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Gastric Cancer Risk Diagnosis and Prevention in Subjects with Helicobacter pylori-related Chronic GastritisShotaro Enomoto1, Mika Watanabe1, Chizu Mukoubayashi1, Hiroshi Ohata1, Hirohito Magari1, Izumi Inoue1, Takao Maekita1, Mikitaka Iguchi1, Kimihiko Yanaoka1, Hideyuki Tamai1, Jun Kato1, Masashi Oka1 and Masao Ichinose1[1] Second Department of Internal Medicine, Wakayama Medical University, Japan1. Gastritis Staging by OLGA system (Rugge & Genta, 2005a, 2005b, 2007), published in Gut in 2007. Summary of management for patients with atrophic gastritis, gastric intestinal metaplasia and gastric epithelial dysplasia.
IntroductionThe gastritis is an inflammatory condition of the gastric mucosa characterized by existence of elementary histological alternations. Gastric cancer risk and prevention of gastric cancer based on Helicobacter pylori (HP)-related chronic gastritis stage.
Jones, 2010Japanese apricots reported to inhibit inflammation and gastritis progression related to Helicobacter pylori infection.
The main criticism was that the some of the commonly used descriptive names were not enabled into the system, like the ‘multifocal atrophic gastritis’ or ‘diffuse antral gastritis’.
The relationship between chronic gastritis, gastric ulceration and carcinoma of the stomach. The staging of gastritis with the OLGA system by using intestinal metaplasia as an accurate alternative for atrophic gastritis. Grading and classification of chronic gastritis: one American response to the Sydney System. This shows the stage classification for HP-related chronic gastritis based on the serum pepsinogen (PG) test and HP antibodies.
In the serum PG test-positive group (extensive chronic atrophic gastritis (CAG)), no reduction in gastric cancer incidence was observed with HP eradication. The atrophy stage defined from the combination of atrophic changes assessed in gastric antral and corporal biopsies. Progression of chronic atrophic gastritis showed a significant stepwise increase in the incidence of gastric cancer. Correa and Yardley criticized the system for missing out certain types of the gastritis and well as it is not a ‘classification’ (Correa & Yardley, 1992). Regarding gastric cancer prevention based on stage, in Group B, with mild atrophy, prevention of gastric cancer mainly by HP eradication can be expected. Long-lasting inflammation in the stomach mucosa leads to a cascade of molecular and morphological changes, representing the gastritis-atrophy-metaplasia-dysplasia-cancer sequence (Correa, 1992). Warren, 1984Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration.
At the same time the discoveries of non-neoplastic gastric diseases, especially gastritis, was really elusive for quite a long time due to less macroscopic features and to post-mortem alternations. The HP infection rate is higher in Japan than in Western countries, with nearly all cases of GC occurring in subjects with underlying HP-related chronic gastritis.
Kurihara, 2004Meta-analysis on the validity of pepsinogen test for gastric carcinoma, dysplasia or chronic atrophic gastritis screening. Perez-Perez, MJ Blaser, 1989Prevalence of Helicobacter pylori infection and histologic gastritis in asymptomatic persons. Parsonnet, 1999Interobserver variability in application of the revised Sydney classification for gastritis.
Original classification of gastritis dividing into acute, chronic and special forms, and grading of chronic inflammation, polymorph activity, atrophy, intestinal metaplasia and H. He stated that some of the erosions can become gangrenous, and described corrosive gastritis as it was the most well-known gastritis form of that time due high number of lye intoxication. In addition, in terms of GC prevention, it has become clear that HP-related chronic gastritis cannot be ignored as an origin of carcinogenesis.Here, we discuss the significance of serum pepsinogen (PG) as a marker of GC risk and GC high-risk groups based on HP-related chronic gastritis.
Meanwhile Baron Carl von Rokitansky besides his major discoveries was the first to note hypertrophic gastritis in 1855. Most of the pathologist agreed with the need of incisural biopsy, since the most degree of atrophy and intestinal metaplasia is found in the incisural region.
GC risk diagnosis based on the natural history of HP-related chronic gastritisNovel risk markers to identify GC high-risk groups based on a detailed natural history of HP-related chronic gastritis have long been awaited.


The next major footstep was done by Samuel Fenwick in 1870, who noted the presence of glandular atrophy due to gastric inflammation when classifying gastric lesions and anatomical alternations of the gastric mucosa (Fenwick, 1870). That would reduce the sampling error of missing premalignant lesions and improve the diagnosis of multifocal gastritis. After the development of the visual analogue scale according to the Up-dated Sydney System, the grading of atrophy still continued to show a considerable inter-observer variability (El-Zimaity et al, 1996). However, accurately diagnosing the extent of CAG based on a few biopsy samples is difficult, because CAG together with intestinal metaplasia is a multifocal process.
The updated system categorised chronic gastritis into ‘non-atrophic’ and ‘atrophic’ forms with the latter divided into autoimmune (diffuse corpus atrophy) and multifocal.
Histological reporting of gastritis should take into account the topographical pattern (antral or corpus predominant), and the final diagnostic term should ideally combine morphology and etiology to maximize the clinical value of gastric biopsy diagnosis (Dixon et al, 1997).
The up-dated system beside its major benefits in further standardizing endoscopic sampling, histological assessment and formality of reporting, still showed weaknesses specially in grading atrophy as pointed out by Johan A.
Classification by ApplemanThe clearest division of gastritis for clinicians was published by Appleman in 1994.
The most common form of gastritis that was called earlier as chronic diffuse antral gastritis, gastritis chronic type B, gastritis chronica active antralis, gastritis non-specifica or gastritis typus hypersecretions was named as Helicobacter pylori related gastritis. According to Appelman’s classification the autoimmune gastritis used to be called as gastritis autoimmunogenes, gastritis chronic atrophica typus A, gastritis chronic typus A and gastritis chronic diffusa corporis, was called to autoimmune chronic atrophic gastritis. Appelman pointed out the presence of autoantibodies against parietal cells and intrinsic factor being important in diagnosis, enterochromaffinlike (ECL) cell hyperplasia and risk of carcinoma. Appelman’s classification of gastritis continues with the multifocal atrophic gastritis earlier called as environmental gastritis or type B chronic atrophic gastritis.
MacKay proposed the classification of gastritis based on additional factors just beside just histology and topography (Strickland & Mackay, 1973). They suggested that immunological and etiological data should be included along with pathomorphological and topographic parameters; gastric parietal cell antibody and serum level of gastrin have to be seen to get better classification of chronic gastritis. This term was aimed to be used for extended gastritis observed in corpus to pre-pyloric region (Glass & Pitchumoni, 1975). Appelman seeing similarity of the histological changes of patients with gastroenteric anastomosis and taking nonsteroidal anti-inflammatory (NSAID) medications, called third division of gastritis caused by bile reflux or NSAIDs to chemical gastropathies. Recognition of this distinction of gastritis greatly helped to simply classification, although many times elements histological changes usually found in chemical gastropathy can be noticed in other forms of gastritis as well as in other gastric disease. All the rest of gastritis was called environmental, which are mostly due to diet and geographic localization (Correa, 1980). Finding them singular and unassociated wit other changes like atrophy, intestinal metaplasia, presence of bacteria, ulcers, polyps, should raise the possibility of chemical gastritis. Appelman kept the name of lymphotic gastritis used by his frontiers for the fourth distinctive form of gastritis (Haot et al, 1988, 1990). By seeing his nomenclature, sometimes showing etiology, sometimes reflecting topography, we are able to see the controversy existed between pathologist and clinicians in the field of gastritis at that time. In this form of chronic gastritis huge lymphocytic infiltration of the surface epithelium, superficial pits and lamina propria can be observed.
Others used to call this as superficial gastritis, gastritis chronic erosive or gastritis varioliformis. That time in 1990, the histological changes seen in lymphocytic gastritis was already described in patients with sprues and gluten-sensitivity. Two years later, examining 316 patients Sobala confirmed that most of reflux gastritis in intact (non-operated) stomach is not due to bile reflux but rather NSAID use. But lymphocytic gastritis also can form giant folds leading clinical symptoms (Ménétrier’s disease). There are many gastritis forms that do not differ significantly from similar inflammations found other organs, including those that occur in syphilis, mycobacterial and cytomegalovirus, human immunodeficiency virus infections, histoplasmosis, candidiasis, cryptosporidiosis and other opportunistic fungi. In a population of middle-aged healthy men, in an atrophy-negative group, the annual incidence of GC was 0.07%.
Their discovery showed that the commonest form of gastritis is simply an infectious disease caused by an otherwise known pathogen.


There are still others which are not associated with any other diseases and designated as ‘isolated granulomatous gastritis’. Appelman also categorized the recently described collagenous gastritis into this miscellaneous group.
Natural history of HP-related chronic gastritis and GC riskIn addition to the serum PG test, the natural history of HP-related chronic gastritis and associations with GC risk have been examined by evaluating HP infection, as the major cause of onset and progression of chronic gastritis in Japan (Ohata et al, 2004; Yanaoka et al, 2008b).
HP infection is diagnosed using anti-HP antibody titers, which, like the serum PG test, is a blood test that is easy to perform. Heilmann, Adrian Lee, Barry Marshall, George Misiewicz, Ashley Price, Penti Sipponen, Enrico Solcia, Manfred Stolte, Robert Strickland, Guido Tytgat) was set up to review the biology and natural course of chronic gastritis and to propose a new classification for gastritis by the leadership of George Misiewicz and Guido Tytgat. The stages of HP-related chronic gastritis, fromFigure 2.Kaplan-Meier analysis of gastric cancer development in subjects classified using the criteria of the serum pepsinogen (PG) test. The histological division of Sydney System intended to be a practical guideline showing which of the morphological features of gastritis in endoscopic biopsy specimens should be documented (Price, 1991). Based on these data, with progression in stage of HP-related chronic gastritis, a stepwise increase is seen for GC incidence (Fig. These results showed that in Japan, almost all cases of GC are associated with HP-related chronic gastritis. Points in the diagnosis of GC risk using the serum PG testThe serum PG test is clearly a highly useful test for a GC risk marker. However, the occurrence of GC (particularly diffuse-type GC) in PG test-negative groups (group B in the stage classification for HP-related chronic gastritis) cannot be ignored. When diagnosing GC risk using the serum PG test, this fact must be carefully considered.We therefore carefully investigated GC occurrence in a PG test-negative group. Among PG test-negative groups, in group A of the stage classification for HP-related chronic gastritis (PG test-negative and HP-negative), we observed no occurrence of GC over a 10-year follow-up period. However, some cautionary points must be considered in a confirmatory diagnosis of Group A status. Prevention of GC based on the natural history of HP-related chronic gastritisThe evaluation of HP-related chronic gastritis is especially important in the analysis of GC prevention. During long-term observation, clear-cut inhibition of gastric carcinogenesis by HP eradication is not seen, but eradication groups with shorter observation periods may display apparent inhibition of GC, with slower growth rates, and without growth of cancer that can be clinically diagnosed.
We therefore conducted a 10-year follow-up study in middle-aged healthy adults in whom progression of atrophic gastritis was monitored by serum PG (Yanaoka et al., 2009). In addition, we conducted a clinical study of GC chemoprevention using a COX-2 inhibitor in patients with metaplastic gastritis (Yanaoka et al., 2010).
This study, although non-randomized, included patients who had undergone endoscopic resection of intestinal-type GC with a background of metaplastic gastritis. The diagnosis of metaplastic gastritis was based on serum testing, as previously described. Regarding HP-related chronic gastritis stage, these patients were classified as Group D [HP(-), PG(+)]. In this study, long-term treatment with etodolac as a selective COX-2 inhibitor effectively inhibited metachronous cancer development in curatively treated, early GC patients with metaplastic gastritis.
Research into HP-related chronic gastritis and promoters and inhibitors of gastric carcinogenesis, and studies of alternative therapies, primarily in the form of functional foods, has thus been conducted. In the progression of HP-related chronic gastritis, besides HP virulence factors such as VacA and CagA (Hatakeyama, 2004), and host factors such as cytokine polymorphisms (El-Omar et al., 2000), environmental factors such as lifestyle and dietary habits have been shown to be involved.
ConclusionIn conclusion, based on the natural history of HP-related chronic gastritis from blood test data, including the serum PG test and HP antibodies, specific prediction of the risk of GC in each individual is now possible.



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