Purpose: To explore stable and sensitive indicators for clinical diagnosis of acute angle closure (AAC) secondary to lens subluxation (LS) through quantitative analysis of CASIA 2 imaging. Design: A prospective cross-sectional study. Setting: Clinical practice. Participants: 23 patients with unilateral acute angle closure secondary to lens subluxation and 23 cataract patients without lens subluxation were recruited. Lens subluxation was confirmed by ultrasound biomicroscope diagnosis. The contralateral eyes without LS served as fellow control group. The cataract eyes without LS were enrolled in blank control group. Intervention: Participants underwent ophthalmologic examinations including slit-lamp biomicroscope, best corrected visual acuity, intraocular pressure, central corneal thickness measurement, axial length, gonioscopy, ultrasound biomicroscope and 360-degree anterior chamber and crystalline lens scan protocols of CASIA 2 system. Main outcome measures: Automated circumferential anterior segment and lens morphological parameters under anterior segment optical coherence tomography were analyzed via three-dimensional analysis. Significant differences were found in the front and back radius of the lens, the front and back radius of steep curvature of the lens, lens thickness, lens decentration, lens diameter, iris-trabecular contact (ITC) index, ITC area, anterior chamber depth (ACD), lens vault (LV), and iris volume between LS and controls. Among these parameters, LV, the anterior radius of steep curvature of the lens and ACD demonstrated the highest prediction power (AUC = 0.87, 0.89, and 0.86, respectively). The prediction power of tilt/axis was much higher in the Gaussian Naive Bayes model (AUCs = 0.90) than in the logistic model (AUCs = 0.74). Combination of LV_mean, LV_std, tilt and tilt axis in Gaussian Naive Bayes model presented as most stable and excellent diagnostic markers for AAC secondary to LS (AUCs = 0.98). The combination of markers including lens tilt and lens vault in the mathematic model facilitate clinical work as it not only provides novel diagnostic indications and possible prompt treatment for AAC secondary to lens subluxations, but also enhances our understanding of the pathogenic role of zonulopathy in angle closure glaucoma.

Objectives: To quantify interleukin‐36 receptor antagonist (IL‐36Ra), interleukin‐37 (IL‐37), and interleukin‐38 (IL‐38) levels in aqueous humor and plasma of patients with primary glaucoma, and investigate their correlations with glaucomatous structural damage. Methods: Matched aqueous humor and plasma samples were collected from patients with acute primary angle‐closure glaucoma (APACG), chronic PACG (CPACG), and primary open‐angle glaucoma (POAG), and age‐related cataract controls (ARC). Levels of IL‐36Ra, IL‐37, and IL‐38 were quantified and correlated with average retinal nerve fiber layer thickness (RNFLT). Results: A total of 96 participants were enrolled, including 25 APACG, 23 CPACG, 23 POAG, and 25 ARC. In aqueous humor, IL‐36Ra was significantly elevated in CPACG compared to all other groups, while IL‐37 and IL‐38 were markedly increased in both CPACG and POAG compared to ARC and APACG (all p < 0.05). In plasma, IL‐36Ra was significantly lower in the POAG and APACG than in ARC and CPACG, and IL‐38 was reduced in APACG compared to all other groups (all p < 0.05). All three cytokines in aqueous humor, as well as plasma IL‐36Ra and IL‐38, showed significant negative correlations with average RNFLT. Notably, aqueous humor IL‐38 exhibited the strongest association with RNFLT, particularly within the POAG ( r = −0.745, p < 0.001) and CPACG ( r = −0.496, p = 0.016) subgroups, suggesting an association with structural damage in chronic glaucoma. Conclusion: Aqueous humor IL‐38 levels correlated with RNFLT thinning in POAG and CPACG, suggesting a potential role as a biomarker associated with structural damage. IL‐36Ra was independently elevated in CPACG, supporting its potential as a subtype‐related biomarker. Further studies are needed to clarify the mechanisms of these cytokines in glaucoma pathogenesis.