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血浆肿瘤坏死因子α水平升高与原发性开角型青光眼的关联。

Association of increased levels of plasma tumor necrosis factor alpha with primary open-angle glaucoma.

作者信息

Kondkar Altaf A, Sultan Tahira, Almobarak Faisal A, Kalantan Hatem, Al-Obeidan Saleh A, Abu-Amero Khaled K

机构信息

Glaucoma Research Chair, Department of Ophthalmology, College of Medicine, King Saud University, Riyadh, Saudi Arabia.

出版信息

Clin Ophthalmol. 2018 Apr 12;12:701-706. doi: 10.2147/OPTH.S162999. eCollection 2018.

Abstract

PURPOSE

Retinal ganglion cell (RGC) death is a key feature of glaucoma. Elevated levels of tumor necrosis factor alpha (TNF-α), a pro-inflammatory cytokine, can induce RGC apoptosis and play a critical role in glaucomatous neurodegeneration. Based on the possible role of inflammation and oxidative stress in the pathogenesis of primary open-angle glaucoma (POAG), we investigated the association between plasma levels of TNF-α and POAG or its clinical indices in comparison to non-glaucomatous controls.

PATIENTS AND METHODS

In a case-control retrospective cohort of 51 POAG cases and 88 controls, plasma TNF-α levels were measured using an enzyme-linked immunosorbent assay (ELISA). The assay was performed in duplicates on an automated ELISA analyzer.

RESULTS

Mean TNF-α level was significantly elevated in POAG cases (1.88 ± 2.17 pg/mL) than the controls (0.93 ± 1.49 pg/mL; = 0.003). The overall dose-response trend was significant ( = 6.12, df = 2; = 0.047). No statistical difference was seen in age, gender and systemic disease distribution. A modest negative and significant correlation was seen between TNF-α level and number of antiglaucoma medications, an important clinical index of POAG severity. Moreover, logistic regression analysis showed that the risk of POAG was most significantly affected by TNF-α level and not by age and sex.

CONCLUSION

High systemic level of an inflammatory cytokine, TNF-α, is associated with POAG; however, its possible use as a biomarker for early glaucoma diagnosis and/or disease severity needs further investigation.

摘要

目的

视网膜神经节细胞(RGC)死亡是青光眼的关键特征。促炎细胞因子肿瘤坏死因子α(TNF-α)水平升高可诱导RGC凋亡,并在青光眼性神经退行性变中起关键作用。基于炎症和氧化应激在原发性开角型青光眼(POAG)发病机制中的可能作用,我们研究了与非青光眼对照组相比,血浆TNF-α水平与POAG及其临床指标之间的关联。

患者和方法

在一项包含51例POAG病例和88例对照的病例对照回顾性队列研究中,使用酶联免疫吸附测定(ELISA)法测量血浆TNF-α水平。该测定在自动ELISA分析仪上重复进行两次。

结果

POAG病例的平均TNF-α水平(1.88±2.17 pg/mL)显著高于对照组(0.93±1.49 pg/mL;P = 0.003)。总体剂量反应趋势具有显著性(P = 6.12,自由度= 2;P = 0.047)。在年龄、性别和全身疾病分布方面未观察到统计学差异。TNF-α水平与抗青光眼药物数量之间存在适度的负相关且具有显著性,抗青光眼药物数量是POAG严重程度的一项重要临床指标。此外,逻辑回归分析表明,POAG风险受TNF-α水平影响最为显著,而不受年龄和性别的影响。

结论

炎症细胞因子TNF-α的全身高水平与POAG相关;然而,其作为青光眼早期诊断和/或疾病严重程度生物标志物的潜在用途需要进一步研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d6a/5905466/d20702d3d9f9/opth-12-701Fig1.jpg

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