Abstract
BackgroundThe clinical endoscopic phenotypes of gastroesophageal reflux disease (GERD) are classified as Barrett's esophagus (BE), erosive esophagitis (EE) and non-erosive gastroesophageal reflux disease (NERD). NERD is subclassified as abnormal acid exposure (AAE) and normal acid exposure (NAE) based on pH monitoring study results. The aim of this study was to characterize genes involved in the pathophysiology and immune response of GERD.MethodsThis is an observational and cross-sectional study. All patients with BE, EE, AAE, and NAE and a control group were subjected to superior endoscopy (with biopsies of esophageal mucosa). Relative mRNA quantification of cytokine and target genes was conducted by quantitative Polymerase Chain Reaction (RT-qPCR). Changes in the expression of genes associated with inflammation were assessed for each disease phenotype. Statistical analysis of differential gene expression was performed using the Mann–Whitney U non-parametric test. A p value < 0.05 was considered significant.ResultsA total of 82 patients were included and were divided into the following groups: Group BE, 16 (19.51%); Group EE, 23 (28.04%); Group AAE, 13 (15.86%); NAE 13 (15.86%); and Control Group, 17 (20.73%). Compared with the control group, patients with BE exhibited increased IL-8 expression (p < 0.05) and increased levels of IL-10, MMP-3, and MMP-9. Patients with EE exhibited increased levels of IL-1B, IL-6 and IL-10 (p < 0.05), and patients with AAE exhibited increased expression of IL-1B, IL-6, IFN-γ and TNF-α (p < 0.05). AAE exhibited increased IL-1B and TNF-α expression compared with NAE (p < 0.05).ConclusionThis study demonstrates the differential expression of mediators of inflammation in the esophageal mucosa of patients with different GERD endoscopic phenotypes. IL-1B and TNF-α could be useful to differentially diagnose AAE and NAE in the non-erosive phenotype using endoscopic biopsies.
Highlights
The clinical endoscopic phenotypes of gastroesophageal reflux disease (GERD) are classified as Barrett’s esophagus (BE), erosive esophagitis (EE) and non-erosive gastroesophageal reflux disease (NERD)
This study proposed initial insights into the genetic background of GERD, which was further supported by genome wide association study (GWAS) analyses that showed that GERD, Barrett’s esophagus and esophageal adenocarcinoma exhibit substantial overlap in terms of genetic etiology
Patients were divided into the following groups: Group BE, 16 (19.51%); Group EE, 23 (28.04%); Group abnormal acid exposure (AAE), 13 (15.86%); normal acid exposure (NAE), 13 (15.86%); and Control Group, 17 (20.73%)
Summary
The clinical endoscopic phenotypes of gastroesophageal reflux disease (GERD) are classified as Barrett’s esophagus (BE), erosive esophagitis (EE) and non-erosive gastroesophageal reflux disease (NERD). NERD is subclassi‐ fied as abnormal acid exposure (AAE) and normal acid exposure (NAE) based on pH monitoring study results. The pathophysiology of GERD is complex, involving mechanical factors, such as the presence of hiatal hernia and transient relaxations of the lower esophageal sphincter [1]. Patients are classified into the following clinical categories based on their clinical endoscopic phenotype: Barrett’s esophagus (BE), erosive esophagitis (EE) and non-erosive gastroesophageal reflux disease (NERD). The NERD group is divided into abnormal acid exposure (AAE) and normal acid exposure (NAE) according to the esophageal exposure time at pH < 4 based on pH monitoring studies
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