Ma Yao, Liu Jia, Liang Zhiqiao, Yang Kangyi, Lv Kun, Liu Wenbo, Wu Huijuan
Department of Ophthalmology, Peking University People's Hospital, No.11 Xizhimen South Street, Xicheng District, Beijing, 100044, China.
Ophthalmol Ther. 2025 Aug;14(8):1985-1997. doi: 10.1007/s40123-025-01176-1. Epub 2025 Jul 3.
The mechanism of primary angle closure disease (PACD) has been extensively investigated, while some cases remain unexplained. Hypothesizing that chronic primary ciliary block (CB) may play a role in PACD pathogenesis and the contribution could be revealed by pharmacologic cycloplegia and mydriasis, this study analyzed changes in anterior segment biometric parameters following cycloplegic intervention.
A total of 170 eyes of 170 Chinese subjects aged between 50 and 80 years were included: 90 in the primary angle closure suspect (PACS) group, 33 in the primary angle closure (PAC)/PAC glaucoma (PACG) group, and 47 in the normal control group. All participants underwent a comprehensive ophthalmic examination, and ultrasound biomicroscopy (UBM) was conducted in patients with PACD at the baseline. Compound tropicamide (Mydrin P, Santen, Osaka, Japan) was administered to patients for pupillary dilation. Intraocular pressure (IOP) measurement and IOLMaster were performed before and 45 min after mydriasis.
Following dilation, PACS and PAC/PACG eyes demonstrated less significant changes in the anterior section compared to normal eyes based on △ACD-△LT (the difference in the changes of anterior chamber depth and lens thickness) (P < 0.01). Nine PACD eyes had a △ACD-△LT greater than 0.10 mm (1 PAC/PACG and 8 PACS eyes). About 8.94% of PACD eyes exhibited an elevated post-IOP. In PACS eyes, significantly higher pre-IOP (P < 0.05), shallower anterior chamber (AC, P < 0.01), more anterior lens position (P < 0.01), and narrower anterior chamber width (ACW, P < 0.05) were observed.
A minority of PACD eyes displayed obvious movement of the ciliary-lens diaphragm, suggesting that primary CB may be an infrequent occurrence in PACD eyes. Additionally, higher IOP, shallower AC, more anteriorly placed lens, and smaller ACW may facilitate the identification of IOP spikes following dilation in clinical practice.
原发性闭角型青光眼(PACD)的发病机制已得到广泛研究,但仍有一些病例无法解释。假设慢性原发性睫状肌阻滞(CB)可能在PACD发病机制中起作用,且这种作用可通过药物性睫状肌麻痹和散瞳来揭示,本研究分析了睫状肌麻痹干预后眼前节生物测量参数的变化。
纳入170例年龄在50至80岁之间的中国受试者的170只眼睛:原发性闭角型青光眼可疑者(PACS)组90只眼,原发性闭角型青光眼(PAC)/原发性闭角型青光眼合并青光眼(PACG)组33只眼,正常对照组47只眼。所有参与者均接受了全面的眼科检查,PACD患者在基线时进行了超声生物显微镜检查(UBM)。给患者使用复方托吡卡胺(美多丽P,参天制药,日本大阪)散瞳。在散瞳前和散瞳后45分钟测量眼压(IOP)并进行IOLMaster检查。
散瞳后,基于△ACD-△LT(前房深度和晶状体厚度变化的差值),PACS和PAC/PACG组的眼前节变化与正常眼相比不太明显(P < 0.01)。9只PACD眼的△ACD-△LT大于0.10 mm(1只PAC/PACG眼和8只PACS眼)。约8.94%的PACD眼散瞳后眼压升高。在PACS眼中,观察到散瞳前眼压显著更高(P < 0.05)、前房更浅(AC,P < 0.01)、晶状体位置更靠前(P < 0.01)以及前房宽度更窄(ACW,P < 0.05)。
少数PACD眼显示睫状肌-晶状体隔膜有明显移动,提示原发性CB在PACD眼中可能不常见。此外,较高的眼压、较浅的前房、更靠前的晶状体位置和较小的ACW可能有助于在临床实践中识别散瞳后的眼压峰值。