Abstract
Serum pepsinogen assay (sPGA), which reveals serum pepsinogen (PG) I concentration and the PG I/PG II ratio, is a non-invasive test for predicting chronic atrophic gastritis (CAG) and gastric neoplasms. Although various cut-off values have been suggested, PG I ≤70 ng/mL and a PG I/PG II ratio of ≤3 have been proposed. However, previous meta-analyses reported insufficient systematic reviews and only pooled outcomes, which cannot determine the diagnostic validity of sPGA with a cut-off value of PG I ≤70 ng/mL and/or PG I/PG II ratio ≤3. We searched the core databases (MEDLINE, Cochrane Library, and Embase) from their inception to April 2018. Fourteen and 43 studies were identified and analyzed for the diagnostic performance in CAG and gastric neoplasms, respectively. Values for sensitivity, specificity, diagnostic odds ratio, and area under the curve with a cut-off value of PG I ≤70 ng/mL and PG I/PG II ratio ≤3 to diagnose CAG were 0.59, 0.89, 12, and 0.81, respectively and for diagnosis of gastric cancer (GC) these values were 0.59, 0.73, 4, and 0.7, respectively. Methodological quality and ethnicity of enrolled studies were found to be the reason for the heterogeneity in CAG diagnosis. Considering the high specificity, non-invasiveness, and easily interpretable characteristics, sPGA has potential for screening of CAG or GC.
Highlights
Gastric cancer (GC) is a global health-related burden and the fourth most common cause of cancer-related deaths worldwide [1]
The sequential cascade of histopathology for development of intestinal-type gastric adenocarcinoma is from normal gastric epithelium to chronic gastritis, chronic atrophic gastritis (CAG), and intestinal metaplasia (IM), followed by dysplasia, and GC [2]
Various cut-off values have been suggested, the combination of pepsinogen I (PG I) ≤70 ng/mL and PG I/PG II ratio ≤3 have been proposed for the prediction of CAG or GC [4,8]
Summary
Gastric cancer (GC) is a global health-related burden and the fourth most common cause of cancer-related deaths worldwide [1]. The sequential cascade of histopathology for development of intestinal-type gastric adenocarcinoma is from normal gastric epithelium to chronic gastritis, chronic atrophic gastritis (CAG), and intestinal metaplasia (IM), followed by dysplasia, and GC [2]. Patients with premalignant lesions, such as CAG or dysplasia, have a considerable risk for developing GC, and early detection of these lesions is important for the screening of GC [3,4]. The endoscopic screening program reduced GC-related mortality by 47% in a nested case-control study in Korea [6]. It is not cost-effective in regions with low incidence of GC, and stepwise or individualized screening according to the risk factors of GC has been recommended [4,5]
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