From the Guidelines
Gastritis can lead to intestinal metaplasia through chronic inflammation of the gastric mucosa, and the most effective way to prevent this progression is by eradicating H. pylori infection, as recommended by the most recent guidelines 1.
Key Points
- Gastritis is a precursor to intestinal metaplasia, which is a precancerous condition that can lead to gastric cancer.
- The progression from gastritis to intestinal metaplasia is influenced by environmental factors, such as H. pylori infection, and genetic predisposition.
- Eradication of H. pylori infection is the most effective way to prevent the progression of gastritis to intestinal metaplasia and gastric cancer, as supported by recent studies 2, 3.
- Early detection and treatment of underlying gastritis, particularly eradication of H. pylori when present, can potentially halt or slow the progression to intestinal metaplasia and gastric cancer.
Mechanism of Progression
The normal gastric epithelium undergoes a protective adaptation in response to chronic inflammation, where native gastric cells are gradually replaced by intestinal-type epithelium with goblet cells, absorptive cells, and Paneth cells—a condition known as intestinal metaplasia. This transformation represents the body's attempt to protect itself from ongoing injury, as intestinal-type cells are more resistant to the harsh gastric environment. However, this adaptation comes with risks, as intestinal metaplasia is considered a precancerous condition and an important step in the Correa cascade leading to gastric cancer.
Importance of H. pylori Eradication
H. pylori infection is a major risk factor for gastric cancer, and eradication of the infection can reduce the risk of gastric cancer, as shown in recent studies 4, 3. The Taipei Consensus recommended an organized screening program in areas with a high incidence rate of gastric cancer, which includes screening for H. pylori infection and eradication treatment for those who test positive 3.
Clinical Implications
The most recent guidelines recommend a risk-stratified approach to endoscopic surveillance, with only patients with high-risk GIM phenotypes or persistent refractory H. pylori infection undergoing regular-interval endoscopic surveillance 1. Early detection and treatment of underlying gastritis, particularly eradication of H. pylori when present, can potentially halt or slow the progression to intestinal metaplasia and gastric cancer.
From the FDA Drug Label
In two 24 month carcinogenicity studies, Sprague-Dawley rats were treated with oral lansoprazole doses of 5 to 150 mg/kg/day, about one to 40 times the exposure on a body surface (mg/m 2) basis of a 50 kg person of average height [1. 46 m 2 body surface area(BSA)] given the recommended human dose of 30 mg/day. Lansoprazole produced dose-related gastric enterochromaffin-like (ECL) cell hyperplasia and ECL cell carcinoids in both male and female rats. It also increased the incidence of intestinal metaplasia of the gastric epithelium in both sexes
Gastritis can lead to intestinal metaplasia as it can cause chronic inflammation of the gastric epithelium, which may result in metaplastic changes. The exact mechanism is not explicitly stated in the drug label, but it is mentioned that lansoprazole increased the incidence of intestinal metaplasia in rats, suggesting a possible link between gastritis and intestinal metaplasia 5.
- Key points:
- Gastritis can cause chronic inflammation of the gastric epithelium
- Chronic inflammation may lead to metaplastic changes
- Lansoprazole increased the incidence of intestinal metaplasia in rats However, the FDA label does not provide a clear explanation of how gastritis leads to intestinal metaplasia.
From the Research
Gastritis and Intestinal Metaplasia
Gastritis can lead to intestinal metaplasia through several mechanisms:
- Chronic infection with Helicobacter pylori (Hp) is a major cause of gastric mucosal damage and is linked to gastric atrophy and cancer 6, 7, 8, 9, 10.
- Hp infection can lead to atrophic gastritis (AG), a chronic disease characterized by atrophy and/or intestinal metaplasia of the gastric glands 6.
- Intestinal metaplasia is a precancerous lesion that can progress to gastric cancer, particularly in the presence of extensive intestinal metaplasia 6, 8, 9, 10.
- The use of proton pump inhibitors (PPIs) can mask Hp infection, leading to a diagnosis of non-Hp gastritis and increasing the risk of intestinal metaplasia 7.
Risk Factors for Intestinal Metaplasia
Several factors can increase the risk of intestinal metaplasia, including:
- Chronic Hp infection 6, 7, 8, 9, 10.
- Atrophic gastritis (AG) 6.
- Use of PPIs 7.
- High bacterial load, high gastric acidity, Hp strain, smoking, low compliance, overweight, and increasing antibiotic resistance 6.
- Excess salt, cigarette smoking, and deficiency of foodstuffs with an antioxidizing effect 9.
Reversibility of Intestinal Metaplasia
Intestinal metaplasia was previously considered an irreversible precancerous lesion, but recent studies suggest that it may be reversible with Hp eradication 8.