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作 者:于洋[1] 蒋沁[1] 曹国凡[1] Yang Yu;Qin Jiang;Guo-Fan Cao(Nanjing Medical University Eye Hospital,Nanjing 210029,Jiangsu Province,China)
机构地区:[1]南京医科大学附属眼科医院,中国江苏省南京市210029
出 处:《国际眼科杂志》2021年第3期497-499,共3页International Eye Science
基 金:国家自然科学基金项目(No.81870679)。
摘 要:目的:检测原发性开角型青光眼(POAG)患者房水中IL-37和IL-6的含量,并分析IL-6和IL-37含量与眼压或视野平均缺损的相关性。方法:采用前瞻性病例对照研究,利用酶联免疫吸附试验(ELISA)对2019-06/2020-01在南京医科大学附属眼科医院连续就诊的25例POAG患者和25例年龄相关性白内障(ARC)患者房水中IL-37和IL-6含量进行检测。同时测定POAG组患者眼压、视野平均缺损。结果:房水中IL-37和IL-6含量POAG组患者为25.80±2.87、43.87±7.75pg/mL,ARC组患者为23.75±3.88、36.53±7.60pg/mL,两组间IL-37和IL-6含量比较均有差异(P<0.05)。IL-6与眼压正相关(r=0.5817,P<0.05),IL-37与视野缺损正相关(r=0.4520,P<0.05)。结论:POAG患者房水中IL-37、IL-6含量均显著高于ARC组。IL-37和IL-6介导的免疫炎症反应可能参与了POAG的发病机制。AIM:To test concentrations of IL-37 and IL-6 in aqueous humor samples of patients with primary open angle glaucoma(POAG),and analyze the potential relationship to intraocular pressure(IOP)and mean defect of visual field.METHODS:Prospective consecutive non-randomized comparative cohort study was conducted.Totally 25 POAG patients and 25 age related cataract(ARC)patients in Nanjing Medical University Eye Hospital from June,2019 to January,2020 were collected.The levels of IL-37 and IL-6 in the aqueous humor were detected by enzyme-linked immunosorbent assay(ELISA).The IOP and mean defect of visual field of patients in the POAG group were also measured.RESULTS:The IL-37 concentrations in aqueous humor of POAG group and control group were 25.80±2.87pg/mL and 23.75±3.88pg/mL respectively(P<0.05).The IL-6 concentrations in aqueous humor of POAG group and control group were 43.87±7.75pg/mL and 36.53±7.60pg/mL respectively(P<0.05).In POAG group,the concentration of IL-37 was significantly positively correlated with mean defect of visual field(r=0.4520,P<0.05),the concentration of IL-6 was significantly positively correlated with IOP(r=0.5817,P<0.05).CONCLUSION:Significant differences in aqueous humor levels of IL-37 and IL-6 between glaucoma and control patients support the hypothesis that immune inflammation are involved in the pathogenesis of POAG.
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