Abstract
ObjectiveThe aim of this study was to integrate the serum exosomal miRNA miR-122-5p with canonical serological biomarkers for the non-invasive screening of chronic atrophic gastritis (CAG) patients.MethodsmiR-122-5p and U6 were amplified by the quantitative reverse transcription polymerase chain reaction (RT-qPCR), gastrin (GAS), pepsinogen I (PG-I), and PG-II and were measured by ELISA. The area under the receiver operating characteristic (ROC) curves and their correlation were analyzed.ResultsIn the present study, GAS level and PG-I/PG-II ratio (PGR) were increased in CAG group, but there was no significant difference in PG-I or PG-II levels between CAG group and chronic non-atrophic gastritis (CNAG) group. Only GAS level and PG-I/PG-II ratio were significantly correlated with atrophy, and not any other clinicopathologic factors. Expression of hsa-miR-122-5p positively correlated with GAS level, PG-I level, and PGR, while it negatively correlated with PG-II level; however, none of them had significant difference. The combination of GAS, PGR, and hsa-miR-122-5p presented as a better model for non-invasive screening of CAG compared to others.ConclusionThese results suggested that serum exosomal hsa-miR-122-5p combined with GAS and PGR would elevate accuracy and specificity in non-invasive screening of CAG.
Highlights
Chronic atrophic gastritis (CAG) is a precancerous, wildspread gastrointestinal disease
Our results showed that serum GAS level was significantly upregulated in CAG group and significantly correlated to the clinicopathologic factor of CAG, but not serum pepsinogen I (PG-I) or pepsinogen II (PG-II) level
There was a significant difference in serum PG-II ratio (PGR) between chronic non-atrophic gastritis (CNAG) group and CAG group
Summary
Chronic atrophic gastritis (CAG) is a precancerous, wildspread gastrointestinal disease. The prevalence of CAG is 10% in 20–50 years old population, and more than 50% in 51–65 years old population [1]. The diagnosis and staging of CAG mainly depended on the presence of chronic inflammatory cells established by endoscopic and histological examination, including lymphocytes and plasma cells that expanded in lamina propria, and the disappearance of the normal glands [3,4,5]. Diagnostic methods of CAG are usually invasive, which are hardly accepted by the patients [2]. Accumulating serological biomarkers were highlighted in CAG diagnosis. It is reported that gastrin (GAS), pepsinogen I (PG-I), or pepsinogen II (PG-II) might be helpful for non-invasive diagnosis of atrophic gastritis [2,6]. Previous study showed that the sensitivity and specificity of a panel test (G-17, PG, and anti-Helicobacter pylori) was 74.7 and 95.6%, respectively [7]
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