Pathologic interpretation of gastroscopic mucosal biopsy
Inflammation
Early stage: chronic superficial, with inflammatory cells infiltrating the superficial mucosal layer between the small gastric recesses.
Progressive stage: inflammatory cells progress to the deeper mucosal layers and can reach the entire gastric mucosa, often accompanied by atrophy of the gastric glands.
Terminal stage: the inflammation subsides and all gastric glands are atrophied.
Under gastroscopic visualization, mucosal congestion, edema, erosion, hemorrhage, ulceration, mucosal whitening, exposure of submucosal vessels, granular mucosal hyperplasia, and toughness to the touch.
According to the number of inflammatory cells, there are three levels of mild to moderate severity. However, the meaning of the representation cannot be understood mechanically, because inflammation is a process, and the reduction of inflammation mostly refers to the improvement of the disease, but if the progression of inflammation is never controlled, the result can also be that the inflammation destroys the tissue and the inflammation disappears. This is similar to the situation of hepatitis leading to cirrhosis: the inflammation triumphs and returns, leaving behind a barren landscape.
Active
The more rigorous pathology reports will have inflammatory activity described on them. By activity, we mean the number of neutrophils in the inflammatory cells that infiltrate the gastric mucosa.
Mild activity – small or moderate amounts of neutrophils in the lamina propria of the gastric mucosa.
Moderate motility – a high number of neutrophils in the lamina propria. And infiltration into the epithelium of the gastric glands.
Severe activity – extensive gastric mucosal cryptitis with mucosal epithelial erosion and crypt abscess formation.
In short, activity represents the degree of acute inflammation or acute activity of chronic inflammation. It is an important sign that active treatment is necessary and is the sign that treatment is most likely to be effective. Chronic gastritis with heavy inflammation but low activity (lymphocytes are the majority of inflammatory cells) is, in turn, not easily treated.
Intestinal chemosis
Changes in the morphology and histochemistry of the epithelium of the gastric mucosal surface and the epithelium of the crypts, becoming similar to the epithelium of the small or large intestine.
Complete intestinal chemosis – the epithelium of the gastric mucosa becomes normal intestinal epithelium.
Incomplete intestinal metaplasia – the morphology remains the same as the epithelium of the gastric mucosa, but the chemical composition of the mucous cells is changed. It is further divided into incomplete small intestinal metaplasia and incomplete large intestinal metaplasia. Incomplete intestinal metaplasia requires special staining to differentiate.
Mild intestinal metaplasia of the gastric mucosa is more common and suggests damage to the gastric mucosa.
Incomplete intestinal metaplasia, especially incomplete colorectal metaplasia, may be closely related to gastric cancer. Therefore, if intestinal metaplasia and atypical hyperplasia appear together in the pathology report, it is necessary to make special staining to identify the type of intestinal metaplasia – complete? or incomplete? Small bowel or large bowel? It is crucial! Clinicians and patients alike need to keep this in mind. However, special staining is not a routine part of the pathology of the gastric mucosa and needs to be requested separately.
Atypical hyperplasia (intraepithelial neoplasia)
Atypical hyperplasia is an abnormal nature of cell proliferation, including abnormal cell size, morphology, and arrangement, decreased mucus secretion, decreased nucleocytoplasm ratio, loss of nuclear polarity, pseudomultilayers, increased nuclear schizophrenia, and atypical nuclear schizophrenia. The disease is classified as mild, moderate or severe. The international academic community now renames atypical hyperplasia as intraepithelial neoplasia, with mild to moderate atypical hyperplasia classified as low-grade intraepithelial neoplasia and severe atypical hyperplasia classified as high-grade intraepithelial neoplasia.
There are two types of atypical hyperplasia.
Adenomatous atypical hyperplasia – considered to progress to highly differentiated intestinal type gastric adenocarcinoma.
Proliferative atypical hyperplasia – closely related to incomplete intestinal metaplasia and thought to progress to poorly differentiated intestinal-type gastric adenocarcinoma.
It is important to understand that mild atypical hyperplasia is often difficult to distinguish from inflammation-induced cell regeneration. However, this differentiation is again very important because it is the true atypical hyperplasia that is considered to be the precancerous state. We clinically found that some pathology reported as mild atypical hyperplasia disappeared after treatment, which probably turned out to be an inflammatory reactive regeneration phenomenon rather than a true atypical hyperplasia. Therefore, patients should not be alarmed when they see the results of mild atypical hyperplasia (low-grade epithelioid neoplasia) reports. It requires comprehensive analysis, close observation and appropriate treatment. As for severe atypical hyperplasia, i.e. high-grade intraepithelial neoplasia is already equivalent to carcinoma in situ and involves surgery.
Atrophy
Gastric mucosal glands are reduced to varying degrees of atrophy or even disappear completely, leaving only the gastric hollows remaining. Depending on the degree of reduction, it is classified as mild, moderate or severe. While the gastric glands are atrophied, the epithelium in the deeper part of the gastric notch proliferates to form glands and can become intestinal hyperplasia, or polyps or even cancer. If the atrophy is severe and there is a large amount of fibrous tissue proliferation in the gastric wall, it can also lead to gastric sclerosis. In this case, it should be differentiated from widely invasive gastric cancer.
Since atrophy occurs in the pylorus (gastric sinus) of the stomach, and the mucosa of the body and fundus of the stomach is less involved and retains its secretory function, it is reasonable that some patients with atrophic gastritis still have symptoms of acidity and heartburn in clinical practice.
The risk of gastric cancer in atrophic gastritis is mainly due to the accompanying intestinalization and polyps (of course there are other factors such as reduced gastric acid which facilitates the accumulation of carcinogenic factors nitrite).
The above brief explanation should be read carefully by patients with chronic gastritis.