El Salvador Atlas of Gastrointestinal VideoEndoscopy. A Large Database of Images and Video Clips with Cases Reported.
El Salvador Atlas of Gastrointestinal VideoEndoscopy
IntestinalMetaplasiazxcv1

Video Endoscopic Sequence 1 of 5.

Intestinal Metaplasia

 

 

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 All endoscopic images shown in this Atlas contain
 video clips

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IntestinalMetaplasiazxcv2

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.

 

IntestinalMetaplasiazxcv3

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.
  •  

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..

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.

Intestianal Metaplasiazxc2

Video Endoscopic Sequence 5 of 5.

 

A 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.

 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. 

 

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.

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.

metaplasia1

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.

 

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.

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

 

Cametaplasia2

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:

  • Antral predominant gastritis is characterized by inflammation and is mostly limited to the antrum. Individuals with peptic ulcers usually demonstrate this pattern of gastritis.
  • 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.
Cametaplasia1

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.

 

 

Cametaplasia3

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
 gastritis.

Cametaplasia4

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: (1) the metaplastic tissue is an
 early step in a multistep induction process; (2) 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 (3) the metaplasia is only a marker for
 chronic gastritis due to H. pylori infection or pernicious
 anemia. With the last mechanism.

Cametaplasia5

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
.

Cametaplasia6

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.

Cametaplasia7

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.