Atrophic Gastritis萎缩性胃炎

Atrophic gastritis is defined by the loss of gastric glands and the thinning of the gastric mucosa. The condition represents the endpoint of chronic gastritis, most commonly driven by persistent Helicobacter pylori infection or autoimmune processes directed against parietal cells. As the gastric glands atrophy, the production of hydrochloric acid, pepsin, and intrinsic factor declines, which may lead to hypochlorhydria, impaired protein digestion, and in autoimmune cases, vitamin B12 deficiency (pernicious anemia).

Classification

• H. pylori-associated atrophic gastritis: The most common form worldwide. Infection with H. pylori causes chronic inflammation that, over years to decades, can lead to progressive glandular loss. The atrophy typically begins in the antrum and may extend to the corpus (pangastritis) in advanced cases.
• Autoimmune atrophic gastritis (AAG): The immune system targets parietal cells and intrinsic factor, leading to corpus-predominant atrophy, hypochlorhydria, and vitamin B12 deficiency. It is associated with other autoimmune conditions, particularly Hashimoto's thyroiditis and type 1 diabetes.
• Mixed forms: In some patients, both H. pylori infection and autoimmune mechanisms contribute.

Epidemiology

The prevalence of atrophic gastritis varies substantially by geography, largely tracking H. pylori infection rates. In East Asian countries (Japan, China, Korea), where H. pylori prevalence is high, atrophic gastritis may be found in 30 to 50 percent of adults over age 50. In Western countries with lower H. pylori prevalence, rates are lower but still significant. Autoimmune atrophic gastritis affects approximately 1 to 2 percent of the general population, with a higher prevalence among women and individuals with other autoimmune diseases.

Diagnostic Criteria

Diagnosis requires endoscopic evaluation with biopsy. Key diagnostic elements include:

• Endoscopy: Visual assessment may show pale, thin mucosa with visible submucosal blood vessels. However, endoscopic appearance alone is insufficient — biopsy confirmation is required.
• Histopathology: The gold standard. Biopsy specimens are assessed for glandular atrophy, intestinal metaplasia, inflammation, and dysplasia using standardized systems such as the Sydney System or OLGA (Operative Link on Gastritis Assessment) staging.
• H. pylori testing: Biopsy-based tests (histology, rapid urease test), urea breath test, or stool antigen test.
• Serology: Parietal cell antibodies and intrinsic factor antibodies suggest autoimmune gastritis. Gastrin levels are typically elevated, and pepsinogen I/II ratio is reduced.
• Vitamin B12 and iron studies: Particularly in autoimmune gastritis, where deficiency is common.

The following describes how TCM practitioners may conceptualize the symptoms of atrophic gastritis. These are traditional theoretical associations, not validated diagnostic correspondences. TCM patterns do not replace histopathological diagnosis.

TCM does not have a concept of gastric mucosal atrophy as defined by histopathology. However, the clinical presentation of atrophic gastritis — poor appetite, epigastric discomfort, fatigue, dry mouth, and progressive wasting — overlaps significantly with several classical TCM patterns. Practitioners who work alongside gastroenterologists often use these pattern frameworks to guide herbal and dietary recommendations while the patient continues conventional surveillance.

Spleen and Stomach Qi Deficiency (Pi Wei Qi Xu, 脾胃气虚)

This is the most commonly discussed pattern in the context of chronic atrophic gastritis, particularly in the early to middle stages. The progressive loss of digestive function and the accompanying fatigue, poor appetite, and abdominal discomfort map onto the TCM concept of Spleen and Stomach weakness. The Spleen lacks the Qi to properly transform food, and the Stomach lacks the Qi to properly receive and descend it. Tongue is typically pale with teeth marks; pulse is weak at the right Guan position.

Stomach Yin Deficiency (Wei Yin Xu, 胃阴虚)

As atrophic gastritis progresses, the loss of gastric secretions (acid, mucus, enzymes) parallels the TCM concept of Stomach Yin depletion. The Stomach “dries out.” This pattern is associated with dry mouth and throat, a burning or uncomfortable sensation in the epigastrium, poor appetite with a sense of emptiness, and a red tongue with little or no coating. Some practitioners consider this pattern to more closely reflect the mucosal atrophy itself. Learn more about Stomach Yin Deficiency.

Blood Stasis (Xue Yu, 血瘀)

In long-standing atrophic gastritis, particularly when intestinal metaplasia or dysplasia is present, some practitioners discuss Blood stasis as a contributing or complicating pattern. Chronic inflammation damages the microcirculation of the gastric mucosa, and in TCM theory, prolonged stagnation leads to stasis. Signs may include fixed, stabbing epigastric pain, a purplish tongue, and a choppy pulse. This pattern is often discussed alongside the deficiency patterns, as chronic deficiency can lead to stasis.

Damp-Heat (Shi Re, 湿热)

In cases where H. pylori is the primary driver, some practitioners associate the infection with Damp-Heat in the Stomach. The bacterium creates chronic inflammation, and the TCM concept of Damp-Heat captures aspects of this: a feeling of fullness, sticky mouth, possible nausea, and a yellow, greasy tongue coating. This pattern is more commonly discussed in active, symptomatic phases rather than in advanced atrophy.

The evidence for TCM in atrophic gastritis faces several significant challenges:

• Most studies are small and from China. A 2019 meta-analysis in Journal of Gastroenterology and Hepatology reviewed TCM formulas for atrophic gastritis and identified over 60 RCTs, but nearly all were single-center, had fewer than 100 participants per arm, and were conducted in China. Publication bias toward positive results is a well-documented concern in Chinese herbal medicine research. PMID: 31320846
• Outcome measures are inconsistent. Some studies assess symptom improvement; others assess endoscopic appearance; still others use histopathological scoring. Few use all three. Without standardized outcomes, comparing and pooling results is problematic.
• Blinding is difficult. Herbal decoctions have distinctive tastes and appearances. Very few trials use adequate placebo controls that match the active treatment in taste, appearance, and smell.
• No reversal of atrophy has been conclusively demonstrated. While some trials have reported improvements in endoscopic or histological scores, these findings have not been replicated in large, well-designed, multicenter trials. Regression of intestinal metaplasia with herbal treatment has been claimed in some studies but remains unproven.
• Pattern heterogeneity. Different TCM patterns are treated with different formulas. Trials that do not stratify by pattern (or that use a single formula for all participants regardless of pattern) may fail to show benefit even if the approach has merit for specific subgroups. However, pattern-stratified trials require much larger sample sizes.

Bottom line: the existing evidence base is suggestive but far from conclusive. TCM should not be presented as an established approach for atrophic gastritis. More rigorous research is needed.

Atrophic gastritis is a condition where safety boundaries are particularly important:

Some herbs traditionally used for gastric conditions may interact with proton pump inhibitors, H2 receptor blockers, or antibiotics commonly prescribed for atrophic gastritis. Product quality is also an ongoing concern — herbal supplements are less regulated than pharmaceuticals, and contamination or adulteration has been documented.