Old Wang usually smoked and drank, but he felt that his body was “quite good”. A relative in his family died of stomach cancer, and he went to the hospital to have a gastroscopy, and the results showed: atrophic gastritis. Wang heard that this disease can become cancerous, so he was very worried about it, but instead, he had epigastric pain and postprandial flatulence.
In fact, Wang’s atrophic gastritis did not come in a day or two, why did he not feel anything different before the examination, but had obvious symptoms after knowing the result? The actual fact is that a lot of the factors are caused by excessive worry, and a lot of unknown atrophic gastritis patients are often also worried after the test results come out.
Atrophic gastritis does not need to be treated as a beast of prey, but rational understanding and scientific treatment
Symptoms
Some patients can be asymptomatic, with only microscopic signs of atrophy. Some patients may have upper abdominal fullness, discomfort or pain, which is more pronounced after meals, along with other non-specific symptoms of dyspepsia such as belching, acid reflux, nausea, vomiting, and loss of appetite.
Atrophic gastritis is divided into two categories
Chronic atrophic gastritis is divided into two types: autoimmune (type A) and multifocal atrophic (type B).
Autoimmune atrophic gastritis, as the name implies, develops from autoimmune induced gastric body gastritis with atrophic changes mainly in the gastric body.
Multifocal atrophic gastritis, in which the lesions are located mainly in the gastric sinus and show multifocal atrophy, mostly develops from chronic gastritis caused by Helicobacter pylori infection and is the most common type of atrophic gastritis.
The normal gastric mucosal surface is smooth, mucus-covered, and rich in folds generally talk pink. In contrast, endoscopic examination of patients with typical atrophic gastritis reveals pale gastric mucosa, thinning of mucosa, reduction or disappearance of mucosal folds, permeability of submucosal vessels, rough and uneven surface, and granular or nodular appearance. Gastroscopy and pathological examination can confirm the diagnosis, of which pathological findings are the gold standard for diagnosis.
Microscopically, atrophic gastritis can be classified into three conditions: glandular atrophy, intestinal epithelial hyperplasia and atypical hyperplasia (abnormal hyperplasia), in order of severity: mild, moderate and severe. Most data suggest that mild and moderate atrophy is reversible, while severe atrophy has little reversibility.
What is the meaning of common intestinal epithelial hyperplasia in the report
Normally there is no intestinal epithelium in the gastric mucosal glands, if there is an undesirable intestinal gland in the small intestine or colon is the occurrence of intestinal metaplasia, which can be considered as a result of gastric mucosal atrophy. The more intestinal gland, the more severe the atrophy.
Intestinal chemosis is further divided into four types: small intestine type, colon type, complete (mature glandular differentiation) and incomplete (immature glandular differentiation), among which only the fourth incomplete colon type intestinal chemosis is closely related to cancer, while the first three are not obviously related to cancer.
Relationship with gastric cancer: there is an association but no need to be overly nervous
The pathological study on the process of gastric cancer found that the cancerous cells evolved from normal-aging-proliferating-atypical hyperplasia-cancer; severe atrophic foci and atypical hyperplasia are often seen around gastric cancer; atrophic gastritis with atypical hyperplasia is a relatively clear precancerous lesion of gastric cancer at present;
It is currently believed that
I. Although atrophic gastritis can become cancerous, the cancer rate is very low, and it cannot be said in general that atrophic gastritis is a precancerous disease of gastric cancer; the risk of cancer depends mainly on whether atypical hyperplasia occurs and its degree.
The risk of cancer depends on the presence and extent of atypical hyperplasia.
Third, in order to monitor the dynamic changes of lesions, gastroscopy should be reviewed regularly. The specific follow-up time should be decided depending on individual factors and treatment, etc. The recommended follow-up time is once every 3 years for atrophic gastritis; once every 1 year for incomplete colonic enterosis or mild atypical hyperplasia; and once every 3 months for moderate atypical hyperplasia.
Fourth, for severe atypical hyperplasia, it should be treated as cancer and can be completely removed endoscopically or surgically.
Seeing here, patients have a number in their mind that some atrophic gastritis may become the prelude of gastric cancer, but only a very few of them are transformed into gastric cancer. Therefore, there is no need to be nervous and pessimistic even if the examination result is severe atrophic gastritis, as long as you treat it seriously and adopt comprehensive therapy, the condition can be improved or cured.
The probability of atrophic gastritis developing into gastric cancer is very low if we adhere to standardized treatment and review, and regular review is the best way to avoid the chagrin of not even knowing the appearance of cancer.