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The inflammatory spectrum of gastric diseases includes different clinico-pathological entities, the etiology of which was recently established in the international Kyoto classification. A diagnosis of gastritis combines the information resulting form the gross examination (endoscopy) and histology (microscopy). It is important to consider the anatomical/functional heterogeneity of the gastric mucosa when obtaining representative mucosal biopsy samples. Gastritis includes self-limiting and non-self-limiting (long-standing) inflammatory diseases, and the latter are epidemiologically, biologically and clinically linked to the onset of gastric cancer (i.e. "inflammation-associated cancer"). Different biological models of inflammation-associated gastric oncogenesis have been proposed. Helicobacter pylori (H. pylori) gastritis is the most prevalent worldwide, and H. pylori is classified as a first-class carcinogen. On these bases, eradicating H. pylori is mandatory for the primary prevention of gastric cancer. Non-self-limiting gastritis may also be triggered by the immune-mediated destruction of gastric parietal cells, resulting in autoimmune gastritis. In both H. pylori -related and autoimmune gastritis, the non-self-limiting inflammation results in atrophy of the gastric mucosa, which is the main factor promoting gastric cancer. Long-term follow-up studies consistently demonstrate the prognostic impact of the histological staging of gastritis in gastric cancer secondary prevention strategies. [ABSTRACT FROM AUTHOR]

Purpose of review: The gastritis constellation includes heterogeneous clinicopathological entities, among which long-standing, non-self-limiting gastritis, mainly due to Helicobacter pylori infection, has been epidemiologically, biologically, and clinically linked to gastric cancer development (i.e. "inflammation-associated cancer"). This review illustrates the updated criteria applied in the taxonomy of gastritis (Kyoto classification), elucidates the biological rationale for endoscopy biopsy sampling (heterogeneity of gastric mucosa), and finally reports the results of long-term follow-up studies supporting the reliability of biopsy-based gastritis staging as predictor of gastritis-associated cancer risk. Recent findings: By assuming gastric atrophy as the "cancerization field" where (non-syndromic) gastric cancer mostly develops, recent long-term follow-up studies consistently demonstrate the prognostic impact of the gastritis OLGA staging system. Summary: Helicobacter pylori eradication is the leading strategy in the primary prevention of gastric cancer. In a multidisciplinary dimension of secondary cancer prevention, the OLGA staging system reliably ranks the patient-specific cancer risk, thus providing the clinical rationale for a tailored follow-up strategy. [ABSTRACT FROM AUTHOR]

Gastric intraepithelial neoplasia (IEN; formerly dysplasia) is an advanced precancerous lesion. Lesions indefinite for IEN mimic the IEN phenotype but lack some morphologic attributes of IEN. Indefinite for IEN lesions may arise in native foveolae (atypical foveolar hyperproliferation [aFH]) or intestinalized glands (hyperproliferative intestinal metaplasia [HIM]). The clinicopathologic outcome of such lesions is debated. We retrospectively studied the clinicopathologic behavior of 129 consecutive indefinite for IEN lesions (HIM, 98; aFH, 31; median follow-up, 31 months) and correlated outcome with the extent and topography of mucosal atrophy (assessed by OLGA staging) at the initial endoscopy/biopsy. At enrollment, aFH never coexisted with severe/extensive atrophy (all cases were in low-risk OLGA stages [0-II]), whereas HIM was associated with low- and high-risk OLGA stages (0-II, 73; III-IV, 25). At follow-up, IEN was never documented among cases enrolled as aFH, while follow-up endoscopy/biopsy documented 6 neoplastic intraepithelial lesions among 98 cases of HIM (6%, all had high-risk OLGA stages at initial biopsy). OLGA staging can stratify indefinite for IEN lesions into different risk classes, potentially contributing to decisions for a patient-specific follow-up strategy. [ABSTRACT FROM AUTHOR]

Summary: Both sulfomucin-type intestinal metaplasia (ie, types II and III intestinal metaplasia, colonic-type intestinal metaplasia) and gastritis in Operative Link for Gastritis Assessment stages III and IV are associated with an increased risk of intestinal-type gastric cancer. This study aimed to verify the hypothesis that gastritis in Operative Link for Gastritis Assessment stages III and IV (both consistently associated with an increased cancer risk) is associated per se with types II and III intestinal metaplasia. Two hundred consecutive cases of atrophic gastritis (Operative Link for Gastritis Assessment stages I, II, III, and IV) were considered (50 cases for each stage). All cases were stained with high iron diamine, and intestinal metaplasia was subtyped accordingly (type I [ie, small-intestinal type] and types II and III). Helicobacter pylori status was also considered, distinguishing H pylori–positive versus H pylori–negative versus H pylori–eradicated patients. A significant association was found between intestinal metaplasia subtype and the Operative Link for Gastritis Assessment stage of gastritis (the higher the stage, the more the colonic-type of intestinal metaplasia, and vice versa; Wilcoxon, P = .001). The strength of the association between Operative Link for Gastritis Assessment stages and the 3 intestinal metaplasia subtypes was confirmed by logistic regression analysis (P < .001; odds ratio, 4.84; 95% confidence interval, 2.97-7.88). Intestinal metaplasia subtyping also correlated with the patient''s age (Kruskal-Wallis, P = .001) and H pylori status (Fisher exact, P < .001). Operative Link for Gastritis Assessment staging incorporates the prognostic message obtainable from histochemical gastric mucin subtyping. [Copyright &y& Elsevier]

Abstract: 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. The current format for histology reporting in cases of gastritis fails to establish an immediate link between gastritis phenotype and risk of malignancy. The histology report consequently does not give clinical practitioners and gastroenterologists an explicit message of use in orienting an individual patient''s clinical management. 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). This tutorial aims to provide unequivocal information on how to consistently apply the OLGA staging system in routine diagnostic histology practice. [Copyright &y& Elsevier]

Geographical differences have been shown in the clinical outcomes of Helicobacter pylori-associated gastritis phenotypes and in gastric cancer risk. This study tested whether the Operative Link on Gastritis Assessment (OLGA) staging correlated with gastric cancer risk in populations from 3 continents. Mapped gastric biopsies were obtained from 316 dyspeptic adults aged less than 41 years from 8 geographic areas that differed in gastric cancer risk. Gastric atrophy was assessed according to internationally validated criteria. Gastritis stage was established according to the OLGA staging system. The most prevalent gastritis stages were 0 to II, which included all subjects entered from Chile, Germany, India, Italy, and Thailand. Gastritis Stages III and IV were limited to the Chinese and Korean populations. Indians had a high prevalence of H pylori infection without high-stage gastritis. In populations at different cancer risk, the gastritis OLGA stage mirrored the gastric cancer incidence. Gastritis staging identifies a subgroup of higher-risk patients. [ABSTRACT FROM AUTHOR]

Gastric cancer (GC) ranks among the most lethal epithelial malignancies, and its striking mortality rate prompts a global prevention strategy. Helicobacter pylori (H. pylori) gastritis is the main GC promoter, and the 2014 Global Kyoto conference recognized H. pylori gastritis as a (treatable) infectious disease. It is therefore plausible that any large‐scale intervention for H. pylori eradication would result in cleansing the world of the fifth cause of cancer‐related death. Atrophic gastritis is the cancerization field in which GCs (both intestinal and diffuse histotypes) mainly develop. Discontinuing the inflammatory cascade triggered by H. pylori is tantamount to preventing GC. For patients (still infected or eradicated) who have already developed gastric atrophy, the severity/topography of the atrophic changes correlates with their cancer risk. Gastritis OLGA (Operative Link for Gastritis Assessment) staging consistently ranks the atrophy‐associated cancer risk, providing a solid clinical/biological rationale for establishing patient‐specific surveillance programs. By combining primary and secondary prevention strategies, gastric cancer is a preventable disease. [ABSTRACT FROM AUTHOR]

As Helicobacter pylori is a first-class carcinogen, eradication of the infection would be expected to be a beneficial measure for the (primary) prevention of gastric cancer. Given the natural history of gastric cancer, it is plausible that eradication before gastric atrophy sets in offers the best chance for cancer risk reduction. The beneficial effects of eradication may, nevertheless, still be achievable in more advanced disease. The reversibility of inflammatory lesions has been supported by undeniable evidence; the regression of mucosal atrophy/metaplasia has also been confirmed by several recent histologic studies., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Abstract: Gastritis is defined as inflammation of the gastric mucosa. In histological terms, it is distinguishable into two main categories, i.e. non-atrophic and atrophic. In the gastric mucosa, atrophy is defined as the loss of appropriate glands. There are several etiological types of gastritis, their different etiology being related to different clinical manifestations and pathological features. Atrophic gastritis (resulting mainly from long-standing Helicobacter pylori infection) is a major risk factor for the onset of (intestinal type) gastric cancer. The extent and site of the atrophic changes correlate significantly with the cancer risk. The current format for histology reporting in cases of gastritis fails to establish an immediate link between gastritis phenotype and risk of malignancy. Building on current knowledge of the biology of gastritis, an international group of pathologists [Operative Link for Gastritis Assessment (OLGA)] has proposed a system for reporting gastritis in terms of its stage (the OLGA Staging System): this system places the histological phenotypes of gastritis on a scale of progressively increasing gastric cancer risk, from the lowest (Stage 0) to the highest (Stage IV). The aim of this tutorial is to provide unequivocal information on how to standardize histology reports on gastritis in diagnostic practice. [Copyright &y& Elsevier]