A Review
Kent Humble MD
Assistant Professor of Family Medicine
LSU School of Medicine
Discuss relationship between gastric IM and gastric cancer
Review pathophysiology and epidemiology of gastric IM
Review guidelines concerning endoscopic surveillance
US Incidence by
Ethnic Background
2008
Int J Cancer 2010;127(12):2893
Highest incidence in
East Asia, Eastern
Europe, and
Western South
America
Intestinal Type Diffuse Type
Intestinal Type
70-80% of cases
Predominantly in high risk areas
Older age (mean 69)
Diffuse Type
20-30% of cases
Uniform across countries
Develops from precursors
Male to Female 2:1
Environmental factors
Younger age (mean 38)
No identified precursors
Male to Female 1:1
Genetic factors
Gastritis
Atrophic
Gastritis
Intestinal
Metaplasia
Dysplasia Cancer
Gastric IM is likely the 'breaking point' between chronic gastritis and dysplasia
Am J Physiol Gastrointest Liver Physiol 291: G999 –G1004, 2006
• Foci appear at junction of Antrum & Body, often at
Angularis
• Enlarge, coalesce, extending to Antrum & Body
• Small foci of dysplasia may appear in areas of IM, subject to sampling error
• Severity & tempo of progression may be influenced by virulence of H Pylori (?cagA), environmental, host genetic factors
Found in up to 25% US Adults
13% of Caucasians
50% of Blacks/Hispanics
H. pylori infection significantly raises IM prevalence
Increases with patient age
Higher in first degree relatives with gastric cancer
Cancer Epidemiol Biomarkers Prev 1992;1:293 –296.
• Systematic review:
Patients with IM
Gastric cancer incidence varied 0-10%
Am J Surg Pathol 2000; 24: 167-176
• Dutch study:
Histology based
• 61,707 pts with IM
• 874 developed gastric CA over 10 years
• 0.18%yearly
Gastroenterology 2008; 134: 945-952
ARE ALL PATIENTS WITH IM AT
EQUAL RISK OF GASTRIC
CANCER?
The presence of incomplete-type IM is associated with a higher gastric cancer risk compared to complete-type IM.
Spain study:
Mean follow-up 12.8 years
• Incomplete IM: 16 of 88 pts (18.2%) developed gastric CA
• Complete IM: 1 of 104 pts (0.96%) developed gastric CA
Int J Cancer 2010; 127: 2654-2660
ARE ALL PATIENTS WITH IM AT
EQUAL RISK OF GASTRIC
CANCER?
Gastric cancer risk is associated with IM topography.
Columbia study:
Compared to antral predominate (focal)
• Extension through angularis- risk 5.7 fold
• Antrum plus body (diffuse)- risk 12.2 fold
Incomplete IM presents as diffuse more commonly than focal
Am J Gastroenterol 2000; 95: 1431-1438
ARE ALL PATIENTS WITH IM AT
EQUAL RISK OF GASTRIC
CANCER?
Extensive IM increases the risk of progression to dysplasia.
Italian Study
• The rate of gastric cancer appeared to increase with increasing
IM extension
Hum Pathol 2006; 37 1489-1497
IM may be considered extensive when it involves at least two locations or when it is moderate or marked in more than one biopsy specimen
H. pylori eradication may slow IM progression .
Hong Kong Study
• 537 pts with IM and H. Pylori randomized to treatment or placebo
• H Pylori eradication prevented IM progression
• Odds ratio 0.48 (95% CI: 0.32-0.74)
Gut 2004; 53: 1244-1249
IM does not appear to regress following H. pylori eradication.
Meta-analysis of 7 studies
• Unlike atrophy, no significant IM regression occurred following H. Pylori eradication
Helicobacter 2007; 12 Suppl 2: 32-38
Meta-analysis of 12 studies
• Atrophy improved in the body but not antrum
• IM did not improve after eradication
Digestion 2011; 83: 253-260
Italian Study
• 6 months of ascorbic acid qOD following H. Pylori eradication helped reduce IM
Aliment Pharma- col Ther 2000; 14: 1303-1309
Taiwan Study
• IM regressed in 24% of 33 pts following 8 wks of treatment with celecoxib 200 mg/d after H. Pylori eradication
J Gastroenterology Hepatol 2010; 25: 48-53
Dutch study : Can extension be predicted?
88 patients with previous IM on gastric biopsy
Repeat EGD & blood tests done
Most important predictors of extensive IM:
Family history of gastric cancer
Alcohol use 10ml per day
Marked IM of index biopsy
Pepsinogen I/II ratio < 3.0
Gastrointestinal Endoscopy Vol 70, No.1:2009
PG
II
PG
II
PG I & II
• Endoscopic surveillance for gastric intestinal metaplasia has not been extensively studied in the U.S. and therefore cannot be uniformly recommended
• Patients at increased risk for gastric cancer due to ethnic background or family history may benefit from surveillance
• Endoscopic surveillance should incorporate topographic mapping of the entire stomach
Gastrointestinal Endoscopy Volume 63, No. 4 : 2006
• Conventional white light endoscopy cannot accurately differentiate between benign and precancerous gastric conditions/lesions
• Magnification chromoendoscopy (MCE) or narrow-band imaging (NBI) endoscopy with or without magnification may be offered in these cases as it improves diagnosis of such lesions
• At least four non-targeted biopsies of the proximal and distal stomach, on the lesser and greater curvatures, are needed for adequate assessment of premalignant gastric conditions
Virchows Arch. 2012 Jan;460(1):19-46. Epub 2011 Dec 22.
• Patients with extensive atrophy and/or extensive IM should be offered endoscopic surveillance every 3 years
• Further studies are needed however, to accurately estimate the cost –effectiveness of such an approach
• Patients with mild to moderate atrophy/IM only in
Antrum do not need follow-up
• Sub-typing of IM is not recommended for clinical practice
Virchows Arch. 2012 Jan;460(1):19-46. Epub 2011 Dec 22.
• COX-2 inhibitors, or the use of dietary supplementation with antioxidants (ascorbic acid and beta-carotene) are not endorsed as approaches to decrease the risk of progression of gastric precancerous lesions
• Neither age, gender, H. pylori virulence factors, or host genetic variations change these clinical recommendations
Virchows Arch. 2012 Jan;460(1):19-46. Epub 2011 Dec 22.
Virchows Arch. 2012 Jan;460(1):19-46. Epub 2011 Dec 22.
IM may be considered extensive when it involves at least two locations or when it is moderate or marked in more than one biopsy specimen
OLGA
Operative Link for Gastritis Assessment
OLGIM
Operative link on Gastric Intestinal Metaplasia Assessment.
Gastritis staging systems that arrange histological phenotypes of gastritis along a scale of progressively increasing gastric cancer risk, from the lowest
(stage 0) to the highest (stage IV).
khumbl@ lsuhsc.edu