青光眼是全球第二大致盲眼病，第一大不可逆性致盲眼病，其中原发性闭角型青光眼(primary angle closure glaucoma，PACG)占25%。激光周边虹膜切除术(laser peripheral iridotomy，LPI)已成为PACG和原发性房角关闭的一线治疗。LPI机制为利用激光在周边虹膜上打孔，解除PACG的瞳孔阻滞，加深前房，扩大房角，恢复生理性房水排出途径，从而降低眼压。研究表明LPI在原发性房角关闭各个疾病进程中均能比较好的控制眼压，是相对安全的治疗方法。

Glaucoma is the second leading cause of blindness and the most common cause of irreversible blindness worldwide. Primary angle closure glaucoma (PACG) accounts for 25% of glaucoma. Laser peripheral iridotomy(LPI) has become the first line treatment for PACG and primary angle closure (PAC). The mechanism of LPI is to use laser to create a hole in peripheral iris to relieve pupil block, deepen anterior chamber, expand chamber angle,restore pathway of physiological aqueous discharge and reduce intraocular pressure. Studies have shown that LPI can control intraocular pressure well in all stages of PAC, which is safe for PAC.

目的：比较单眼发作的原发性急性房角关闭(acute primary angle closure，APAC)患者发作眼与未发作眼眼部生物学参数的差异，分析急性房角关闭发作的可能危险因素。方法：回顾性分析2008年1月至2020年3月中山眼科中心青光眼科222例45岁以上单眼发作的APAC病例。排除双眼发作、另眼有发作史及晶状体源性、外伤性等继发因素。A超测量晶状体厚度、眼轴长度，超生生物显微镜测前房深度。对单眼发作APAC患者的发作眼与未发作眼眼轴长度、前房深度、晶状体厚度、晶状体相对位置等进行统计学分析。结果：患者发作年龄为(62.57±9.14)岁。发作眼与未发作眼前房深度分别为(1.75±0.27) mm和(1.88±0.31) mm，眼轴长度分别为(22.34±0.80) mm和(22.35±0.83) mm，晶状体厚度分别为(5.14±0.38) mm和(5.17±0.42) mm，晶状体相对位置分别为0.195和0.198。发作眼前房深度较浅，晶状体相对位置较靠前，差异有统计学意义(均P<0.001)，发作眼的眼轴长度、晶状体厚度较未发作眼差异无统计学意义(P>0.05)。APAC发作年龄较小(45~59岁)的患者双眼眼轴均短于发作年龄较大(60~69、70岁以上)的患者；发作年龄70岁以上患者双眼前房深度均较浅，双眼晶状体相对位置均较靠前，差异均有统计学意义(P<0.05)。相关性分析表明APAC发作年龄较小的患者双眼眼轴均较短(P<0.001)。结论：APAC发作眼的前房较浅、晶状体相对位置靠前。短眼轴、女性与不同个体的APAC发作相关。浅前房、晶状体厚、晶状体相对位置靠前可能是高龄人群APAC发作的危险因素。

Objective: To compare the ocular biometric parameters between the acute primary angle closure (APAC) eyes and the fellow eyes as well as the risk factors associated with APAC. Methods: From January 2008 to March 2020,222 monocular APAC patients over 45 years old from the Glaucoma Department of Zhongshan Ophthalmic Center, Sun Yat-sen University were retrospectively studied. Patients with binocular attack, previous attack in the fellow eyes, and secondary factors such as lens-induced and traumatic glaucoma were excluded. Ocular biometric parameters including axial length (AL) and lens thickness (LT) were measured with A-scan ultrasound, while the anterior chamber depth (ACD) was measured by ultrasonic biological microscope. AL, ACD, LT and relative lens position (RLP) were compared between the APAC and the fellows eyes. Results: The average age of onset was (62.57±9.14) years. The ACD was (1.75±0.27) and (1.88±0.31) mm, AL was (22.34±0.80) and (22.35±0.83) mm,LT was (5.14±0.38) and (5.17±0.42) mm, and the RLP was 0.195 and 0.198 for the APAC and the fellow eyes,respectively. Compared with the fellow eyes, the ACD of the APAC eyes was shallower, and the RLP was more anterior (both P<0.001), while the differences of AL and LT were not statistically significant (both P>0.05).Furthermore, AL of patients with a younger age of onset (aged 45 to 59 years) was shorter than that of those with an older age of onset (aged 60 to 69 or over 70 years); patients with an onset age of over 70 years have shallower ACD and more anterior RLP, all statistically significant (P<0.05). In addition, correlation analysis indicated that younger onset age was significantly correlated to shorter axial length of APAC eyes (P<0.001). Conclusion:APAC eyes had shallower ACD and more anterior RLP. Shorter AL and female were associated with APAC attack between individuals. Shallower ACD, thicker lens and more anterior RLP are potential risk factors for APAC among aged population.

晶状体悬韧带异常（包括松弛和断裂）可引起晶状体虹膜隔前移、前房变浅、房角关闭和眼压升高，即闭角型青光眼（angle closure glaucoma，ACG）的发生。特发性悬韧带异常多发生于原发性闭角型青光眼（primary angle closure glaucoma，PACG），可能是PACG的发病机制之一，但仍需前瞻性队列研究进一步证实。此类患者双眼前房深度不等，虹膜/晶状体震颤等体征及超声生物显微镜（ultrasound biomicroscopy, UBM）检查能够诊断的悬韧带异常比例较低，通常在青光眼白内障联合手术前未能被诊断而在术中被发现，故被称为隐匿性晶状体悬韧带异常。目前根据术中表现如充分散瞳可见晶状体赤道部，连续环形撕囊破囊时可见前囊放射状皱褶，超声乳化时囊袋赤道部移位或卷曲，灌注抽吸时囊袋异常飘动，囊袋口不规则等可明确诊断。根据悬韧带异常的程度、范围，选择超声乳化晶状体吸除联合人工晶体植入，联合或不联合囊袋张力环植入或人工晶体缝合固定术。PACG患者术前和术中应关注是否存在悬韧带异常，制定个体化治疗方案，以保证手术安全和疗效。

Zonulopathy (including zonular laxity and dehiscence) can cause anterior displacement of iris-lens diaphragm, shallow anterior chamber, anterior chamber angle closure and elevated intraocular pressure, resulting in angle closure glaucoma (ACG). Idiopathic zonulopathy is common in primary angle closure glaucoma (PACG), which may be one of the pathogenic mechanisms of PACG. But further prospective cohort studies are needed to verify that. ?e proportion of diagnosis ofzonulopathy in PACG patients before cataract extraction in combination with anti-glaucoma surgery is low by signs of anterior chamber depth differences between both eyes, iridodonesis / phacodonesis and UBM examination. Hence, most cases with zonulopathy in PACG are found during the operation, which is called occult zonulopathy. At present, the diagnosis of zonulopathy in PACG is often made according to the intraoperative manifestations, such as visible capsular equator aěer mydriasis, wrinkling of the anterior capsule during manual capsulorhexis, infolding of peripheral capsule or visualization of the capsular equator during the cortical or nuclear removal; loose or ěoppy capsular bag. According to different ranges and severities ofzonulopathy, phacoemulsi?cation combined with intraocular lens (IOL) implantation, with or without capsule tension ring implantation, or sclera-fixated IOL is selected. PACG patients should be paid more attention to the diagnosis and differentiation ofzonulopathy before and during operation, fully improved the preoperative examination, and formulated individualized treatment plans to ensure the safety and efficacy of operation.