Causes and management strategies for elevated intraocular pressure after implantable collamer lens implantation.

With the widespread application of Implantable Collamer Lens (ICL) implantation surgery in the field of myopia correction, a comprehensive understanding of its potential complications, especially those related to intraocular pressure (IOP), becomes crucial. This article systematically reviews various complications that may lead to IOP elevation after ICL surgery. Firstly, common complications after ICL surgery, including residual viscoelastic, steroid response, and excessive vault of the ICL, are detailed, emphasizing their potential impact on intraocular pressure. Regarding residual viscoelastic, we delve into its direct relationship with postoperative elevated IOP and possible preventive measures. For steroid response, we stress the importance of timely adjustment of steroid therapy and monitoring intraocular pressure. Additionally, excessive vault of the ICL is considered a significant potential issue, and we elaborate on its mechanism and possible management methods. In further discussion, we focus on relatively rare complications such as Toxic Anterior Segment Syndrome (TASS), Urrets-Zavalia Syndrome (UZS), Pigment Dispersion Syndrome (PDS), and malignant glaucoma. For these relatively rare complications, this review thoroughly explores their potential mechanisms, emphasizes the importance of prevention, and provides guidance for early diagnosis and treatment. This is a comprehensible review that aims to offer eye care professionals a comprehensive understanding and effective management guidance for complications of elevated IOP after ICL surgery, ultimately providing optimal care for patients' visual health.

First Evidence Indicates the Physiology- and Axial-Myopia-Dependent Profiles of Steroid Hormones in Aqueous Humor.

The quantitative level of steroid hormones (SHs) in some body fluids have been accepted for clinical diagnosis, whereas their distribution in aqueous humor (AH) is unknown yet. Herein, a profiling study was conducted with a total of 171 AH and 107 plasma samples using liquid chromatography coupled with tandem mass spectrometry (LC MS/MS). For the first time, six kinds of SHs in AH were quantitatively estimated, and their abundances were ranked at cortisol (F), corticosterone (COR), androstenedione (A2), and 11-deoxycortisol (11DOC). The corresponding abundance of all SHs in AH was significantly lower than those in plasma, while there was a lack of a proportional relationship with the abundance of plasma SHs. Dehydroepiandrosterone sulfate, the most abundant plasma SH, was undetectable in AH, implying that the blood-aqueous barrier might specifically block its transferral. Axial myopia generally results from many factors throughout the entire eye from tissues and molecules; furthermore, the correlation of AH SHs and axial myopia was assessed to look for their indication in such myopia. The panel with five kinds of AH SHs (F, COR, CORT, ALD and A2) was functional as a discriminator for axial myopia and control. The abundance of SHs, therefore, has a specific distribution in AH and can potentially contribute to axial myopia.

Polymorphisms and Circulating Plasma Protein Levels of Immune Checkpoints (CTLA-4 and PD-1) Are Associated With Posner-Schlossman Syndrome in Southern Chinese.

Cytotoxic T-lymphocyte associated protein 4 (CTLA-4) and programmed cell death 1 (PD-1) are well-known key immune checkpoints that play a crucial dampening effect on regulating T-cell homeostasis and self-tolerance. In this study, we aimed to evaluate the association between immune checkpoints (CTLA-4 and PD-1) and Posner-Schlossman syndrome (PSS) in a southern Chinese population. A total of 137 patients with PSS and 139 healthy controls from a southern Chinese population were recruited. Five single nucleotide polymorphisms (SNPs) of CTLA-4 (rs733618, rs4553808, rs5742909, rs231775, and rs3087243) and five SNPs of PD-1 (rs10204525, rs2227981, rs2227982, rs41386349, and rs36084323) were genotyped by SNaPshot technique. Soluble CTLA-4 (sCTLA-4) and soluble PD-1 (sPD-1) were determined by ELISA and antibody array assay, respectively. The frequencies of T allele at rs733618 and A allele at rs231775 of CTLA-4 were significantly higher in PSS patients than in healthy controls (corrected p (Pc ) = 0.037; Pc = 0.044, respectively). The haplotype frequencies of CACGG haplotype (rs733618-rs4553808-rs5742909-rs231775-rs3087243) of CTLA-4 and TGAGC haplotype (rs10204525-rs2227981-rs2227982-rs41386349-rs36084323) of PD-1 in the PSS group was significantly lower than those in the control group (Pc = 0.015, p = 0.034, respectively). Circulating plasma levels of sCTLA-4 and sPD-1 in PSS patients were significantly higher than those in controls (all p < 0.001). The present study suggests that CTLA-4 and PD-1 genetic polymorphisms are associated with the susceptibility to PSS in a southern Chinese population. The upregulated circulating plasma protein levels of sCTLA-4 and sPD-1 might provide some hints regarding the dysfunction of immune checkpoints in PSS during the active status.

Polar value analysis of astigmatic change and rotational stability after implantation of V4c toric implantable collamer lens.

BACKGROUND: To evaluate the clinical results and rotational stability of V4c toric implantable collamer lens (TICL, STAAR Surgical Company, Monrovia, CA, USA) in patients with moderate to high myopic astigmatism. Retrospective, interventional case series was performed at Shenzhen Eye Hospital, Shenzhen, Guangdong, China. METHODS: This study enrolled 43 patients (72 eyes) who received TICL implantation to correct myopia and myopic astigmatism. The patients underwent visual and refractive examinations before and 1 month after surgery. Astigmatic changes were estimated using polar value analysis. The difference between the achieved axis and the intended axis at the last follow-up was taken as the rotation of the V4c TICL. RESULTS: At 1 month postoperatively, the mean safety and efficacy indices were 1.17 and 1.13, respectively. A significant reduction of 8.92±2.58 D was observed in the spherical equivalent refraction (SER), which decreased from -9.29±2.41 D preoperatively to -0.37±0.55 D postoperatively. The astigmatic error of treatment in cylinder format was calculated to 0.50±0.41 @ 15.08° relative to the preoperative stronger meridian at 1 month, postoperatively. At 1 month postoperatively, the mean absolute rotation was 8.30±10.00 degrees (median =5.46 degrees; range, 0.00-58.88 degrees). CONCLUSIONS: TICL could achieve good astigmatic outcomes for correcting moderate to high myopic astigmatism. After TICL implantation, corneal astigmatism remained unchanged. To optimize postoperative astigmatic outcomes in TICL, polar value analysis can be used to build a nomogram.

Involvement of the JNK signaling in granular corneal dystrophy by modulating TGF-ß-induced TGFBI expression and corneal fibroblast apoptosis.

Granular corneal dystrophy (GCD) is featured by corneal deposits of transforming growth factor beta-induced gene (TGFBI) mediated by the TGF-ß (transforming growth factor-ß)/Smad signaling. However, the roles of c-Jun amino-terminal kinase (JNK) pathway in GCD pathogenesis remains unexplored, which was investigated in this study. JNK signaling activation and inhibition in primary corneal fibroblasts were obtained by treatments with anisomycin and SP600125, respectively. Protein abundance and phosphorylation were detected by immunoblotting. Cell viability and apoptosis were analyzed by CCK-8 and flow cytometry respectively. TGFBI deposit and autophagy progression were assessed by immunofluorescence. The results found that JNK1 expression and phosphorylation were greatly increased in corneal tissues from GCD2 patients. JNK signaling activation impaired the viability and promoted apoptosis and autophagy processes in primary corneal fibroblasts, along with Smad2/3 phosphorylation, TGFBI accumulation and Bcl-2 suppression. Autophagy related proteins, such as ATG5 (autophagy related 5), ATG12 (autophagy related 12) and LC3B (microtubule-associated protein 1 light chain 3 beta), were also increased in anisomycin or TGF-ß1 treated corneal fibroblasts. However, SP600125 effectively reversed the above effect induced by TGF-ß1 treatment in corneal fibroblasts, including the TGF-ß-induced autophagy progression. The results suggested that JNK signaling was activated in GCD2 corneal tissues, and it mediated the TGF-ß-induced TGFBI protein accumulation and apoptosis of corneal fibroblasts during GCD2 pathogenesis.

[Higher-order aberrations in myopic and astigmatism eyes].

OBJECTIVE: To analyze the distribution of the higher order aberrations in the population of Chinese with myopia and astigmatism and determine whether the pupil size, degree of myopia and astigmatism affects the higher order aberrations. METHODS: Using a Tscherning method, 147 myopic and astigmatism eyes were evaluated before LASIK. The root mean square (RMS) values of higher order aberrations for each subject with pupil diameters of 4.5, 5.0, 5.5, 6.0, 6.5 and 7.0 mm were calculated. The subjects were divided into following groups: high myopia (> -6.00 D) and low myopia (or= 0.75 D) and astigmatism group II (< 0.75 D). RESULTS: The root mean square (RMS) values was decreased from 3rd order to sixth order aberrations in the same eye. The individual difference was from 6.1-fold to 36.6-fold in same type of aberration. All types of aberrations, in particular spherical and coma aberration, was increased significantly with increasing pupil size. Secondary spherical aberration, spherical and secondary coma aberration were affected by myopia, but coma aberration; astigmatism only affected the coma aberration, but spherical aberration. CONCLUSIONS: The aberrations were increased with the increasing of refractive error such as myopia and astigmatism. Spherical aberration is more common in high myopia, Coma aberrations is related with astigmatism.

[Contrast sensitivity function in myopic LASIK].

OBJECTIVE: To evaluate near contrast sensitivity function before and after myopic laser in situ keratomileusis (LASIK). METHODS: With FACT 101 test chart, static near contrast sensitivity was measured in randomly selected 47 subjects (93 eyes) before, 1 month and 6 months after LASIK. The contrast sensitivity was measured at 1.5, 3.0, 6.0, 12.0 and 18.0 cycles per degree (c/d) spatial frequency respectively and made comparison in them. RESULTS: The patients achieved the mean uncorrected visual acuity (UCVA) of 1.07 +/- 0.18 and 1.12 +/- 0.20 at postoperative 1-month and 6-months respectively. There was a general reduction in near contrast sensitivity in all spatial frequencies at postoperative 1-month when they were compared with the preoperative contrast sensitivity. The difference at 12 and 18 c/d spatial frequency was statistically significant (t test, P < 0.01). By the 6-month visit, all eyes showed a recovery of static contrast sensitivity function. The group of high myopia (preoperative > or = -6.00 D) and group with complaining of glare and halos after the surgery had a higher decrease rate of contrast sensitivity compared with that of the group preoperative < - 6.00 D and the group of patients without such complaints respectively. The differences at 6.0, 12.0 and 18.0 c/d spatial frequency at 1-month visit was statistically significant (t test, P < 0.05). CONCLUSIONS: The contrast sensitivity function test offers a more sensitive and comprehensive measure of functional vision than does standard Snellen acuity. The near contrast sensitivity in post-LASIK patients at early stage is reduced despite normal visual acuity and this can affect the quality of vision.