sore tongue. Anorexia with moderate weight loss occasionally associated with diarrhea may result from 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. Signs and symptoms include numbness and paresthesias in the extremities, weakness, and ataxia. Sphincter disturbances may be present. Mental function disturbances vary from mild irritability to severe dementia or psychosis. Neurologic disease may occur in patients with normal hematocrit and normal red cell parameters.


Patients with pernicious anemia have an increased frequency of gastric polyps and have a 2.9-fold increase in gastric cancer.

Additionally, patients with autoimmune atrophic gastritis and H pylori infection may manifest iron deficient anemia that may be refractory to oral iron treatment. H pylori eradication in combination with continued oral iron therapy has been shown to result in a significant increase in hemoglobin levels.

Primary hyperparathyroidism

Massironi et al found evidence of a noncausal association between chronic autoimmune atrophic gastritis (CAAG) and primary hyperparathyroidism (PHPT). In a prospective study, they evaluated the prevalence of PHPT in 107 patients with CAAG and the prevalence of CAAG in 149 patients with sporadic PHPT. The results indicate that PHPT is about three-fold more prevalent in patients with CAAG than in the general population and that CAAG is about four-fold more prevalent in patients with PHPT than in the general population.[11]



Physical examination is of little contributory value in atrophic gastritis; however, some findings are associated specifically with the complications of H pylori–associated atrophic gastritis and autoimmune atrophic gastritis.

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.

Findings in a patient with autoimmune atrophic gastritis 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.



Atrophic gastritis usually is associated with either chronic H pylori infection or with autoimmune gastritis. The environmental subtype of atrophic gastritis corresponds mostly with H pylori–associated atrophic gastritis, although other unidentified environmental factors may play a role in the development of gastric atrophy. Yagi et al used magnifying endoscopy to distinguish atrophic gastritis caused by H pylori from autoimmune gastritis.[12]

Chronic gastritis caused by H pylori infection of the stomach

H pylori infection of the stomach is by far the most common cause of chronic atrophic gastritis.

The risk of atrophic gastritis is increased by 10-fold if an H pylori infection is present.

Whether H pylori infection follows the multifocal atrophic gastritis pathway or the nonatrophic antral gastritis pathway may be related to genetic susceptibility factors, environmental factors that modulate the host-bacterial interaction, or bacterial strains.

Although H pylori possessing the cag (cytotoxin-associated gene) pathogenicity island have been shown to have increased virulence, to cause higher levels of mucosal inflammation, and to be present more frequently in individuals infected with H pylori who develop gastric cancer, no specific virulence factors have been identified that might be useful to predict specific H pylori disease outcome.

Host factors or the effects of other environmental agents are likely to be the determinant elements modulating patterns of disease progression. For example, family relatives of individuals with gastric cancer develop pangastritis more frequently in response to H pylori infection and they also develop multifocal intestinal metaplasia more often, a preneoplastic lesion of the stomach and a component of H pylori–associated atrophic gastritis.

Autoimmune atrophic gastritis

Autoimmune atrophic gastritis is a type of chronic atrophic gastritis limited to corpus-fundus mucosa and characterized by marked diffuse atrophy of parietal and chief cells.

Autoimmune gastritis is associated with serum antiparietal and anti-IF antibodies that cause IF deficiency, which, in turn, causes decreased availability of cobalamin and, eventually, pernicious anemia in some patients.

In some families, the disease appears to be transmitted with an autosomal dominant pattern of inheritance.

A large population-based study by Zhang et al suggested that the presence of antigastric parietal cell antibodies (APCAs) may contribute to the development of chronic atrophic gastritis even in the absence of H pylori infection. The study, which included 9684 persons aged 50-74 years, reported an overall seroprevalence of APCA in this population of 19.5%, with a strong association found between the existence of APCAs and the presence of chronic atrophic gastritis. The more severe the disease, the greater the association with APCA was found. However, the link between APCAs and the severity of chronic atrophic gastritis was greatest in persons who were negative for H pylori.[13]

Contributor Information and Disclosures

Nafea Zayouna, MD Fellow, Department of Internal Medicine, Division of Gastroenterology, St John Providence Hospital

Nafea Zayouna, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.


Michael H Piper, MD Clinical Assistant Professor, Department of Internal Medicine, Division of Gastroenterology, Wayne State University School of Medicine; Consulting Staff, Digestive Health Associates, PLC

Michael H Piper, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Gastroenterology, American College of Physicians, Michigan State Medical Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Additional Contributors

Gregory William Rutecki, MD Professor of Medicine, Fellow of The Center for Bioethics and Human Dignity, University of South Alabama College of Medicine

Gregory William Rutecki, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society of Nephrology, National Kidney Foundation, Society of General Internal Medicine

Disclosure: Nothing to disclose.


Simmy Bank, MD Chair, Professor, Department of Internal Medicine, Division of Gastroenterology, Long Island Jewish Hospital, Albert Einstein College of Medicine

Disclosure: Nothing to disclose.

Sandeep Mukherjee, MB, BCh, MPH, FRCPC Associate Professor, Department of Internal Medicine, Section of Gastroenterology and Hepatology, University of Nebraska Medical Center; Consulting Staff, Section of Gastroenterology and Hepatology, Veteran Affairs Medical Center

Disclosure: Merck Honoraria Speaking and teaching; Ikaria Pharmaceuticals Honoraria Board membership

Antonia R Sepulveda, MD, PhD Professor of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine; Director of Surgical Pathology, Department of Pathology and Laboratory Medicine, Hospital of the University of Pennsylvania

Antonia R Sepulveda, MD, PhD is a member of the following medical societies: American Association for Cancer Research, American Gastroenterological Association, American Society for Investigative Pathology, College of American Pathologists, and United States and Canadian Academy of Pathology

Disclosure: Genentech Honoraria Consulting; Leica Honoraria Consulting

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Atrophic gastritis. Schematic representation of Helicobacter pylori–associated patterns of gastritis. Involvement of the corpus, fundus, and gastric antrum, with progressive development of gastric atrophy as a result of loss of gastric glands and partial replacement of gastric glands by intestinal-type epithelium, or intestinal metaplasia (represented by the blue areas in the diagram) characterize multifocal atrophic gastritis. Individuals who develop gastric carcinoma and gastric ulcers usually present with this pattern of gastritis. Inflammation mostly limited to the antrum characterizes antral-predominant gastritis. Individuals with peptic ulcers usually develop this pattern of gastritis, and it is the most frequent pattern in Western countries.
Patterns of atrophic gastritis associated with chronic Helicobacter pylori infection and autoimmune gastritis.
Atrophic gastritis. Helicobacter pylori–associated chronic active gastritis (Genta stain, 20X). Multiple organisms (brown) are observed adhering to gastric surface epithelial cells. A mononuclear lymphoplasmacytic and polymorphonuclear cell infiltrate is observed in the mucosa.
Atrophic gastritis. Intestinal metaplasia of the gastric mucosa (Genta stain, 20X). Intestinal-type epithelium with numerous goblet cells (stained blue with the Alcian blue stain) replace the gastric mucosa and represent gastric atrophy. Mild chronic inflammation is observed in the lamina propria. This pattern of atrophy is observed both in Helicobacter pylori–associated atrophic gastritis and autoimmune gastritis.
Marked gastric atrophy of the stomach body.
Severe gastric atrophy of the stomach antrum.
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