I. Pathological histology
1, the definition of atrophy: gastric mucosal atrophy refers to the reduction of gastric intrinsic glands, and there are two types of histology: ① chemogenic atrophy: gastric intrinsic glands are replaced by enteric or pseudopyloric chemogenic glands: ② non-chemogenic atrophy: gastric mucosal layer intrinsic glands are replaced by fibrous or fibromuscular tissue or inflammatory cell infiltration causes a decrease in the number of intrinsic glands.
The definition of “gastric mucosal atrophy” was debated internationally and a consensus was reached in 2002 [1], which was adopted in China in early years [2] and explained in the first national consensus conference on chronic gastritis [3]. Intestinalization or pseudopyloric glandular hyperplasia is not an intrinsic gastric gland and is therefore atrophy despite the fact that the number of gastric glands is not reduced.
In cases of significant gastric mucosal inflammation, the mucosal layer is densely infiltrated with inflammatory cells and the glands are reduced, for which the international term “inde “nite for atrophv” has been proposed [1]. However, this consensus opinion is not adopted because the density of inflammatory cells does not affect the judgment of atrophy, which can be judged by the reduction of intrinsic glands. The inflammation can be completely repaired (no atrophy) or incompletely repaired (intestinalization or fibrosis) after the inflammation subsides.
2, chronic gastritis has 5 histological changes should be graded. That is, H. pylori infection, chronic inflammation, active, atrophy and intestinalization, divided into four grades: none, mild, moderate and severe. The diagnostic criteria were adopted from the pathological diagnostic criteria of chronic gastritis in China (see Appendix) and the visual analogue scale (Visual
analogue scale, see Figure 1) [4].
The visual analogue scale was proposed by the updated Sydney System (1996) to improve the international exchange agreement rate of chronic gastritis. The pathological diagnostic criteria for chronic gastritis in China are more specific and easy to operate, and are basically similar to the new Sydney system. However, our criteria only have textual descriptions, which can cause diagnostic differences due to different understanding. If it can be combined with the New Sydney System scoring chart, the consistency with international diagnostic standards can be improved.
3. The pathological examination should report the histological changes of each biopsy specimen.
This reporting method can provide more detailed information to the clinician, help to reduce the bias of the conclusions caused by random errors in biopsy, and facilitate the clinician to make a comparison before and after treatment.
4, chronic gastritis pathology biopsy shows atrophy of the intrinsic glands, can be diagnosed as atrophic gastritis, without considering the number and degree of atrophy of the biopsy specimen. The clinician can make a final judgment of the extent and degree of atrophy based on the pathological findings and combined with what is seen by endoscopy.
In early or multifocal atrophic gastritis, the gastric mucosal atrophy is focally distributed. Even if the number of biopsies is small, as long as the pathologic biopsy shows atrophy of the intrinsic glands, the diagnosis of atrophic gastritis can be made. It is important to note that mucosa taken from the edges of erosions or ulcers often has glandular destruction, and the resulting reduction in the number of glands cannot be considered atrophic gastritis. In addition, factors such as biopsy tissue being too shallow or improperly oriented tissue embedding can affect the judgment of atrophy.
5. AB-PAS and HlD-AB mucus staining can distinguish enteric subtypes, but the value of enteric subtypes for predicting the risk of gastric cancer development is still controversial. The small intestinal and complete intestinal subtypes have no significant precancerous significance, and the risk of gastric carcinogenesis is increased in large intestinal intestinal intestinal type, thus causing the observer to evaluate one feature at a time, compare the histological image of the pathological section with the standard map, and find the best matching image before grading. When the intensity was significantly different on the same biopsy specimen, the entire section was observed and scored on average.
Clinical importance. However, the value of the New Sydney system to alert the enteric subtype to predict the risk of gastric carcinogenesis is controversial and limited to studies [4]. Recent studies [5~8] have shown the limited value of enteric subtypes to predict the risk of gastric cancer occurrence, while more emphasis is placed on the importance of the range of entericization, the wider the range, the higher the risk of gastric cancer occurrence. The development of carcinoma from colorectal type of intestinalization has been rarely reported for more than a decade. In addition, the actual situation of pathological examination shows that intestinal chemistry is mostly of mixed type, and the detection rate of colorectal intestinal chemistry is closely related to the number of biopsy blocks, that is, the more the number of biopsy blocks, the higher the detection rate of colorectal intestinal chemistry.
6.Heterotypic hyperplasia (intraepithelial neoplasia) is an important precancerous lesion of gastric cancer, which can be divided into mild and severe (or low grade and high grade).
Heterozygous hyperplasia (dysl~lasia) and intraepithelial neoplasia are synonymous, and the latter is the term recommended by the WHO International Agency for Research on Cancer. At present, the international application of this terminology [9~11] and domestic opinions on the adoption and translation of the terminology are not uniform, and the group of experts on harmonics noted this point and made the above-mentioned preferential opinions.
II. Endoscopic part
7, The endoscopic diagnosis of chronic gastritis refers to the mucosal changes seen by the naked eye under endoscopy, which needs to be combined with pathological findings to make a judgment.
With the development of endoscopic instruments, endoscopic observation is clearer and has greatly improved the endoscopic diagnostic rate of chronic gastritis. However, the diagnosis of atrophic gastritis still relies mainly on pathological examination, i.e., the presence of reduced intrinsic gastric glands to confirm the diagnosis. The compliance rate between endoscopic visual observation and pathological examination for the diagnosis of atrophy is 38%-78% [12,13].
8, Endoscopic classification of chronic gastritis into non-atrophic (superficial)
gastritis and atrophic gastritis as the two basic types. The presence of signs such as flat erosions, elevated erosions, bleeding, coarse folds or bile reflux at the same time is diagnosed as non-atrophic gastritis or atrophic gastritis with erosions and bile reflux.
Since the underlying lesion of most chronic gastritis is inflammation, exudation or atrophy, it is reasonable to divide chronic gastritis into non-atrophic gastritis and atrophic gastritis, which is conducive to unification with pathologic diagnosis. When other pathological signs are more prominent, the diagnosis of non-atrophic gastritis or atrophic gastritis with erosion, with bile reflux, etc. can be made.
9, non-atrophic gastritis endoscopically visible erythema (dotted, lamellar and striped), mucosal roughness, hemorrhagic spots (spots), mucosal edema, exudation and other basic manifestations.
10, atrophic gastritis endoscopically visible mucosa red and white. The white is predominant, the folds flatten or even disappear, the mucosal vessels are revealed; the mucosa is granular or nodular and other basic manifestations.
There are two types of endoscopic atrophic gastritis, namely simple atrophic gastritis and atrophic gastritis with hyperplasia. The main manifestation of pure atrophic gastritis is red and white mucosa, mainly white, flattening or even disappearing of the folds and revealing of blood vessels: atrophic gastritis with hyperplasia is mainly manifested by granular or nodular mucosa.
The endoscopic diagnosis of specific types of gastritis must be combined with etiology and pathology.
The classification of specific types of gastritis is related to the etiology and pathology, including chemical, radiological, lymphocytic, granulomatous, eosinophilic, and other infectious diseases.
12.According to the distribution of lesions, endoscopic chronic gastritis can be classified as gastric sinusitis, gastric body inflammation, total gastritis sinus predominant or total gastritis gastric body predominant.
13.It is difficult to grade the severity of chronic gastritis according to the endoscopic findings.
It is difficult to grade the mild, moderate and severe degree of various lesions of chronic gastritis according to what is seen by endoscopy, mainly because of the shortcomings of the existing endoscopic classification such as artificial subjective factors or too cumbersome [13], and a reasonable and practical grading needs further study.
14, pigmented endoscopy and magnifying endoscopy are helpful for endoscopic classification of gastritis.
Pigmented endoscopy combined with magnifying endoscopy can make the observation of gastric mucosa more fine, and the structure of gastric cell and gastric hollows can be clearly seen [14], which has certain reference value for the diagnosis and differential diagnosis of gastritis. The compliance rate between plain endoscopy and histological diagnosis of chronic gastritis was reported to be 38%, while that of magnified endoscopy was 82.4% [12].
15, biopsy sampling: depending on the lesion and the need, it is recommended to take 2-5 pieces. The endoscopist should provide the pathology department with information on the sampling site, endoscopic findings and a brief medical history.
In addition to the mucosa of the gastric sinus, biopsies of the gastric horn and the lower lesser curved side of the gastric body should be taken to help estimate the extent of atrophy. Because the atrophy and intestinalization of the gastric horn are also more obvious in patients with atrophic gastritis, and this part is also one of the most frequent sites of heterogeneous hyperplasia.
H.pylori infection and chronic gastric non
16, H. pylori infection is the main cause of chronic active gastritis.
Australian scholars Barry Marshall and Robin Warren were awarded the 2005 Nobel Prize in Physiology or Medicine for the successful culture of H. pylori in 1983 and its association with the development of peptic ulcer and chronic active gastritis [15]. the relationship between H. pylori infection and chronic active gastritis is consistent with Koch’s proposal to identify Koch’s four basic requirements for identifying the pathogen as the cause of disease (Koch’s
postulates). Studies have shown that 80% to 95% of patients with chronic active gastritis have H. pylori infection in the gastric mucosa, and the 5% to 20% negative rate of H. pylori reflects the diversity of the etiology of chronic gastritis; the intragastric distribution of H. pylori in those with H. pylori-associated gastritis is consistent with inflammation; eradication of H. pylori results in regression of gastric mucosal inflammation, with general neutrophil regression is faster, while lymphocytes and plasma cells take longer to regress [16]. H.pylori infection has been shown to cause gastritis in volunteers [17] and animal models.
17, H. pylori infection causes active inflammation of the gastric mucosa; after prolonged infection, gastric mucosal atrophy and intestinalization can occur in some patients. The synergistic effect of host, environmental and H.pylori factors determines the type and development of gastritis associated with H.pylori infection.
H.pylori infection is closely associated with active inflammation of the gastric mucosa, and the presence of active inflammation of the gastric mucosa is highly suggestive of H.pylori infection [16]. The inflammatory immune response due to long-term H. pylori infection can lead to gastric mucosal atrophy and intestinalization in some patients [18,19].There are two prominent types of H. pylori-associated chronic gastritis: total gastritis sinus predominant and total gastritis gastric body predominant. The former has increased gastric acid secretion and an increased risk of duodenal ulcer development: the latter often has decreased gastric acid secretion and an increased risk of gastric ulcer and gastric cancer development. The synergy of host (e.g. cytokine gene polymorphisms such as interleukin-lB [20,21]), environmental and H. pylori factors (virulence genes) determines the type of H. pylori infection-associated gastritis and the onset and development of atrophy and intestinalization [22].
18, eradication of H. pylori leads to long-term improvement of dyspeptic symptoms in some patients.
Most patients with H. pylori-associated gastritis are asymptomatic, and those with dyspeptic symptoms can be classified as functional dyspepsia in terms of their symptoms [23]. Therefore, whether eradication of H. pylori eliminates dyspeptic symptoms in chronic gastritis can be based on the results of studies of functional dyspepsia. Meta-analysis showed that eradication of H. pylori resulted in long-term improvement of symptoms in some patients with functional dyspepsia and was a cost-effective strategy in the treatment regimen to eliminate or improve dyspeptic symptoms [24]. Studies [25] have shown that the improvement of symptoms after eradication of H. pylori is more significant in those with a high degree of inflammation and activity of the gastric mucosa before treatment.
19, eradication of H. pylori prevents further development of gastric mucosal atrophy and intestinalization, but whether it can be reversed remains to be confirmed by more studies.
Numerous studies [26,27] have confirmed that H. pylori eradication can lead to the disappearance of active inflammation of the gastric mucosa and a reduction in the degree of chronic inflammation, but the effect on gastric mucosal atrophy and intestinalization is not fully understood. Certain factors can affect the judgment of the results, such as the difference of the biopsy site; when H.pylori infection, the gastric mucosa is heavily infiltrated with inflammatory cells, which looks like atrophy: after the eradication of H.pylori, the gastric mucosal inflammation subsides, and the mucosal atrophy is expected to recover, but the reversal may take a long time: there may be the point of no return in the development of atrophy, such as beyond the point of no return), which is difficult to reverse. Most studies [26-27] have shown that eradication of H. pylori can prevent the further development of gastric mucosal atrophy and intestinalization, but whether atrophy and intestinalization can be reversed remains to be confirmed by more studies [28].
IV. Diagnosis and treatment
20. Most patients with chronic gastritis do not have any symptoms. Those with symptoms are mainly non-specific dyspepsia: the presence or absence of dyspeptic symptoms and their severity do not correlate significantly with the endoscopic findings and histological grading of chronic gastritis.
Epidemiological studies [29] have shown that most patients with chronic gastritis are asymptomatic. Patients with functional dyspepsia may or may not have chronic gastritis, and the histology of chronic gastritis improves significantly after eradication of H. pylori, but most of those with improved histology do not have elimination of dyspeptic symptoms, suggesting that chronic gastritis and dyspeptic symptoms are not closely related. Correlation analysis of endoscopic and gastric mucosal histological findings with the symptoms of patients with chronic gastritis showed that the symptoms of patients with chronic gastritis lacked specificity, and the presence or absence of symptoms and their severity did not correlate significantly with endoscopic findings and histological grading [30].
21, Confirmation of the diagnosis of chronic gastritis relies mainly on endoscopy and histological examination of gastric mucosal biopsy, with the latter in particular being of greater diagnostic value.
Given that most patients with chronic gastritis do not have any symptoms, and even if they have symptoms, they lack specificity and lack specific signs, the diagnosis is based on symptomatic examination and histological examination of gastric mucosal biopsy, especially the latter is of greater diagnostic value (see “I. Pathological histology” and “II. Endoscopic section” in this article for details). The latter in particular is of greater diagnostic value (see “I. Pathological histology” and “II.)
22. The diagnosis of chronic gastritis should seek to clarify the etiology and should be routinely tested for H. pylori. serum gastrin, vitamin B12 and related autoantibodies (anti-mural cell antibodies and anti-internal factor antibodies) are recommended for patients with atrophic gastritis. Serum gastrin G17 and pepsinogen I and II may be helpful in determining the presence and site of gastric mucosal atrophy.
H. pylori infection is the main cause of chronic gastritis and should be routinely tested for etiologic diagnosis. Atrophic gastritis can be caused by H. pylori infection or autoimmunity [31,32]. Serum gastrin, vitamin B12 levels and related autoantibodies (anti-mural cell antibodies and anti-internal factor antibodies) should be tested for atrophic gastritis suspected to be of autoimmune origin. In chronic gastritis, serum gastrin G17 levels are significantly increased and pepsinogen I or pepsinogen I/II ratio is decreased in gastric body atrophy; serum gastrin G17 levels are decreased and pepsinogen I or pepsinogen I/II ratio is normal in gastric sinus atrophy; both are decreased in total gastric atrophy. The detection of serum gastrin G17 and pepsinogen I and II can help determine the presence or absence of gastric mucosal atrophy and the site of atrophy.
23. The treatment of chronic gastritis aims to relieve symptoms and improve gastric mucosal inflammation. Treatment should target the cause as much as possible and follow the principle of individualization.
The aim of treatment for chronic gastritis is to relieve symptoms and improve the histology of the gastric mucosa, including inflammation, atrophy and intestinalization. However, the reversal of atrophy/enterolization has yet to be confirmed by further studies. The management of dyspeptic symptoms in chronic gastritis is the same as in functional dyspepsia. Eradication of H.pylori can eliminate or improve gastric mucosal inflammation and prevent further development of atrophy and intestinalization; asymptomatic, H.pylori-negative non-atrophic gastritis does not require special treatment; for atrophic gastritis, especially severe atrophic gastritis or with heterogeneous hyperplasia, attention should be paid to prevent its malignant transformation.
24, H.pylori-positive chronic gastritis with gastric mucosal atrophy, erosion or indigestion symptoms is recommended to eradicate H.pyloriH.pylori-associated gastritis whether all need to eradicate H.pylori there is a lack of uniform opinion. The European Consensus Report on H.pylori 2000 recommends eradication of H.pylori for atrophic gastritis [36], and domestic consensus opinion recommends eradication of H.pylori in chronic gastritis with significant abnormalities (pathological biopsy showing moderate to severe atrophy, moderate to severe intestinalization, heterogeneous hyperplasia or endoscopic gastric mucosal erosion) or with a family history of gastric cancer, poor outcome of conventional therapy, with eradication therapy for those with duodenitis [37]. The main symptom of chronic gastritis is dyspepsia, and those whose symptoms should be functional dyspepsia should be treated with eradication therapy [36,37]. Therefore, patients with H. pylori-positive chronic gastritis with dyspepsia symptoms should undergo eradication therapy. Eradication of H. pylori can improve the histology of gastric mucosa, which is important for the prevention of peptic ulcer and gastric cancer, etc., and has a cost-one efficacy ratio advantage for improving or eliminating dyspeptic symptoms.
25, the upper abdominal fullness, nausea or vomiting as the main symptoms can be applied to prokinetic drugs. Gastric mucosal damage and (or) symptoms are obvious to apply gastric mucosal protective agents. In cases with bile reflux, prokinetic agents and/or gastric mucosal protectors with bile acid binding effect can be used.
Bile reflux is also a cause of chronic gastritis. Pyloric sphincter insufficiency leads to bile reflux into the stomach, weakening or destroying the gastric mucosal barrier function. Digestive juices act on the gastric mucosa, producing lesions such as inflammation, erosion, bleeding and epithelial metaplasia. The occurrence of epigastric fullness or nausea and vomiting may be associated with delayed gastric emptying, and prokinetic agents such as domperidone, trimebutine maleate, mosapride, and etopride hydrochloride may improve these symptoms [38-40] and prevent or reduce bile reflux. Gastric mucosal protective agents, such as aluminum thioglycollate [41], rebapate [42], teprenone [43], gefalte [44], and ecabet [45] can improve the gastric mucosal barrier, reduce the destruction of the gastric mucosal barrier by bile reflux, and promote the healing of gastric mucosal erosion, but their effect on the improvement of symptoms is controversial. Magnesium aluminum carbonate preparation can enhance the gastric mucosal barrier function and can bind bile acid, thus reducing or eliminating the gastric mucosal damage caused by bile reflux [46].
26, Those with gastric mucosal erosion and/or predominantly acid reflux and epigastric pain can be treated with antacids, H2 receptor antagonists, or proton pump inhibitors (PPl) depending on the condition or severity of symptoms.
Gastric acid and pepsin play an important role in the development of symptoms such as gastric mucosal erosion (especially flat erosion), acid reflux and epigastric pain, and antacid or acid suppressive therapy is effective in healing erosion and eliminating symptoms. Antacids have a short-lived effect, while PPIs have a strong and long-lasting acid-suppressive effect and can be chosen according to the severity of the disease or symptoms [47].
27, Antidepressants or anxiolytics can be used in chronic gastritis with dyspepsia with significant psychiatric factors.
Patients with chronic gastritis with dyspepsia symptoms who have obvious mental factors should be given patient explanation or psychotherapy. Psychological factors play a role in the development of functional dyspepsia and are also associated with the occurrence of dyspeptic symptoms in chronic gastritis. Poor sleep or obvious psychiatric factors, as well as indigestion symptoms of conventional treatment is ineffective and poor efficacy can be combined with the application of antidepressants, sedative treatment.
The treatment of chronic gastritis can be broadened by traditional Chinese medicine.
V. Regression of chronic gastritis, follow-up of atrophic gastritis and cancer prevention
29. Chronic gastritis can persist.
Since the vast majority of chronic gastritis occurs in association with H. pylori infection, and spontaneous clearance of H. pylori is rare, chronic gastritis can persist [29].
30, Those with H. pylori-associated sinusitis are prone to duodenal ulcers, and those with multifocal atrophy are prone to gastric ulcers.