Usefulness of OLGA and OLGIM system not only for intestinal type but also for diffuse type of gastric cancer, and no interaction among the gastric cancer risk factors

Abstract

Background The operative link on gastric atrophy (OLGA) and operative link on gastric intestinal metaplasia (OLGIM) stages have been suggested for risk estimation of gastric cancer (GC). However, usefulness of OLGA/OLGIM systems in diffuse type of GC was not investigated so far. The aims of this study were to evaluate the OLGA/OLGIM systems in estimating the GC risk according to Lauren's classification and to investigate the interaction among the risk factors. Materials and methods The OLGA/OLGIM stages were evaluated in 1398 (765 control and 633 GC patients) who were prospectively enrolled in the Seoul National University Bundang Hospital. Synergistic interaction among the risk factors for GC was calculated using an additive model. Results Among 387 intestinal‐type GC patients, 71 (18.3%) were high‐risk OLGA stages (III, IV) and 113 (29.2%) were high‐risk OLGIM stages (III, IV). Of the 246 patients with diffuse‐type GC, 36 (14.6%) were high‐risk OLGA stages and 39 (15.9%) were high‐risk OLGIM stages. Multivariable analysis revealed family history of GC, Helicobacter pylori infection, high‐risk OLGA stages, and high‐risk OLGIM stages as independent risk factors for GC regardless of histologic type (odds ratios [ORs] 1.78, 1.94, 2.63, and 3.18, respectively). There was no significant risk modification among the H. pylori infection, family history of GC, and high‐risk OLGA/OLGIM stages. Conclusion High‐risk OLGA/OLGIM stages are important prediction markers for GC regardless of H. pylori infection or family history of GC not only for the intestinal type but also for diffuse‐type GC.

Natural history of autoimmune atrophic gastritis: a prospective, single centre, long‐term experience

“…Similarly, severity of intestinal metaplasia has an increasing trend over time, with no regression during AAG natural history. Intestinal metaplasia is another risk factor for the development of gastric neoplasms, which depends on the severity of intestinal metaplasia, regardless of H pylori infection . According to our results, it was not possible to identify a specific time point or a time lapse during which stage progression is more likely to occur, as this was stable over time.…”

The prevalence of histologic atrophy and intestinal metaplasia in the corpus has decreased over 15 years in females in the Korean population

“…Four specimens from the greater curvature and six biopsy specimens were obtained from the lesser curvature, evenly from the mid‐antrum and mid‐corpus (Figure ) . In this study, we determined H pylori ‐positive as a result of histologic examination (modified Giemsa test), rapid urease test (Campylobacter‐like organism [CLO] test), and culture . One experienced pathologist (HSL, an expert pathologist with over 20 years of experience) consistently performed a histologic evaluation of all specimens without subject information.…”

Gastric cancer prevention targeted on risk assessment: Gastritis OLGA staging

“…This observation generated the hypothesis of GC developing irrespective of any atrophy: Due to the possible dedifferentiation of intestinal‐type GC into a diffuse phenotype, the real prevalence of such a situation is hard to estimate, and the biological link between a non‐atrophic background and diffuse‐type GC has by no means been consistently demonstrated. Moreover, there is solid evidence of cancer promotion (any histotype) being associated with hypoacidity (mostly atrophy‐related), and this supports the possibility of both diffuse and intestinal GCs originating from a non‐metaplastic cell lineage (ie, non‐metaplastic atrophy) …”

“…Gastric atrophy includes two major phenotypes (Table ): (a) the disappearance of glandular units, replaced by fibrotic lamina propria (ie, a reduced glandular mass, but no change in the native commitment of glandular epithelia; so‐called non‐metaplastic atrophy); or (b) the replacement of the native glandular epithelium by (newly committed) metaplastic cells (the so‐called metaplastic atrophy) involving intestinal metaplasia and/or SPEM. The SPEM variant (restricted to the oxyntic mucosa by definition) can be more easily assessed by exploiting its positive immuno‐staining with TFF2 antibodies (Figure , Table ) …”

“…Moreover, there is solid evidence of cancer promotion (any histotype) being associated with hypoacidity (mostly atrophy-related), and this supports the possibility of both diffuse and intestinal GCs originating from a non-metaplastic cell lineage (ie, non-metaplastic atrophy). 15,16 Gastric mucosal atrophy is defined as the "loss of appropriate glandular units." 17,18 Atrophic transformation of the gastric mucosa (almost) invariably results from long-standing (non-self-limiting) inflammatory conditions.…”