眼科 ›› 2026, Vol. 35 ›› Issue (1): 1-8.doi: 10.13281/j.cnki.issn.1004-4469.2026.01.001

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从眼内液体循环异常和腔室压力失衡的病理生理进程重新认识原发性闭角型青光眼

赵晗雪 余晓伟 范志刚 石砚   

  1. 首都医科大学附属北京同仁医院 北京同仁眼科中心 眼科学与视觉科学北京市重点实验室,北京 100730
  • 收稿日期:2025-10-27 出版日期:2026-01-25 发布日期:2026-01-13
  • 通讯作者: 石砚,Email: yansmile4433@163.com E-mail:yansmile4433@163.com
  • 基金资助:
    国家自然科学基金(82471072)

Reconsidering primary angle-closure glaucoma from the pathophysiological perspective of abnormal intraocular fluid circulation and imbalance of chamber pressure

Zhao Hanxue, Yu Xiaowei, Fan Zhigang, Shi Yan   

  1. Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University; Beijing Key Laboratory of Ophthalmology and Visual Sciences, Beijing 100730, China
  • Received:2025-10-27 Online:2026-01-25 Published:2026-01-13
  • Contact: Shi Yan, Email: yansmile4433@163.com E-mail:yansmile4433@163.com
  • Supported by:
    National Nature Science Fundation of China (82471072)

摘要: 原发性闭角型青光眼(primary angle-closure glaucoma,PACG)是一类严重威胁视功能的致盲性眼病,其发病机制长期存在争议。传统观点将虹膜膨隆、晶状体前移及睫状体前旋等解剖学因素视为主要病因,但基于这些结构异常的治疗效果不一,提示这些更可能是疾病进展过程中的伴随结果,而非真正病因。基于此认识,本文聚焦于眼内液体循环异常所致腔室压力失衡对眼内各结构和功能的影响,以阐明PACG发生发展中的病理生理进程,主要包括脉络膜病理性膨胀或脉络膜上腔液体转运异常导致脉络膜-玻璃体压力改变,睫状体-悬韧带-晶状体-玻璃体前界膜-前部玻璃体复合体(ciliary body- zonules-crystalline lens-hyaloid-anterior vitreous complex, CZLHV)异常引起玻璃体腔-后房压力改变,CZLHV复合体再向前推挤虹膜导致后房-前房压力改变,最终虹膜根部关闭房角使得房水从小梁网引流受阻。通过系统总结脉络膜膨胀、玻璃体缓冲体系以及CZLHV复合体在PACG发生发展中的作用机制,以期为PACG的精准诊疗与发病机制研究提供新思路。

关键词: 原发性闭角型青光眼, 眼内液体循环, 脉络膜膨胀, 玻璃体缓冲体系, 睫状体-悬韧带-晶状体-玻璃体前界膜-前部玻璃体复合体

Abstract: Primary angle-closure glaucoma (PACG) is a vision-threatening eye disease that can lead to blindness, and its pathogenesis has long been debated. Traditionally, anatomical factors such as iris bombe, anterior lens displacement, and anterior rotation of the ciliary body have been considered the primary causes. However, the inconsistent therapeutic outcomes targeting these structural abnormalities suggest that they may represent concomitant changes during disease progression rather than the fundamental cause. Drawing from this insight, this article explores how intraocular chamber pressure imbalances, triggered by abnormal intraocular fluid circulation, affect different intraocular structures and functions, with the goal of clarifying the pathophysiological mechanisms underlying the development and progression of PACG. The proposed mechanisms mainly include: pathological choroidal expansion or abnormal suprachoroidal fluid transport leading to altered choroidal-vitreous pressure; abnormalities of the ciliary body-zonules-crystalline lens-hyaloid-anterior vitreous complex (CZLHV) resulting in changes in vitreous cavity-posterior chamber pressure; and forward displacement of the CZLHV complex compressing the iris, thereby creating a posterior-anterior chamber pressure gradient. This sequence ultimately causes iridotrabecular contact, angle closure, and obstruction of aqueous humor outflow through the trabecular meshwork. By systematically summarizing the roles of choroidal expansion, the vitreous buffering system, and the CZLHV complex in the pathogenesis and progression of PACG, this article aims to provide new insights for precision management and future pathogenesis research in PACG.

Key words: Primary angle-closure glaucoma, Intraocular fluid circulation, Choroidal expansion, Vitreous buffering system, Ciliary body-zonules-crystalline lens-hyaloid-anterior vitreous complex