Gastric Intestinal Metaplasia
What is gastric intestinal metaplasia
Gastric intestinal metaplasia is defined as the replacement of gastric surface epithelium with intestinal epithelial cells. If it holds only one area in the stomach, it is defined as limited intestinal metaplasia. If it includes multiple regions between the areas of corpus antrum and incisura angularis, it is defined as common intestinal metaplasia.
In the example of the complete intestinal metaplasia, there are the formations of eosinophilic enterothesis, goblet cells, and brushy edge. In the incomplete intestinal metaplasia, there is colonic epithelial type in pathology without brushy limit and goblet cells; however, musin droplets are seen in the colonic cells.
Precancerous is a lesion. The risk of gastric cancer is low in low prevalence areas. It is 2.5/1000 person-year. In cases of the incomplete intestinal type and the common intestinal metaplasia, the rate slightly rises. It is 16.5 /1000 person-year.
Gastric intestinal metaplasia is important for several aspects. It has no specific complaints. Beside that, it is possible to see excessive bacterial proliferation in the small intestine swells since these patients have gastric hypochlorite. In parallel with it, bloating, abdominal distension, and diarrhea may occur.
In the display of endoscopy there may be not only nonspecific images but also images of bloated villous from the mucous as white swellings in patches.
People with stomach cancer in their family and ethnically except the Caucasian race, which are Asians, Hispanics, African-Americans, are considered the risk group for gastric cancer.
While applying endoscopy in such risky groups and in people with common and incomplete intestinal metaplasia, biopsy mapping should be completed from five region. Screening endoscopy is recommended for these people in every 2-3 years.
When there is helicobacter pylori, even if eradicated intestinal metaplasia does not return, gastric cancer will slow the rate of transformation.
What is the importance of gastric intestinal metaplasia?
Stomach cancer ranks the second among the cancer-related death causes in the world. . Gastric intestinal metaplasia is considered as precancerous lesion in terms of stomach cancers. It increases the risk of stomach cancer by six times.
On the other hand, it appears quite highly in the general population. Almost a quarter of patients who are applied endoscopy may have intestinal metaplasia. Intestinal metaplasia is seen more in people who have helicobacter pylori infection, have gastric cancer in their first degree relatives, and smoke. It also increases with aging.
It does not return with the helicobacter pylori eradication however, the infection control may slow down the progression of mucosal damage and transformation into dysplasia. The risk of gastric cancer is even higher in the incomplete intestinal metaplasia.
It is higher in the cases holding both the antrum and the corpus. In addition, when gastric mucosa holds more than 20%, the risk increases even more. Periodic endoscopic checking is cost effective in patients with intestinal metaplasia (it is more economical).
Recommendation for annual control
With a pragmatic approach, annual endoscopic control can be accepted in patients with intestinal metaplasia in the following cases:
- In cases where more than 20% surface is covered
- In people with incomplete type intestinal metaplasia
- In people with intestinal metasplasia who have first-degree relatives who are gastric cancer
- In people with intestinal metaplasia who smoke
For other intestinal metaplasia (IM) patients, endoscopic screening may be recommended in less frequency that is every 2-3 years.
Gastric intestinal metaplasia epidemiology
Intestinal metaplasia is 33% positive for helicobacter pylori positive, while in those with disinfected show 15% around of a prevalence. At the same time, age of contracting IM lower even in people with helicobacter pylori infection.
In general, IM increases with aging. While it is around of 5% under the age of 40, this rate rises to 46% over the age of 80. IM with helicobacter pylori rates may differ from different countries. According to publications, there are 29% in China, 13% in Hong Kong, and around 25% in the Netherlands.
While gastric intestinal metaplasia is around 30% in cases with non ulcer dyspepsia, it is 55% in patients with gastric ulcers, and it is 100% in patients with intestinal type gastric cancer.
It is thought that intestinal metaplasia occurs as a result of chronic inflammatory gastric mucous membranes damage. Helicobacter pylori infections also appear to be the main etiological factors in this aspect. Helicobacter pylori increases the risk of intestinal metaplasia by 4.5 to 9 times. In the studies, it has been reported that prevalence of IM increases significantly in Cag-A positive H pylori types.
The risk increases 4.5 times in those who are positive for helicobacter pylori and smokes more than 20 cigarettes a > day.
It increases by two times in people who use high level of oil. . There are studies have been made from countries such as Germany, Korea, Iran, and Brazil about that progress of intestinal metaplasia is more common in patients who have first-degree relatives who are stomach cancer. With the family history, the risk increases in patients with IM, which is also positive for H pylori.
Is gastric intestinal metaplasia recyclable?
Although helicobacter pylori is a chronic inflammatory process involved in the development of intestinal metaplasia, there are no studies supporting IM recycling in the antrum and corpus mucosa after eradication treatment.
As a result of eight meta-analyzes, there is only one study in this subject argues that in antrum IM is recyclable after the helicobacter pylori eradication, all other studies asserts that in both antrum and corpus IM is not recyclable after the helicobacter pylori eradication.
On the other hand, mucosal atrophy can recycle after helicobacter pylori eradication. On the other side, there is a study in Hong Kong includes 435 cases that reports that although helicobacter pylori eradication treatment does not provide the regression, it slows the progression.
Some studies for gastric intestinal metaplasia treatment
According to the studies, ascorbic acid is an additive treatment for six months after the eradication for people with intestinal metaplasia and helicobacter pylori positive. Intestinal metaplasia decreases in these patients.
In addition, cox-2 receptor expression is high in patients with helicobacter pylori positive and intestinal metaplasia. For this reason, in a Taiwan study conducted with COX-2 receptor blockers such as celecoxib for two months, it is claimed that precancerous gastric lesions recovered after the helicobacter pylori eradication. . After this publish, according to another study in China, there is no difference between the placebo and celecoxib with regard to regression in intestinal metaplasia. As a result, further studies are needed.
The risk of gastric cancer in patients with gastric intestinal metaplasia
In a study from Japan including 1246 cases, patients with helicobacter pylori positivity and intestinal metaplasia positive in the beginning are observed for an average of 7 to 8 years. 36 people of them have gastric cancer. In this study, the risk increased by 6.4 percent.
For the cases with intestinal metaplasia in the stomach, lewis blood type a antigen and sulphomusin expression is one of the parameters that increase the risk of gastric cancer.
Incomplete intestinal metaplasia can be classified further as type 2 and type 3. In type 2 there are cells that secrete sialomucin and the paneth cells are positive. In type 3, there are columnar cells that secrete sulphomusine and there are no paneth cells. Type 2 and type 3 separated by painting with high iron diamine paint.
In patients with incomplete intestinal metaplasia, the risk for progression of gastric cancer is even higher. A recent study in Spain, after the 12 years follow-up, found gastric carcinoma in 16 of the 88 patients containing incomplete metaplasia, and only one in 104 cases containing complete intestinal metaplasia.
Similarly, in a study in Portugal, there are 58 patients with incomplete intestinal metaplasia and while 31% of them have low grade displasia, 6% of them have high grade displasia. In 62 patients with complete intestinal metaplasia, 8% of them have low grade displasia.
The risk of gastric cancer in cases of type 3 intestinal metaplasia was found to be higher than type 2.
Who are gastric intestinal metaplasia patients at high risk of gastric cancer?
- People with first-degree relatives who have stomach cancer
- People with incomplete intestinal metaplasia
- People with intestinal metaplasia in corpus or people with common intestinal metaplasia
African-Americans, Hispanics, and Asians
A generation of migrants migrating from high-risk areas (east Asia and Latin America mountainous regions)
Is endoscopic follow-up of patients with intestinal metaplasia in the stomach cost effective?
According to the studies, the answer is yes. In cases with incomplete metaplasia with helicobacter pylori positive, annual follow-up in certain conditions (these conditions are written above), and it is recommended every 2-3 years in other cases of intestinal metaplasia. .
What is metaplasia?
It is defined a complete transformation of a normal differential cell type into to another type of cell due to the environmental factors. It is potentially reversible. The progress of intestinal metaplasia in the gastric mucosa may occur due to helicobacter pylori, bile reflux, or radiotherapy.
What is dysplasia?
Dysplasia is the point that has histological, cytological, and structural abnormalities, so it creates a suspicion of being neoplastic, but it is not.