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Olga staging system for diagnosis of gastritis
- 1. OLGA staging sytem SamirHaffar M.D. Assistant Professor of Gastroenterology
- 2. Histological classification ofgastritis • 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 forgastric 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 Eradicationof 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 gastriccancer 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 systemfor 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 samplingprotocol 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 & atrophicglandular 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 systemfor 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 systemfor 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 RuggeM 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 RuggeM 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 RuggeM 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 RuggeM et al. Dig Liver Dis 2011 ; 43S : S373 – S384. GU encountered more frequently than in OLGA stages 0 – I – II
- 16. Stage III gastritis Corpuspredominant atrophy should suggest an autoimmune etiology Rugge M et al. Dig Liver Dis 2011 ; 43S : S373 – S384.
- 17. Stage IV gastritis Pan-atrophicgastritis Endoscopic surveillance in stage III–IV patients Rugge M et al. Dig Liver Dis 2011 ; 43S : S373 – S384.
- 18. Assessment of elementarylesions • 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 gastriccancer has long been a dream Now this dream can come true Rugge M et al. Nat Rev Gastroenterol Hepatol 2012 ; 9 : 128 – 129.
- 21.
Editor's Notes
- #2 Gram-negative bacterium with helical rod shape.Prominent flagellae facilitating penetration of thick mucous layer in the stomach.
- #3 (OLGA) system may afford a reliable indication of the cancer risk of individual patients.
- #7 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.
- #9 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.
- #15 Antral atrophy scoreCorpus atrophy score
- #19 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).