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Atrophic Gastritis Symptoms and How to Determine If the Condition Is Worsening

Atrophic gastritis is a common diagnosis made during endoscopic examinations. Since there is currently no definitive cure for atrophic gastritis, and considering it is recognized as a precancerous condition with potential for malignant transformation, many people are concerned about how to identify signs of worsening disease.

Common Symptoms of Atrophic Gastritis

The clinical symptoms of atrophic gastritis are often nonspecific. Some individuals may not experience any noticeable symptoms, while others may report digestive discomfort such as upper abdominal fullness, nausea, vomiting, or pain in the upper abdomen. Additional symptoms can include burning sensations, acid reflux, belching, bitter taste in the mouth, or bad breath. These symptoms can usually be managed with medications that aid digestion, suppress gastric acid production, or enhance gastrointestinal motility.

Signs of Progression or Worsening Atrophic Gastritis

When atrophic gastritis worsens—especially if cancerous changes occur—the symptoms become more severe. Persistent abdominal pain that doesn't respond to medication is a key indicator. Digestive symptoms also intensify, potentially leading to reduced appetite, weight loss, anemia, fatigue, and in serious cases, vomiting, hematemesis (vomiting blood), or melena (black tarry stools). Notably, atrophic gastritis can impair intrinsic factor production, which is essential for vitamin B12 absorption. This deficiency can lead to megaloblastic anemia. Therefore, unexplained cases of nutritional anemia should prompt further investigation into possible progression of atrophic gastritis.

How to Assess the Severity of Atrophic Gastritis

Despite the variety of symptoms patients may experience, these do not always correlate directly with the severity of the underlying condition. The most reliable way to determine if atrophic gastritis is worsening is through histological biopsy findings.

Endoscopic Evaluation of Gastric Atrophy

During endoscopy, atrophic gastritis typically presents with a mixed red and white mucosal appearance, where the white areas dominate. The mucosal folds may flatten or disappear, visible blood vessels may appear, and there could be granular or nodular surface changes. The Kimura-Takemoto classification is commonly used to categorize atrophic gastritis based on endoscopic findings:

Type C (closed type): Atrophy confined to the antrum

Type O (open type): Atrophy extends beyond the cardia

Type C is further classified as C1 (limited to the antrum), C2 (extends beyond the angularis), and C3 (approaches the cardia). Type O includes O1 (just beyond the cardia), O2 (involves the fundus), and O3 (extends into the corpus). The higher the classification, the more extensive the atrophy and the greater the risk.

Pathological Assessment of Gastric Atrophy

A definitive diagnosis of atrophic gastritis requires both endoscopic and histopathological evaluation. The gold standard remains biopsy confirmation showing reduction or loss of gastric mucosal glands.

Degree of Atrophy

Histologically, atrophic gastritis is categorized as mild, moderate, or severe. Mild atrophy involves less than one-third loss of native glands, moderate refers to a reduction between one-third and two-thirds, and severe means over two-thirds of glands have been lost, leaving only sparse or no glands remaining. A shift from mild to moderate or severe atrophy in pathology reports indicates disease progression.

Intestinal Metaplasia Grading

Intestinal metaplasia refers to the transformation of gastric epithelium into intestinal-like tissue, serving as a marker of mucosal damage and a subtype of atrophic gastritis. It's graded by extent:

Mild: Intestinal metaplasia occupies less than one-third of the glandular and surface epithelial area

Moderate: One-third to two-thirds involvement

Severe: More than two-thirds involvement

Higher grades of intestinal metaplasia correlate with increased cancer risk.

Intraepithelial Neoplasia and Dysplasia

Intraepithelial neoplasia and dysplasia are essentially synonymous terms indicating precancerous changes in epithelial tissue. While "dysplasia" emphasizes morphological alterations, "intraepithelial neoplasia" highlights the progression toward malignancy. It is now more commonly used in pathology reporting and is divided into low-grade and high-grade categories. High-grade intraepithelial neoplasia may include early or in situ cancer. Low-grade corresponds to mild or moderate dysplasia, and high-grade aligns with severe dysplasia. A diagnosis of high-grade dysplasia or high-grade intraepithelial neoplasia warrants aggressive management, including possible surgical or endoscopic intervention.

Gastric Function Tests for Early Detection

Serum biomarkers, known collectively as the "four gastric function tests," play a vital role in early detection and monitoring of atrophic gastritis:

Pepsinogen I (PGI): Levels decrease with atrophy of the corpus and fundus

Pepsinogen II (PGII): Elevated levels are associated with peptic ulcer disease and inflammation

Pepsinogen Ratio (PGR = PGI/PGII): Progressive decline suggests increasing mucosal atrophy

Gastrin-17 (G-17): Reflects antral mucosal health; lower levels indicate more severe atrophy

Helicobacter pylori Antibodies: Higher prevalence in atrophic gastritis patients compared to healthy controls

These non-invasive, cost-effective tests are valuable tools for large-scale screening and monitoring of gastric atrophy.

Conclusion

Atrophic gastritis is a prevalent condition with generally favorable outcomes for most patients. However, due to its premalignant potential, regular endoscopic and histological follow-up is essential. Monitoring symptoms, endoscopic features, and pathological changes—including the presence of intestinal metaplasia, dysplasia, or intraepithelial neoplasia—helps assess disease progression and guide treatment decisions. Early identification and appropriate management are crucial, particularly when high-grade lesions are detected.

TimeTooReal2025-07-10 08:56:25
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