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酒石酸溴莫尼定对青光眼患者嗜碱性粒细胞活化的影响。

Effect of brimonidine tartrate on basophil activation in glaucoma patients.

作者信息

Rosenfeld Eldar, Barequet Dana, Rabina Gilad, Langier Sheila, Lazar Moshe, Shemesh Gabi, Kurtz Shimon, Kivity Shmuel

机构信息

Division of Ophthalmology, Sourasky Medical Center, Sackler School of Medicine, Tel Aviv University, Tel Aviv 6423906, Israel.

Department of Allergy and Immunology, Sourasky Medical Center, Sackler School of Medicine, Tel Aviv University, Tel Aviv 6423906, Israel.

出版信息

Int J Ophthalmol. 2020 Mar 18;13(3):509-512. doi: 10.18240/ijo.2020.03.21. eCollection 2020.

Abstract

AIM

To evaluate the mechanism of which brimonidine tartrate 0.15% causes clinical hypersensitivity.

METHODS

A prospective case-control study comparing 8 glaucoma patients with clinical hypersensitivity to brimonidine to a control group consisting 13 healthy volunteers. Blood samples were stimulated with brimonidine 0.15%, timolol 0.5% or brimonidine tartrate/timolol maleate 0.2%/0.5%. Premixed antibodies (CD63/FITC and aIgE/PE) were added for direct staining and whole-blood samples were lysed, fixed and analyzed by a flow cytometer. The basophil population was defined by high IgE cell expression. Degranulation was identified by the expression of the activation molecule CD63.

RESULTS

Basophil activation was not significant when comparing percent of activated basophils of patients and healthy controls after exposure to brimonidine (2.58%, 2.45%, respectively, =0.72). There was a significant suppression of basophil activation when a combination of brimonidine-timolol (0.87%) was compared to timolol (2.27%; =0.012) and to brimonidine alone (2.58%; =0.017).

CONCLUSION

The results of our study do not support the hypothesis that brimonidine induces an immediate allergic reaction. Basophil activation was suppressed by the presence of β-blockers in patients hypersensitive to brimonidine and in healthy individuals. This finding indicates that timolol suppress brimonidine drug reaction by a different mechanism.

摘要

目的

评估0.15%酒石酸溴莫尼定引起临床超敏反应的机制。

方法

一项前瞻性病例对照研究,将8例对酒石酸溴莫尼定有临床超敏反应的青光眼患者与由13名健康志愿者组成的对照组进行比较。用0.15%酒石酸溴莫尼定、0.5%噻吗洛尔或0.2%/0.5%酒石酸溴莫尼定/马来酸噻吗洛尔刺激血样。加入预混抗体(CD63/异硫氰酸荧光素和抗免疫球蛋白E/藻红蛋白)进行直接染色,全血样本经裂解、固定后用流式细胞仪分析。通过高免疫球蛋白E细胞表达定义嗜碱性粒细胞群体,并通过激活分子CD63表达鉴定脱颗粒情况。

结果

比较患者和健康对照者接触酒石酸溴莫尼定后活化嗜碱性粒细胞百分比,嗜碱性粒细胞活化不显著(分别为2.58%和2.45%,P=0.72)。与噻吗洛尔(2.27%;P=0.012)和单独使用酒石酸溴莫尼定(2.58%;P=0.017)相比,酒石酸溴莫尼定与噻吗洛尔联合使用时(0.87%)嗜碱性粒细胞活化有显著抑制作用。

结论

我们研究结果不支持酒石酸溴莫尼定诱导速发型过敏反应这一假说。在对酒石酸溴莫尼定过敏的患者和健康个体中β受体阻滞剂抑制了嗜碱性粒细胞活化。这一发现表明噻吗洛尔通过不同机制抑制酒石酸溴莫尼定药物反应。

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Pilot study on basophil activation induced by contrast medium.造影剂诱导嗜碱性粒细胞活化的初步研究。
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