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OLGA staging system for gastritis

Thursday 23 February 2012

Building on current knowledge of the biology of gastritis and incorporating experience gained worldwide by applying the Sydney System for more than 15 years, an international group of pathologists (Operative Link for Gastritis Assessment) has proposed a system for reporting gastritis in terms of stage (the OLGA staging system).

Gastritis staging arranges the histological phenotypes of gastritis along a scale of progressively increasing gastric cancer risk, from the lowest (stage 0) to the highest (stage IV).

Gastric mucosal atrophy is the precancerous condition in which intestinal-type gastric cancer (GC) most frequently develops.

The OLGA system

According to internationally accepted criteria, at each biopsy sample site, gastritis was distinguished in non‐atrophic gastritis (ie, no loss of appropriate glands) and atrophic gastritis (ie, loss of appropriate glands).

Mucosal atrophy (both phenotypes, ie, with and without metaplastic epithelial transformation (ie, intestinal metaplasia in both antral and/or oxyntic biopsy samples and pseudo‐pyloric metaplasia in oxyntic biopsy samples)) was scored according to the Sydney system using a visual analogue scale (0 = absent; 1 = mild; 2 = moderate; 3 = severe).

On the basis of the topographic locations (oxyntic and angular/antral) of the histology changes, the gastritis stage is assessed according to the OLGA proposal.

In particular, all the biopsy samples obtained from both the antrum and angularis incisura are considered together as representative of the distal, non‐oxyntic, gastric mucosa, and any atrophic changes were scored according to the visual analogue scale.

The same scoring system is applied in the assessment of atrophic changes in oxyntic biopsy samples.

The OLGA gastritis stage is finally obtained by combining antral with oxyntic scores.

OLGIM

Gastritis staging systems (both OLGA and OLGIM) convey prognostically important information on the gastritis-associated cancer risk.

Because of its clinical impact, the stage of gastritis should be included as a conclusive message in the gastritis histology report.

Since it focuses on IM alone, OLGIM staging is less sensitive than OLGA staging in the identification of patients at high risk of gastric cancer.

Atrophic gastritis (resulting mainly from long-standing Helicobacter pylori infection) is a major risk factor for (intestinal-type) gastric cancer development and the extent/topography of the atrophic changes significantly correlates with the degree of cancer risk.

Gastritis staging systems (both OLGA and OLGIM) convey prognostically important information on the gastritis-associated cancer risk.

Because of its clinical impact, the stage of gastritis should be included as a conclusive message in the gastritis histology report.

Since it focuses on IM alone, OLGIM staging is less sensitive than OLGA staging in the identification of patients at high risk of gastric cancer.

In different epidemiological settings, both cross-sectional and long-term follow-up studies have consistently allocated a small minority of gastritis patients to stages III-IV, associating only this population with a significantly higher GC risk (high-risk OLGA stages).

OLGA stages III-IV have also been consistently associated with molecular tissue markers of high-risk gastritis.

These correlations potentially support the advisability of endoscopic follow-up for such high-stage patients.

A significant correlation has been demonstrated between high-risk OLGA stages and pepsinogen serology; this correlation between organic and functional disease supports the rationale for implementing serology in GC secondary prevention programs.

A recently-proposed modification of the OLGA staging system (OLGIM) basically incorporates the same staging frame, but replaces the “global” score for atrophy (in its different phenotypic variants) with the histological assessment of intestinal metaplasia (IM) alone.

The rationale behind the OLGIM proposal lies in the fact that intestinal metaplasia is easier to assess histologically than the “global” spectrum of the atrophic lesions (as in the OLGA approach).

OLGA system

For OLGA staging purposes, atrophy is defined as the loss of appropriate glands with or without epithelial metaplasia (i.e., IM in antral and/or oxyntic biopsy samples; pseudo-pyloric metaplasia in oxyntic biopsy samples).

Glandular atrophy was scored according to the recommendations in the OLGA staging tutorial.

For OLGIM staging purposes, only IM is considered and scored according to the recommendations of the OLGIM proposers.

Open references

- Operative link for gastritis assessment vs operative link on intestinal metaplasia assessment. Rugge M, Fassan M, Pizzi M, Farinati F, Sturniolo GC, Plebani M, Graham DY. World J Gastroenterol. 2011 Nov 7;17(41):4596-601. PMID: 22147965 [Free]

- Gastritis staging in clinical practice: the OLGA staging system. Rugge M, Meggio A, Pennelli G, Piscioli F, Giacomelli L, De Pretis G, Graham DY. Gut. 2007 May;56(5):631-6. PMID: 17142647 [Free]

- Assessing risks for gastric cancer: new tools for pathologists. Genta RM, Rugge M. World J Gastroenterol. 2006 Sep 21;12(35):5622-7. PMID: 17007013

References

- Gastritis: the histology report. Rugge M, Pennelli G, Pilozzi E, Fassan M, Ingravallo G, Russo VM, Di Mario F; Gruppo Italiano Patologi Apparato Digerente (GIPAD); Società Italiana di Anatomia Patologica e Citopatologia Diagnostica/International Academy of Pathology, Italian division (SIAPEC/IAP). Dig Liver Dis. 2011 Mar;43 Suppl 4:S373-84. PMID: 21459343

- The staging of gastritis with the OLGA system by using intestinal metaplasia as an accurate alternative for atrophic gastritis. Capelle LG, de Vries AC, Haringsma J, Ter Borg F, de Vries RA, Bruno MJ, van Dekken H, Meijer J, van Grieken NC, Kuipers EJ. Gastrointest Endosc. 2010 Jun;71(7):1150-8. PMID: 20381801

- OLGA staging for gastritis: a tutorial. Rugge M, Correa P, Di Mario F, El-Omar E, Fiocca R, Geboes K, Genta RM, Graham DY, Hattori T, Malfertheiner P, Nakajima S, Sipponen P, Sung J, Weinstein W, Vieth M. Dig Liver Dis. 2008 Aug;40(8):650-8. PMID: 18424244