Predicting the development of gastric cancer from combining Helicobacter pylori antibodies and serum pepsinogen status: a prospective endoscopic cohort study

Watabe, Hirotsugu

doi:10.1136/gut.2004.055400

Cited by 361 publications

(377 citation statements)

References 30 publications

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“…3). Similar results were reported by Watabe et al (Watabe et al, 2005). During the 10-year follow-up study, all patients who developed GC were HP infection-positive.…”

Section: Natural History Of Hp-related Chronic Gastritis and Gc Risksupporting

confidence: 80%

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

Enomoto¹,

Watanabe²,

Mukoubayashi³

et al. 2011

Gastritis and Gastric Cancer - New Insights in Gastroprotection, Diagnosis and Treatments

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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. In this section, we discuss the emerging significance of serum PG as a GC risk marker for more precise identification of GC high-risk groups. Serum PG testHP-related chronic gastritis usually starts in the antrum and expands proximally towards the body of the stomach (Kimura, 1972;Tatsuta et al., 1973). As several studies dealing with endoscopic biopsies or chromoendoscopic testing have found that progression of chronic atrophic gastritis (CAG) increases the risk of cancer (Meister et al., 1979;Sipponen et al., 1985;Siurala et al., 1966;Tatsuta et al., 1993;Testoni et al., 1987), accurate and reliable evaluation of the extent of CAG is considered important for identifying individuals at high risk of cancer. 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. Furthermore, histological diagnosis of gastric atrophy depends on subjective judgment without a gold standard (Guarner et al., 1999;Plummer et al., 1997). A test for CAG progression that is more convenient, free of discomfort or risk, economical and based on objective parameters is needed. PG is the inactive precursor of pepsin, a digestive enzyme specifically produced in the stomach. Immunologically, two isozymes exist (Kageyama, 2003). PGI is produced by chief cells and mucus neck cells of the gastric fundic glands. In contrast, PGII is produced not only by chief cells and mucus neck cells, but also in cardiac glands, pyloric glands, and Brunner's glands, with localization of producing cells in a wide range from the stomach to the duodenum. The majority of PG produced (about 99%) is secreted in the stomach lumen and functions as a digestive enzyme. However, a small amount of PG (about 1%) is also present in blood and can be evaluated by measuring serum PG levels. Serum PG levels are generally agreed to reflect the morphological and functional status of the stomach mucosa (Hirschowitz, 1957;Samloff et al., 1982). In an endoscopic study with Congo red staining, we have shown a strong correlation between an increase in glandular boundary, associated with diagnosed progression of gastric mucosal atrophy, and stepwise reductions in serum PGI levels and the PGI/PGII ratio ( Fig. 1) (Miki et al., 1987). In other words, by measuring serum PGI and the PGI/II ratio, the progression of CAG, which is involved in GC carcinogenesis, can be objectively evaluated (Ichinose et al., 2001). In addition, during HP infection, serum PGI and PGII increase, and the PG I/II ratio decreases. These findings are improved after eradication treatment (Furuta et al., 1997) and are useful as gastric mucosal inflammatory markers. Several criteria are used in the serum PG test. As criteria for GC screening, the combination of PGI ≤70 ng/ml and PGI/II ratio ≤3.0...

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“…3). Similar results were reported by Watabe et al (Watabe et al, 2005). During the 10-year follow-up study, all patients who developed GC were HP infection-positive.…”

Section: Natural History Of Hp-related Chronic Gastritis and Gc Risksupporting

confidence: 80%

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

Enomoto¹,

Watanabe²,

Mukoubayashi³

et al. 2011

Gastritis and Gastric Cancer - New Insights in Gastroprotection, Diagnosis and Treatments

View full text Add to dashboard Cite

show abstract

“…The direction of its influence, if it existed, would have been toward the null. Measurement of serum pepsinogen I and II levels would have been helpful in terms of identifying participants with premalignant lesions and preventing the misclassification (Watabe et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

CagA-producing Helicobacter pylori and increased risk of gastric cancer: a nested case–control study in Korea

et al. 2006

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“…Decrease in PgI, the ratio of PgI/PII and G17 may reflect the presence of abnormalities in gastric mucosa including atrophic gastritis and GC (Watabe et al, 2005;Oishi et al, 2006;Yanaoka et al, 2008;Kikuchi et al, 2011). Therefore, it is proposed that a combination of Pg and G17 may be helpful for diagnosis of atrophic gastritis and GC and consequently may be considered to develop a GC screening program (Shiotani et al, 2005;Rollan et al, 2006;Cao et al, 2007).…”

Section: Gastrin-17 For Screening Gastritis and Gastric Cancer In A Hmentioning

confidence: 99%

Diagnostic Values of Serum Levels of Pepsinogens and Gastrin-17 for Screening Gastritis and Gastric Cancer in a High Risk Area in Northern Iran

Nejadi-Kelarijani

Roshandel²,

Semnani³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Background: Gastric cancer (GC) is the second cause of cancer related death in the world. It may develop by progression from its precancerous condition, called gastric atrophy (GA) due to gastritis. The aim of this study was to evaluate the accuracy of serum levels of pepsinogens (Pg) and gastrin-17 (G17) as non-invasive methods to discriminate GA or GC (GA/GC) patients. Materials and Methods: Subjects referred to gastrointestinal clinics of Golestan province of Iran during 2010 and 2011 were invited to participate. Serum levels of PgI, PgII and G17 were measured using a GastroPanel kit. Based on the pathological examination of endoscopic biopsy samples, subjects were classified into four groups: normal, non-atrophic gastritis, GA, and GC. Receiver operating curve (ROC) analysis was used to determine cut-off values. Indices of validity were calculated for serum markers. Results: Study groups were normal individuals (n=74), non-atrophic gastritis (n=90), GA (n=31) and GC patients (n=30). The best cut-off points for PgI, PgI/II ratio, G17 and HP were 80 μg/L, 10, 6 pmol/L, and 20 EIU, respectively. PgI could differentiate GA/GC with high accuracy (AUC=0.83; 95%CI: 0.76-0.89). The accuracy of a combination of PgI and PgI/II ratio for detecting GA/GC was also relatively high (AUC=0.78; 95%CI: 0.70-0.86). Conclusions: Our findings suggested PgI alone as well as a combination of PgI and PgI/II ratio are valid markers to differentiate GA/GC. Therefore, Pgs may be considered in conducting GC screening programs in high-risk areas.

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Predicting the development of gastric cancer from combining Helicobacter pylori antibodies and serum pepsinogen status: a prospective endoscopic cohort study

Cited by 361 publications

References 30 publications

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

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

CagA-producing Helicobacter pylori and increased risk of gastric cancer: a nested case–control study in Korea

Diagnostic Values of Serum Levels of Pepsinogens and Gastrin-17 for Screening Gastritis and Gastric Cancer in a High Risk Area in Northern Iran

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