2. Histological classification of gastritis
• Sydney system1 1990
• Houston version of Sydney system2 1994
• Operative Link for Gastritis Assessment3 2005
OLGA
1 Price AB. J Gastroenterol Hepatol 1991 ; 6 : 209 – 22.
2 Dixon MF et al. Am J Surg Pathol 1996 ; 20 : 1161 – 81.
3 Rugge M & Genta RM. Human Pathol 2005 ; 36 : 228 – 233.
reporting gastritis according to gastric cancer risk
from lowest (stage 0) to highest (stage IV)
3. Risk factor for gastric cancer
• H. pylori Most consistent risk factor
Eradication reduces risk of cancer
• Genetic factors Cytokines: IL-1β, IL-8, IL-10, TNF-α
No recommended marker at present
• Environmental factors N-nitroso compounds
Salted foods, tobacco, alcohol
Subordinate to effect of HP infection
Protective effect of NSAID & aspirin
Malfertheiner P et al. Gut 2012 ; 61: 646 – 664.
4. Gastric cancer pathways
Eradication of H pylori reduces risk of gastric cancer
But not eliminate cancer due to predetermined genetic pathways:
Hereditary diffuse gastric cancers & autoimmune gastritis
Talley NJ. Lancet 2008 ; 372 : 350 – 352.
5. Carcinogenicity of H. pylori
Atrophic corpus gastritis
H. pylori infection
Hypochlorhydria
Overgrowth of non-HP
organisms
Reduce nitrates to nitrites
& N-nitrosamines
Reduced/absent concentrations
of ascorbic acid
Ascorbic acid scavenges
carcinogenic N-nitrosamines
Malfertheiner P et al. Gut 2012 ; 61: 646 – 664.
6. Prevention of gastric cancer
Identification of subjects with high risk of gastric cancer
• Non-invasive tests Validated serology for H. pylori
Low incidence + Markers of atrophy (pepsinogens)
PGI: chief cell
PGII: chief cell – pyloric glands
Low PGI or low PG1/PGII → atrophy
• Invasive test Gastroscopy & biopsies
High incidence OLGA staging system*
* OLGA: Operative Link for Gastritis Assessment
Dinis-Ribeiro M et al. Endoscopy 2012 ; 44 : 74 – 94.
Malfertheiner P et al. Gut 2012 ; 61: 646 – 664.
7. OLGA staging system for gastritis
International group of gastroenterologists & pathologists
• Applies histology reporting format for chronic hepatitis
• Given number of portal tracts for staging of hepatitis
Well-defined biopsy protocol Antrum (3) – Corpus (2)
• Main lesion of cirrhosis risk Fibrosis
Main marker of gastric cancer Mucosal atrophy
• Staging by combining degree of atrophy & topography
• Assess risk of gastric cancer Stage 0 to stage 4
OLGA: Operative Link for Gastritis Assessment
Rugge M & Genta RM. Gastroenterology 2005 ; 129 : 1807 – 8 .
8. Gastric biopsy sampling protocol
A1 – A2
Greater & lesser curvatures of distal antrum
A3
Lesser curvature at incisura angularis
C1 – C2
Anterior & posterior walls of proximal corpus
At least five biopsies
Rugge M et al. Dig Liver Dis 2008 ; 40 : 650 – 658.
Minimum requirement for reliable staging of gastritis
9. Normal & atrophic glandular units in stomach
Nl mucosecreting gland Non-metaplastic atrophy
Normal oxyntic gland Non-metaplastic atrophy Metaplastic atrophy
Pseudopyloric metaplasia
Metaplastic atrophy
Intestinal metaplasia
Ruggea M et al. Dig Liver Dis 2008 ; 40 : 650 – 658.
AntrumCorpus
10. OLGA staging system for gastritis
Combining degree of atrophy & location
• Atrophy No atrophy (0%) Score 0
Mild (1 – 30%) Score 1
Moderate (31 – 60%) Score 2
Severe (> 60%) Score 3
• Location Antral atrophy score (Aas) Mean A1 + A2 + A3
Corpus atrophy score (Cas) Mean C1 + C2
• OLGA Overall Aas & Cas Stage 0, I, II: low risk
Stage III, IV: high risk
Rugge M et al. Dig Liver Dis 2008 ; 40 : 650 – 658.
11. OLGA staging system for gastritis
Ruggea M et al. Dig Liver Dis 2008 ; 40 : 650 – 658.
A
n
t
r
u
m
No atrophy
Score 0
Mild atrophy
Score 1
Moderate atrophy
Score 2
Severe atrophy
Score 3
Stage 0 Stage I Stage II Stage II
Stage I Stage I Stage II Stage III
Stage II Stage II Stage III Stage IV
Stage III Stage III Stage IV Stage IV
Atrophy score
Corpus
No atrophy
Score 0
Mild atrophy
Score 1
Moderate atroph
Score 2
Severe atrophy
Score 3
12. Stage 0 gastritis
Rugge M et al. Dig Liver Dis 2011 ; 43S : S373 – S384.
Visual analog scales at each of biopsy level to stage a given patient
H. pylori-status has to be reported
13. Stage I gastritis
Rugge M et al. Dig Liver Dis 2011 ; 43S : S373 – S384.
Atrophy most frequently detected in angularis incisura
In patients on PPI, HP may be difficult or impossible to identify
Coexisting polymorphs & lymphoid infiltrate suggest presence of HP
14. Stage II gastritis
Rugge M et al. Dig Liver Dis 2011 ; 43S : S373 – S384.
Stages 0, I, and II are associated with DU more than GU
15. Stage III gastritis
Rugge M et al. Dig Liver Dis 2011 ; 43S : S373 – S384.
GU encountered more frequently than in OLGA stages 0 – I – II
16. Stage III gastritis
Corpus predominant atrophy should suggest an autoimmune etiology
Rugge M et al. Dig Liver Dis 2011 ; 43S : S373 – S384.
17. Stage IV gastritis
Pan-atrophic gastritis
Endoscopic surveillance in stage III–IV patients
Rugge M et al. Dig Liver Dis 2011 ; 43S : S373 – S384.
18. Assessment of elementary lesions
• H. pylori status Positive – Negative
Absent in PPI user & atrophic gastritis
• Inflammation Lympho-monocytic – Polymorphic
May suggest presence of HP
• Metaplasia Intestinal – Pseudo-pyloric
• Precancerous lesions IEN (formerly dysplasia)*
* IEN: Intra-Epithelial Neoplasia
Rugge M et al. Dig Liver Dis 2011 ; 43S : S373 – S384.
Information on likely etiology: H. pylori, autoimmune,..
19. Staining for H. pylori
• Basic stain Hematoxylin & eosin
• Special stain Modified Giemsa
• Triple stain Genta
El-Zimaity
• Immunohistochemical
HP status assessed by special stain has to be reported
20. Eradicating epidemic gastric cancer has long been a dream
Now this dream can come true
Rugge M et al. Nat Rev Gastroenterol Hepatol 2012 ; 9 : 128 – 129.
Gram-negative bacterium with helical rod shape.Prominent flagellae facilitating penetration of thick mucous layer in the stomach.
(OLGA) system may afford a reliable indication of the cancer risk of individual patients.
Inflammation of the gastric mucosa leads to an increase in both PGI and PGII serum levels, usually with a more marked increase of PGIIand thus a decrease in the PGI/II ratio. With the development of atrophy and loss of specialized cells, both PGI and PGII may decrease, but PGI usually shows a more marked decrease than PGII, thus there is a further decline in the PGI/II ratio (see review by Kuipers EJ: “In through the out door: serology for atrophic gastritis,” Eur J GastroenterolHepatol 2003: 877–879). Thus, a low PGI level, a lowPGI/II ratio, or both, are good indicators of atrophic changes in the gastric mucosa.Subjects with severe gastric atrophy, in whom H pylori has disappeared and who are therefore serologically negative for H pylori, are at a particularly high risk.
both the oxyntic and the antral mucosa have to be “explored”and also considering the incisuraangularis “highly informative” for purpose of establishing earliest onset of atrophic–metaplastic transformation.
Antral atrophy scoreCorpus atrophy score
Patients on PPI, H. pylori may be difficult (or even impossible) to identify histologically at antral or corpus level, in which case coexisting inflammatory lesions (polymorphs and lymphoid infiltrate) may suggest the bacterium’s presence and a comment on the suspectedbacterial etiology (“suspicious for H. pylori infection”) should be added (whatever the stage of atrophy recorded).
