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色素性青光眼

Pigment Dispersion Glaucoma

作者信息

Zeppieri Marco, Tripathy Koushik

机构信息

University Hospital of Udine, Italy

ASG Eye Hospital, BT Road, Kolkata, India

Abstract

Glaucoma is an ocular disease characterized by ocular hypertension that leads to optic neuropathy and visual field loss. Aqueous humor is secreted in the posterior chamber (PC) by the ciliary body, then moves into the anterior chamber (AC) through the pupil. The aqueous is then drained from the trabecular meshwork (TM) located at the angle between the cornea and iris. Glaucoma due to blockage of aqueous outflow from the TM by the iris or angle is defined as closed-angle glaucoma. When gonioscopy shows no evidence of angle closure, the optic neuropathy related to elevated intraocular pressure (IOP) is defined as open-angle glaucoma. Pigment dispersion glaucoma or pigmentary glaucoma (PG) is considered secondary open-angle glaucoma. PG and pigment dispersion syndrome (PDS) have similar clinical characteristics, representing a disease spectrum. PDS can convert into PG when there is the presence of elevated intraocular pressure (IOP) with visual field defects and glaucomatous optic neuropathy. Friedrich E. Krukenberg described Krukenberg spindle in 1899. An interesting triad of symptoms for PG was first reported by Sugar et al. in 1949, defined by corneal endothelial pigment depositions on the posterior side of the cornea, mid-peripheral radial iris transillumination defects, and heavy pigmentation in the TM. Campbell reported that pigment dispersion and accumulation in PG could be caused by pigment loss (melanin granules) from constant friction and rubbing between the posterior iris pigment epithelium and the lens zonules during physiological pupil movement, which may be facilitated by the posterior bowing of the iris and reverse pupillary block that tends to be more prevalent in myopic eyes with a large iris. The pigment deposited in the AC contributes to chronic damage and death of TM cells over time, limiting the proper function and efficiency. Elevated IOP in PG results from aqueous buildup and reduction of TM aqueous humor outflow, leading to visual field loss associated with chronic optic neuropathy. The disease, which is typically bilateral, is prevalent in males with myopia and is typically diagnosed between 30 to 50 years.

摘要

青光眼是一种以眼压升高为特征的眼部疾病,可导致视神经病变和视野缺损。房水由睫状体在后房分泌,然后通过瞳孔进入前房。接着,房水从位于角膜和虹膜夹角处的小梁网排出。因虹膜或房角阻塞小梁网房水流出而导致的青光眼被定义为闭角型青光眼。当房角镜检查未显示房角关闭的迹象时,与眼压升高相关的视神经病变被定义为开角型青光眼。色素性青光眼或色素播散性青光眼(PG)被认为是继发性开角型青光眼。PG和色素播散综合征(PDS)具有相似的临床特征,代表了一种疾病谱。当存在眼压升高伴视野缺损和青光眼性视神经病变时,PDS可转变为PG。弗里德里希·E·克鲁肯伯格在1899年描述了克鲁肯伯格纺锤体。1949年,休格等人首次报告了PG的一组有趣的三联征症状,其定义为角膜后表面的角膜内皮色素沉着、中周部放射状虹膜透照缺损以及小梁网重度色素沉着。坎贝尔报告称,PG中的色素播散和积聚可能是由于生理瞳孔运动期间后虹膜色素上皮与晶状体小带之间持续摩擦和摩擦导致色素丢失(黑色素颗粒)引起的,虹膜后凸和反向瞳孔阻滞可能会促进这种情况,而这种情况在虹膜较大的近视眼中更为普遍。前房内沉积的色素随着时间的推移会导致小梁网细胞的慢性损伤和死亡,限制其正常功能和效率。PG中的眼压升高是由于房水积聚和小梁网房水流出减少导致的,从而导致与慢性视神经病变相关的视野缺损。这种疾病通常是双侧性的,在患有近视的男性中较为普遍,通常在30至50岁之间被诊断出来。

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