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视网膜脱离患者玻璃体液和视网膜下液中的凝血酶生成

Thrombin Generation in Vitreous and Subretinal Fluid of Patients with Retinal Detachment.

作者信息

Mulder Verena C, Bastiaans Jeroen, van Leuven Cornelis J M, van Meurs Jan C, Kluft Cornelis

机构信息

Rotterdam Ophthalmic Institute, Rotterdam Eye Hospital, Rotterdam, the Netherlands.

Department of Immunology, Erasmus Medical Centre, Rotterdam, the Netherlands.

出版信息

Ophthalmologica. 2018;240(1):23-28. doi: 10.1159/000487757. Epub 2018 Apr 4.

DOI:10.1159/000487757
PMID:29617690
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6050638/
Abstract

PURPOSE

To measure prothrombin fragments (F1+2) and thrombin-antithrombin complex (TAT) in vitreous and subretinal fluid (SRF) of rhegmatogenous retinal detachment (RRD) patients and to validate and further specify our earlier finding of increased thrombin activity in patients with proliferative vitreoretinopathy (PVR).

METHODS

F1+2 and TAT were measured in 31 vitreous and 16 SRF samples using the Enzygnost® immunoassays.

RESULTS

We found significant levels of F1+2 and TAT in the vitreous of all patients with RRD compared to patients with macular hole or macular pucker. However, there was no significant difference between patients who would develop PVR in the future, had established PVR, and patients with uncomplicated RRD both in vitreous concentrations of F1+2 (Kruskal-Wallis p = 0.963) and TAT (p = 0.516).

CONCLUSION

The analysis of F1+2 and TAT confirmed significant thrombin generation in both vitreous and SRF of patients with RRD. An imbalance between the thrombin regulation mechanisms TAT and α2-macroglobulin possibly explains the difference from our previous findings.

摘要

目的

检测孔源性视网膜脱离(RRD)患者玻璃体液和视网膜下液(SRF)中的凝血酶原片段(F1+2)和凝血酶-抗凝血酶复合物(TAT),并验证和进一步明确我们之前关于增生性玻璃体视网膜病变(PVR)患者凝血酶活性增加的发现。

方法

使用Enzygnost®免疫分析法检测31份玻璃体液样本和16份视网膜下液样本中的F1+2和TAT。

结果

与黄斑裂孔或黄斑皱襞患者相比,我们发现所有RRD患者玻璃体液中F1+2和TAT水平均显著升高。然而,未来会发生PVR的患者、已确诊PVR的患者以及无并发症RRD患者的玻璃体液中F1+2浓度(Kruskal-Wallis检验p = 0.963)和TAT浓度(p = 0.516)之间均无显著差异。

结论

F1+2和TAT分析证实RRD患者的玻璃体液和视网膜下液中均有显著的凝血酶生成。凝血酶调节机制TAT和α2-巨球蛋白之间的失衡可能解释了与我们之前研究结果的差异之处。

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本文引用的文献

1
Correlation between Interleukin-6 and Thrombin-Antithrombin III Complex Levels in Retinal Diseases.视网膜疾病中白细胞介素-6与凝血酶-抗凝血酶III复合物水平的相关性
Curr Eye Res. 2017 Sep;42(9):1269-1272. doi: 10.1080/02713683.2017.1313432. Epub 2017 Jun 20.
2
Vitreous and subretinal fluid concentrations of orally administered dabigatran in patients with rhegmatogenous retinal detachment.孔源性视网膜脱离患者口服达比加群后的玻璃体液和视网膜下液浓度
Acta Ophthalmol. 2016 Nov;94(7):663-667. doi: 10.1111/aos.13186. Epub 2016 Aug 6.
3
The role of thrombin in proliferative vitreoretinopathy.凝血酶在增生性玻璃体视网膜病变中的作用。
Invest Ophthalmol Vis Sci. 2014 Jul 11;55(7):4659-66. doi: 10.1167/iovs.14-14818.
4
Thrombin induces epithelial-mesenchymal transition and collagen production by retinal pigment epithelial cells via autocrine PDGF-receptor signaling.凝血酶通过自分泌 PDGF 受体信号诱导视网膜色素上皮细胞发生上皮-间充质转化和胶原产生。
Invest Ophthalmol Vis Sci. 2013 Dec 19;54(13):8306-14. doi: 10.1167/iovs.13-12383.
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α-2-Macroglobulin: a physiological guardian.α-2-巨球蛋白:一种生理性保护蛋白。
J Cell Physiol. 2013 Aug;228(8):1665-75. doi: 10.1002/jcp.24266.
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The paradoxical stimulation by a reversible thrombin inhibitor of thrombin generation in plasma measured with thrombinography is caused by alpha-macroglobulin-thrombin.用血栓描记术测定的血浆中可逆转的凝血酶抑制剂对凝血酶生成的矛盾性刺激是由α-巨球蛋白-凝血酶引起的。
J Thromb Haemost. 2010 Jun;8(6):1281-9. doi: 10.1111/j.1538-7836.2010.03822.x. Epub 2010 Feb 24.
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Estimating the rate of thrombin and fibrin generation in vivo during cardiopulmonary bypass.体外循环期间体内凝血酶和纤维蛋白生成速率的评估。
Blood. 2003 Jun 1;101(11):4355-62. doi: 10.1182/blood-2002-08-2400. Epub 2002 Dec 12.
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Dexamethasone concentration in the subretinal fluid after a subconjunctival injection, a peribulbar injection, or an oral dose.结膜下注射、球周注射或口服给药后视网膜下液中的地塞米松浓度。
Ophthalmology. 2000 Oct;107(10):1932-8. doi: 10.1016/s0161-6420(00)00344-4.
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Activated alpha 2-macroglobulin and transforming growth factor-beta 1 induce a synergistic smooth muscle cell proliferative response.活化的α2-巨球蛋白和转化生长因子-β1诱导协同的平滑肌细胞增殖反应。
J Biol Chem. 1993 Aug 25;268(24):18340-4.
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