Luo Hua-Nan, Yang Qi-Mei, Sheng Ying, Wang Zheng-Hui, Zhang Qing, Yan Jing, Hou Jin, Zhu Kang, Cheng Ying, Wang Bo-Tao, Xu Ying-Long, Zhang Xiang-Hong, Ren Xiao-Yong, Xu Min
Department of Otolaryngology-Head and Neck Surgery, The Second Hospital, Xi'an Jiao Tong University, Xi'an.
Laryngoscope. 2014 Jul;124(7):E294-300. doi: 10.1002/lary.24538. Epub 2014 Jan 15.
OBJECTIVES/HYPOTHESIS: To analyze the relationship between laryngopharyngeal reflux (LPR) represented by pepsin and pepsinogen, and pathogenesis of otitis media with effusion (OME).
Prospective case-control study.
Children with OME who required adenoidectomy and tympanostomy/tympanostomy tubes placement were enrolled in OME group, whereas children with adenoid hypertrophy (AH) who required adenoidectomy and individuals who required cochlear implantation (CI) were enrolled in AH and CI groups, respectively. Pepsinogen mRNA and protein levels were assessed by real-time fluorescence-based quantitative polymerase chain reaction and immunohistochemistry in adenoid specimens from the OME and AH groups. Pepsin and pepsinogen concentrations were evaluated by enzyme-linked immunosorbent assay in middle ear fluid and plasma from the OME and CI groups.
The levels of pepsinogen protein expressed in cytoplasm of epithelial cells and clearance under epithelial cells in adenoid specimens from the OME group were significantly higher than those in the AH group. Furthermore, the concentrations of pepsin and pepsinogen in the OME group were 51.93±11.58 ng/mL and 728±342.6 ng/mL, respectively, which were significantly higher than those in the CI group (P<.001). In addition, the concentrations of pepsin in dry ears were significantly lower than those in serous and mucus ears in the OME group (F=22.77, P<.001).Finally, the concentration of pepsinogen in middle ear effusion was positively correlated with the expression intensity of pepsinogen protein in cytoplasm of epithelial cells (r=0.73, P<.05) in the OME group.
Pepsin and pepsinogen in middle ear effusion are probably caused by LPR and may be involved in the pathogenesis of OME.
3b.
目的/假设：分析以胃蛋白酶和胃蛋白酶原表示的喉咽反流（LPR）与分泌性中耳炎（OME）发病机制之间的关系。
前瞻性病例对照研究。
需要行腺样体切除术和鼓膜切开术/鼓膜置管术的OME患儿纳入OME组，而需要行腺样体切除术的腺样体肥大（AH）患儿和需要行人工耳蜗植入术（CI）的个体分别纳入AH组和CI组。通过实时荧光定量聚合酶链反应和免疫组织化学法评估OME组和AH组腺样体标本中胃蛋白酶原mRNA和蛋白水平。通过酶联免疫吸附测定法评估OME组和CI组中耳积液和血浆中胃蛋白酶和胃蛋白酶原浓度。
OME组腺样体标本中上皮细胞胞质中表达的胃蛋白酶原蛋白水平及上皮细胞下清除率显著高于AH组。此外，OME组胃蛋白酶和胃蛋白酶原浓度分别为51.93±11.58 ng/mL和728±342.6 ng/mL，显著高于CI组（P<0.001）。另外，OME组干耳中胃蛋白酶浓度显著低于浆液性和黏液性耳（F=22.77，P<0.001）。最后，OME组中耳积液中胃蛋白酶原浓度与上皮细胞胞质中胃蛋白酶原蛋白表达强度呈正相关（r=0.73，P<0.05）。
中耳积液中的胃蛋白酶和胃蛋白酶原可能由LPR引起，并可能参与OME的发病机制。
3b。
