Masao Ichinose

COMPLETE AND INCOMPLETE PYLORIC GLAND METAPLASIA OF HUMAN GALLBLADDER

The features of pyloric gland metaplasia in the gallbladder epithelium were studied by histochemical staining for mucin and the immunoperoxldase method for pepsinogens (Pg) I and II. Pyloric gland metaplasia was found in 48 of 72 gallbladders removed surgically. All the pyloric gland metaplastic cells contained class III mucin demonstrated by paradoxical concanavalin A (Con A) staining. Pyloric gland metaplasia was classified into complete and incomplete types on the basis of the immunohistochemical reactivities of Pgs I and II: The complete type of pyloric gland metaplasia contained neutral mucins and weak Pg I and strong Pg II activities, like normal pyloric gland cells. Almost all speciments of the incomplete type of pyloric gland metaplasia contained acid mucins and were further classified into two types: an incomplete type 1, which had Pg II but no Pg I activity, and an incomplete type 2, which had no Pg I or II activity.

Gastric Cancer Risk Diagnosis and Prevention in Subjects with Helicobacter pylori-related Chronic Gastritis

Helicobacter pylori (HP) is recognized as a major pathogenic factor for persistent inflammation in the human stomach (Dooley et al., 1989; Marshall & Warren, 1984). In 1994, the International Agency for Research on Cancer (IARC) classified HP infection as a definite class I carcinogen (International Agency for Research on Cancer (IARC), 1994). HP triggers chronic inflammation of the infected stomach mucosa and is considered a major risk factor for gastric cancer (GC) and associated precursor lesions. Long-lasting inflammation in the stomach mucosa leads to a cascade of molecular and morphological changes, representing the gastritis-atrophymetaplasia-dysplasia-cancer sequence (Correa, 1992). 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. HP infection is widely accepted as a major risk factor for the development of GC and its precursor lesions, based on extensive evidence derived from many studies (Blaser et al., 1995; EUROGAST Study Group, 1993; Forman et al., 1991; Hirayama et al., 1999; Honda et al., 1998; Huang et al., 1998; Nomura et al., 1991; Parsonnet et al., 1991; Shimizu et al., 1999; Sipponen et al., 1992; Sugiyama et al., 1998; Talley et al., 1991; Tokieda et al., 1999; Uemura et al., 2001; Watanabe et al., 1998; Zheng et al., 2004). However, in countries such as Japan, where the HP infection rate is high, prediction of GC risk based solely on the presence or absence of HP infection does not offer sufficient specificity. Elucidation of groups at high risk based on the natural history of GC is clearly necessary. The identification of useful markers of GC risk is thus hoped for. Evaluating HPrelated chronic gastritis and determining which subjects are at high risk for developing GC is very important, and would likely increase the efficacy of GC screening by endoscopic or other examinations (Enomoto et al., 2010a; Mukoubayashi et al., 2007; Ohata et al., 2005), and strategic approaches to metachronous multiple GC after endoscopic mucosal resection (EMR) or endoscopic submucosal dissection (ESD) performed as minimally invasive treatment for early GC (Gotoda, 2007; Kakushima & Fujishiro, 2008; Nakajima et al., 2006). In addition, in terms of GC prevention, it has become clear that HP-related chronic gastritis cannot be ignored as an origin of carcinogenesis.