ConditionDigestive system

Atrophic Gastritis

Atrophic gastritis is a long-term inflammation of the stomach lining that gradually destroys the glands that make acid and intrinsic factor. It is caused mainly by long-standing H. pylori infection or by an autoimmune attack on the stomach. Many people have no symptoms; others develop indigestion, anemia from low vitamin B12 or iron, and nerve symptoms. It slightly raises the risk of stomach cancer, so treatment focuses on clearing H. pylori, replacing vitamins and, for some, regular endoscopy.

Also called: Chronic atrophic gastritis, autoimmune atrophic gastritis, type A gastritis, type B gastritis, gastric atrophy

At a glance

What it is
Chronic stomach inflammation with loss of acid- and intrinsic factor-producing glands.
Main causes
Long-term H. pylori infection, or autoimmune gastritis.
Symptoms
Often none. Indigestion, early fullness, fatigue from anemia, numbness from B12 deficiency.
Diagnosis
Upper endoscopy with biopsies; blood tests for B12, iron, gastrin and antibodies.
Treatment
Eradicate H. pylori, replace B12 and iron, endoscopic surveillance in higher-risk cases.

When to get help

Call 911 or go to the ER

  • Vomiting blood or material like coffee grounds, or black, tarry stools

See a doctor within a day or two

  • Difficulty swallowing, persistent vomiting or unintended weight loss
  • Severe tiredness, breathlessness, chest pain or a racing heart from anemia
  • Numbness, tingling, unsteady walking or confusion that is getting worse

Book a routine appointment

  • Ongoing indigestion, upper belly discomfort or early fullness
  • Anemia found on a blood test, especially with low B12 or iron
  • Autoimmune thyroid disease or type 1 diabetes with tiredness or digestive symptoms
  • A family history of stomach cancer and stomach symptoms

What happens in atrophic gastritis

The stomach lining contains specialized glands. In the upper stomach (body and fundus), parietal cells make acid and intrinsic factor, a protein needed to absorb vitamin B12. In the lower stomach (antrum), cells make the hormone gastrin.

In atrophic gastritis, chronic inflammation destroys these glands, and the lining becomes thin. The glands may be replaced by tissue that looks like intestinal lining (intestinal metaplasia). This is the change most associated with cancer risk.

Two main types

H. pylori-associated (environmental)Autoimmune
CauseLong-term infection with H. pylori bacteriaImmune system attacks parietal cells
Where it startsAntrum, spreading upwardBody and fundus; antrum spared
Acid levelReducedVery low or absent
GastrinNormal or lowHigh
Main consequencesStomach cancer riskB12 deficiency (pernicious anemia), iron deficiency, neuroendocrine tumors
Associated conditionsPeptic ulcers earlier in lifeAutoimmune thyroid disease, type 1 diabetes, vitiligo

Causes and risk factors

  • H. pylori infection: the most common cause worldwide. The infection is usually acquired in childhood and persists for decades without treatment.
  • Autoimmunity: antibodies against parietal cells and intrinsic factor. More common in women and people of Northern European descent, and often runs in families.
  • Age: atrophy becomes more common with age.
  • Smoking, high-salt diet and a family history of stomach cancer increase risk.

Symptoms

Many people have no symptoms for years. When symptoms occur, they include:

  • indigestion, upper belly discomfort, bloating or feeling full quickly
  • nausea and reduced appetite
  • Vitamin B12 deficiency: fatigue, pale skin, shortness of breath, a sore red tongue, numbness and tingling in the hands and feet, balance problems, memory problems or low mood
  • Iron deficiency anemia: fatigue, breathlessness, brittle nails and restless legs. Stomach acid helps absorb iron, so low acid causes iron deficiency, often years before B12 runs out

B12 deficiency from autoimmune gastritis is called pernicious anemia. Nerve damage from B12 deficiency can become permanent if untreated, so early diagnosis matters.

Diagnosis

  • Upper endoscopy with biopsies: the key test. Biopsies are taken from several areas of the stomach (following a standard protocol) to confirm atrophy, look for intestinal metaplasia or dysplasia, and test for H. pylori.
  • H. pylori testing: breath test, stool antigen test or biopsy.
  • Blood tests: - full blood count, B12, folate, iron and ferritin - anti-parietal cell and anti-intrinsic factor antibodies for autoimmune gastritis - gastrin (high in autoimmune gastritis) and pepsinogen levels, which are low with atrophy - thyroid function, since autoimmune thyroid disease often coexists

Treatment

Eradicate H. pylori

If H. pylori is present, it is treated with a combination of antibiotics and an acid-reducing medicine for 14 days, followed by a test to confirm it has gone. Eradication stops further damage and lowers cancer risk, though established atrophy and metaplasia may not fully reverse. Family members living in the same household may also be tested.

Replace vitamins and iron

  • Vitamin B12: given as injections, or high-dose tablets, which can work even without intrinsic factor because a small amount is absorbed passively. Treatment is usually lifelong in autoimmune gastritis.
  • Iron: oral iron, or intravenous iron if tablets are not absorbed or tolerated.
  • Folate and vitamin D levels may also be checked.

Surveillance endoscopy

Because atrophic gastritis increases the risk of gastric cancer, people with extensive atrophy or intestinal metaplasia, or a family history of stomach cancer, may be offered endoscopy every few years. Intervals are individualized. Autoimmune gastritis also raises the risk of gastric neuroendocrine tumors (type 1 carcinoids), which are usually small and slow-growing.

Symptom relief

Acid-reducing medicines are generally unhelpful in autoimmune gastritis, where acid is already low. Small meals and treating anemia often improve energy and digestion.

Complications

  • pernicious anemia and nerve damage from B12 deficiency
  • iron deficiency anemia
  • gastric neuroendocrine tumors
  • stomach cancer (adenocarcinoma), a small but real increased risk
  • bacterial overgrowth from low acid

Outlook

With H. pylori treated, vitamins replaced and appropriate monitoring, most people live normally. B12 injections fully correct anemia, and nerve symptoms often improve if treated early.

Frequently asked questions

What is atrophic gastritis?

It is long-term inflammation of the stomach lining that destroys the glands making stomach acid and intrinsic factor. The lining becomes thin. It is caused mostly by long-standing H. pylori infection or an autoimmune reaction.

What are the symptoms of atrophic gastritis?

Many people have none. Others have indigestion, nausea, early fullness, and symptoms of vitamin B12 or iron deficiency: tiredness, pale skin, breathlessness, numbness or tingling in the hands and feet, and memory problems.

Can atrophic gastritis be reversed?

Treating H. pylori stops further damage, and mild atrophy may partly improve. Advanced atrophy and intestinal metaplasia usually do not reverse fully, especially in autoimmune gastritis, so vitamin replacement and monitoring continue.

Does atrophic gastritis lead to cancer?

It increases the risk of stomach cancer, especially when intestinal metaplasia is extensive, but most people with atrophic gastritis never develop cancer. Surveillance endoscopy helps detect early changes in people at higher risk.

Sources

This guide was written from current patient and clinical guidance, including:

  • American Gastroenterological Association: Clinical Practice Update on the Diagnosis and Management of Atrophic Gastritis
  • American College of Gastroenterology: Clinical Guideline: Treatment of Helicobacter pylori Infection
  • MedlinePlus: Pernicious anemia
  • NIDDK: Gastritis
  • British Society of Gastroenterology: Guidelines on the diagnosis and management of patients at risk of gastric adenocarcinoma