Evaluation of Salivary Pepsin Levels and Dental Erosion in Patients With Gastroesophageal Reflux Disease

格尔德 医学 胃蛋白酶 回流 唾液 胃肠病学 内科学 疾病 书呆子 反流(循环) 生物化学 酶 化学
作者
Yousif Shaban Rajab,Taghreed F. Zaidan
出处
期刊:Cureus [Cureus, Inc.]
卷期号:15 (2): e34744-e34744 被引量:9
标识
DOI:10.7759/cureus.34744
摘要

Background Gastroesophageal reflux disease (GERD) is a common gastrointestinal condition affecting many individuals worldwide. GERD is characterized by esophageal symptoms and may contribute to various extraesophageal symptoms, including dental erosion (DE). This study aimed to estimate the levels of pepsin in the saliva of GERD patients to evaluate and compare the activity of pepsin between the GERD and healthy groups and investigate the prevalence of DE in the GERD group. Methodology In this case-control study, 40 patients with GERD, diagnosed with an endoscope, and 35 healthy subjects were included. Patients and healthy individuals were subjected to the GERD questionnaire (GerdQ). A dental assessment was performed using the Basic Erosive Wear Examination (BEWE). A total score of the BEWE risk level was obtained by summing the scores obtained in each sextant (no risk = ≤2, low risk = 3-8, medium risk = 9-13, and high risk = >13). Five milliliters of unstimulated saliva were collected in a sterile tube. The salivary pepsin levels examined using the enzyme-linked immunosorbent assay were recorded for both groups. Results DE was significantly more frequent in GERD patients compared to healthy subjects. Overall, 32 (80%) GERD patients and 11 (31.4%) healthy individuals had DE risk. The mean salivary pepsin was 43.60 ± 10.61 ng/mL in the GERD group and 20.60 ± 9.27 ng/mL in the healthy group. A statistically significant difference was found in pepsin levels between the two groups (p < 0.001). Conclusions The study concluded that GERD patients had a higher prevalence of DE than healthy individuals. Our findings suggest that elevated salivary pepsin levels and their role as a factor responsible for DE need further evaluation to understand the mechanisms of pepsin-mediated damage leading to DE.
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