Intestinal Metaplasia
Intestinal Metaplasia

Video Endoscopic Sequence 1 of 5.

Intestinal Metaplasia.

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Endoscopy of Intestinal Metaplasia

Video Endoscopic Sequence 2 of 5.

Endoscopy of Intestinal Metaplasia

Intestinal metaplasia (IM) of the stomach is a risk factor
in developing intestinal-type gastric cancer and hence the
question of reversibility is vital. There is emerging
epidemiological evidence that with long term follow up,
IM may be reversible although a combination of
antioxidant agents and eradication of H pylori may be
necessary to achieve this. The pathogenesis of IM is
currently being elucidated and it is likely that a
combination of bacterial, host, and environmental factors
will be shown to lead to IM. In assessing gastric cancer
risk, histochemical typing of IM will most probably be
replaced by molecular markers.

Intestinal Metaplasia

Video Endoscopic Sequence 3 of 5.

Of the different types of metaplasia in the stomach,
intestinal-type is the most common and it is associated with
H pylori infection and bile reflux. Experimentally,
irradiation induces IM.

“H pylori has been implicated as a major cause of IM”

Atrophic gastritis and IM were strongly associated with H pylori and not with aging, leading to the conclusion that with a high prevalence of the precursor lesion the risk of development of early gastric cancer will continue to remain high in Japan. However, H pylori most likely acts in concert with other factors to promote IM.

Intestinal Metaplasia

Video Endoscopic Sequence 4 of 5.

There is no concerted view on regression following eradication of H pylori. A randomised one year follow up study reported that H pylori eradication was beneficial in preventing progression of atrophy and IM of the gastric mucosa and recent presentation of the results of this study at five years has reinforced these findings, although other studies are less conclusive. In a 2–4 year prospective study there was no significant change in antral IM during four years of follow up although antral atrophy declined significantly in the period from 1 to 3 years of follow up. However, a recent report from Japan demonstrated that there are more studies showing regression following eradication therapy than progression. Long term studies are necessary to answer this question and a recent review of the literature shows these are lacking.

Intestinal Metaplasia

Video Endoscopic Sequence 5 of 5.

The metaplasia is of the small intestinal type which completely replaces the normal gastric mucosa.

Intestinal Metaplasia

Diffuse Intestinal Metaplasia.

An 85 year-old female two years ago, she underwent open cholecystectomy. The patient complained of epigastric discomfort, an upper video gastroscopy was performed. A deformed antrum was appreciated, biliar reflux is observed, biopsies where taken to rule out carcinoma. Intestinal metaplasia is the most dramatic epithelial transformation, the acquisition of the epithelium that is normally observed only in the intestine. Intestinal metaplasia has not only morphologic and biochemical properties of the small intestinal epithelium but also functional ones. The metaplastic stomach changes from a secretory organ to an “intestinal” organ capable of the absorption of certain substances such as lipid, from the gastric lumen.


Intestinal Metaplasia

Video Endoscopic Sequence 1 of 3.

Intestinal Metaplasia of the Pre-Piloric Antrum.

Biopsies revealed chronic gastritis with intestinal metaplasia.

The video clip displays more intensive areas of Intestinal
Metaplasia of the antrum as well as biliar reflux.
Metaplasia is a potentially reversible change from a fully
differentiated cell type to another cell type implying
adaptation to environmental stimuli. In the stomach
intestinal type metaplasia is most common. This occurs as
a result of Helicobacter pylori infection or bile reflux.

Intestinal Metaplasia

Video Endoscopic Sequence 2 of 3.

Other promoters of IM

These include lack of vitamin C and cigarette smoking. The concept of atrophy, subsequent hypochlorhydria with bacterial overgrowth, and nitrate generation that damage DNA must also be considered. A European study showed that patients with IM had a significantly higher proportion of gastric juice samples containing bacteria and nitrite and had a gastric pH >6. The role of hypochlorhydria is interesting; studies in rats with IM induced by irradiation showed reversal following lowering of gastric pH. Bile is also a major factor in promotion of IM. An early study from Leeds showed that after stratification for previous surgery, age, and H pylori status, the histological feature most strongly associated with bile reflux was IM, including all subtypes. Bile in combination with H pylori in rats promotes cyclooxygenase 2 (COX-2) expression in body mucosa and when bile was added, COX-2 expression in histologically normal appearing body mucosa was associated with cell proliferation, atrophy, and IM in the antrum. Sung et al also showed that both premalignant and malignant gastric lesions in human subjects demonstrate high COX-2 expression. Successful eradication of H pylori caused downregulation of COX-2 expression but failed to reverse IM at one year.


Intestinal Metaplasia

Video Endoscopic Sequence 3 of 3.

Additional intervention strategies to reverse IM

As it is unlikely that H pylori is solely responsible for
induction and progression of IM, other interventions may
be necessary to reverse this condition. In an Italian study,
co-administration of ascorbic acid with H pylori eradication
significantly resolved IM of the gastric mucosa, and the
authors concluded that chemoprevention treatment should
be considered.

“Co-administration of ascorbic acid with H pylori eradication significantly resolved IM of the gastric mucosa”

Similarly, Correa et al’s study in Colombia has shown that effective anti-H pylori treatment and dietary supplementation with antioxidant micronutrients may interfere with the precancerous process, mostly by increasing the rate of regression of cancer precursor lesions

Intestinal Metaplasia

Video Endoscopic Sequence 1 of 7.

Intestinal Metaplasia and Gastric Cancer

In this clinical case shows the relationship between intestinal metaplasia and gastric cancer, the videos are seen many islands of intestinal metaplasia.

H pylori- associated chronic gastritis progresses with the following 2 main topographic patterns that have different clinical consequences:

ˇ Antral predominant gastritis is characterized by inflammation and is mostly limited to the antrum. Individuals with peptic ulcers usually demonstrate this pattern of gastritis.

ˇ Multifocal atrophic gastritis is characterized by involvement of the corpus and gastric antrum with progressive development of gastric atrophy (loss of the gastric glands) and partial replacement of gastric glands by an intestinal-type epithelium (intestinal metaplasia). Individuals who develop gastric carcinoma and gastric ulcers usually demonstrate this pattern of gastritis.

Intestinal Metaplasia

Video Endoscopic Sequence 2 of 7.

There are islands of intestinal metaplasia around the tumor as well as in the gastric body.

Gastric cancers may take place in advance ages and originatemg from pre-cancerous states such as severe atrophic gastritis and colonic type of intestinal metaplasia.

Especially alcian blue plus high iron diamine positive sulphomucin contents of metaplastic epithelia is suggestive for cancer development and it may be proven by histochemical studies.

It has been suggested that the subtyping of intestinal metaplasia in the stomach is useful in stratifying patients with regard to risk of developing gastric cancer.

Intestinal Metaplasia

Video Endoscopic Sequence 3 of 7.

It still remains controversial whether gastric mucosal
atrophy and intestinal metaplasia are reversible after
eradication of Helicobacter pylori infection.

Another complication of H pylori gastritis is the
development of gastric carcinomas, especially in individuals
who develop extensive atrophy and intestinal metaplasia of
the gastric mucosa. Although the relationship between H
pylori and gastritis is constant, only a small proportion of
individuals infected with H pylori develop gastric cancer.
The incidence of gastric cancer usually parallels the
incidence of H pylori infection in countries with a high
incidence of gastric cancer and is consistent with H pylori
being the cause of the precursor lesion, chronic atrophic

Intestinal Metaplasia

Video Endoscopic Sequence 4 of 7.

Intestinal metaplasia in the stomach increases the risk of
gastric cancer, and the increased risk is proportional to the
extent of the metaplasia. This risk could be generated by
one or more mechanisms: the metaplastic tissue is an
early step in a multistep induction process; the
metaplastic tissue is an epigenetic change that raises the
pH of gastric juice by replacing oxyntic mucosa, favoring
the growth of a bacteria capable of generating endogenous
mutagens; and/or the metaplasia is only a marker for
chronic gastritis due to H. pylori infection or pernicious
anemia. With the last mechanism


Intestinal Metaplasia

Video Endoscopic Sequence 5 of 7.

The inflammatory response favors intramural mutagenesis that might result in metaplasia or neoplasia as independent events. Finding gene rearrangements common to both metaplastic and neoplastic tissue may establish a direct link between them, but too few have been identified to account for the large number of stomach cancers that develop in high risk populations. Histochemical and immunochemical stains that identify enzymes or mucosubstances may suggest that metaplastic epithelial cells resemble small or large intestinal cells, but they are distinctly different from both. Moreover, these stains do not indicate whether a given cytologic change is genetic or epigenetic; therefore, they cannot be used to define the relationship between metaplasia and neoplasia. It is unnecessary for practicing physicians to await resolution of this question. It can be assumed that any person with extensive metaplasia is at high risk for gastric cancer and should be subject to periodic screening. The extent of the metaplastic process is probably more important than the metaplastic subtype.


Intestinal Metaplasia

Video Endoscopic Sequence 6 of 7.

Chronic gastritis is a histopathologic entity characterized by chronic inflammation of the stomach mucosa. Gastritides can be classified based on the underlying etiologic agent (eg, Helicobacter pylori, bile reflux, nonsteroidal anti-inflammatory drugs [NSAIDs], autoimmunity, allergic response) and the histopathologic pattern, which may suggest the etiologic agent and clinical course (eg, H pylori –associated multifocal atrophic gastritis).

Other classifications are based on the endoscopic appearance of the gastric mucosa (eg, varioliform gastritis). Although minimal inflammation is observed in some gastropathies, such as those associated with NSAID intake, these entities are discussed in this article because they are frequently included in the differential diagnosis of chronic gastritis.

Chemical or reactive gastritis is caused by injury of the gastric mucosa by reflux of bile and pancreatic secretions into the stomach, but it can also be caused by exogenous substances, including NSAIDs, acetylsalicylic acid chemotherapeutic agents, and alcohol. These chemicals cause epithelial damage, erosions, and ulcers that are followed by regenerative hyperplasia detectable as foveolar hyperplasia, and damage to capillaries, with mucosal edema, hemorrhage, and increased smooth muscle in the lamina propria.

Intestinal Metaplasia

Video Endoscopic Sequence 7 of 7.

Inflammation in these lesions caused by chemicals is minimal or lacking; therefore, the term gastropathy or chemical gastropathy is more appropriate to describe these lesions than is the term chemical or reactive gastritis as proposed by the updated Sydney classification of gastritis. Importantly, mixed forms of gastropathy and other types of gastritis, especially H pylori gastritis, may coexist.

Intestinal-type gastric carcinoma is frequently accompanied by widespread intestinal metaplasia. Gastric cancer is believed to arise via a multistage process that includes chronic gastritis, gastric atrophy, usually with intestinal metaplasia, and finally dysplasia. It remains unclear whether intestinal metaplasia is a premalignant condition or a marker for increased risk of malignancy. The fact that intestinal metaplasia in the antrum is also found with duodenal ulcer disease, a condition associated with a low risk for the development of gastric cancer, suggests that other conditions or events are important in the pathogenesis of gastric cancer.

The risk of developing gastric adenocarcinoma is highest in those with the most extensive atrophy associated with hypochlorhydria or achlorhydria. It has been suggested that there is a relation between cancer risk and the subtype of intestinal metaplasia, with the incidence of cancer being highest among patients with intestinal metaplasia subtype III. Confirmation of this hypothesis would suggest that typing of intestinal metaplasia could provide a simple approach to identify those at highest risk, and would allow resources to be directed to surveillance of that small group. Our study was designed to ask whether the results regarding the presence and type of intestinal metaplasia are reproducible or consistent on follow up of the same individual and whether type III metaplasia led to a high frequency of dysplasia.



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