标题:Impaired gastric mucosal integrity identified by confocal endomicroscopy in Helicobacter pylori-negative functional dyspepsia
作者:Ji R.; Wang P.; Kou G.-J.; Zuo X.-L.; Wang X.; Li Y.-Q.
作者机构:[Ji, R] Department of Gastroenterology, Qilu Hospital, Shandong University, Jinan, China;[ Wang, P] Department of Gastroenterology, Qilu Hospital, Sha 更多
通讯作者:Li, YQ(liyanqing@sdu.edu.cn)
通讯作者地址:[Li, Y.-Q] Department of Gastroenterology, Qilu Hospital, Shandong UniversityChina;
来源:Neurogastroenterology and Motility
出版年:2020
卷:32
期:1
DOI:10.1111/nmo.13719
关键词:confocal endomicroscopy; functional dyspepsia; mast cell; permeability
摘要:Background: Low-grade inflammation may be involved in the pathogenesis of functional dyspepsia (FD). We hypothesis that altered gastric permeability is involved in the onset and persistence of this disorder. Therefore, our aim was to evaluate gastric mucosal integrity and mast cell numbers in patients with FD. Methods: We enrolled 58 patients with FD fulfilling the Rome III criteria (H Pylori negative), 20 inflammatory control subjects (H Pylori positive), and 20 healthy controls (H Pylori negative). Probe-based confocal endomicroscopy was performed using intravenous fluorescein to assess the paracellular fluorescein leakage and cell shedding. Mast cells were identified with quantitative immunohistochemistry on mucosal biopsies. Key Results: Endomicroscopic score of paracellular permeability was significantly higher in H pylori-negative FD patients compared with healthy controls (1.45 ± 1.27 vs 3.69 ± 3.18, P =.006). However, FD patients and healthy controls did not show differences in cell shedding score (0.75 ± 0.79 vs 1.29 ± 1.14, P =.069). Mast cell numbers were significantly increased compared with healthy control samples (18.91 ± 5.47 vs 14.1 ± 3.88, P <.001). The magnitude of increase in permeability was positively correlated with mast cell numbers of FD patients (rs =.6588, P <.0001), but not dyspepsia symptom scores. Conclusion and Inferences: Impaired gastric barrier function is present in FD patients. This might provide a new pathophysiological mechanism and therapeutical target in FD. © 2019 John Wiley & Sons Ltd
收录类别:SCOPUS
资源类型:期刊论文
原文链接:https://www.scopus.com/inward/record.uri?eid=2-s2.0-85073959532&doi=10.1111%2fnmo.13719&partnerID=40&md5=f7f485d99976ece2a3a19a09be8a475d
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