To evaluate the potential risk factor of visual-threatening posterior capsule opacification (PCO) via the analysis of National Health Insurance Research Database in Taiwan. A total of 8571 patients (3767 male and 4804 female) were recruited in the study group and 17,142 patients (7534 male and 9608 female) in the control group. Patients undergoing cataract surgery, acrysof single-piece intraocular lens implantation and Nd:YAG capsulotomy were selected as the study group. After exclusion which aimed to standardize the ocular condition and exclude the possibility that patients undergoing cataract surgery and Nd:YAG capsulotomy in different eyes, each patient in the study group was age-gender matched to two patients undergoing cataract surgery but without Nd:YAG capsulotomy. The demographic data, systemic disease, and ocular co-morbidities were obtained and analyzed. Adjusted odds ratio (OR) of each demographic data and co-morbidities to the development of visual-threatening PCO, and adjusted OR of co-morbidities to visual-threatening PCO develop within 1 year postoperatively. The dry eye disease (DED), glaucoma, uveitis, age-related macular degeneration (AMD), hyperlipidemia, peptic ulcer disease and liver disease showed significant crude OR while the DED, glaucoma, AMD, hyperlipidemia and peptic ulcer disease revealed a significant adjusted OR. In the subgroup analysis, the DED, glaucoma, AMD, and hyperlipidemia still illustrated a higher adjusted OR to develop visual-threatening PCO within 1 year after the cataract surgery. The DED, glaucoma, AMD, hyperlipidemia and peptic ulcer disease may serve as the risk factor for the developing of visual-threatening PCO.

The effects of lutein and zeaxanthin on lipopolysaccharide- (LPS-) induced secretion of IL-8 by uveal melanocytes (UM) were tested in cultured human UM. MTT assay revealed that LPS (0.01–1 μg/mL) and lutein and zeaxanthin (1–10 μM) did not influence the cell viability of cultured UM. LPS caused a dose-dependent increase of secretion of IL-8 by cultured UM. Lutein and zeaxanthin did not affect the constitutive secretion of IL-8. However, lutein and zeaxanthin decreased LPS-induced secretion of IL-8 in cultured UM in a dose-dependent manner. LPS significantly increased NF-κB levels in cell nuclear extracts and p-JNK levels in the cell lysates from UM, but not p-p38 MAPK and p-ERG. Lutein or zeaxanthin significantly reduced LPS-induced increase of NF-κB and p-JNK levels, but not p38 MAPK and ERG levels. The present study demonstrated that lutein and zeaxanthin inhibited LPS-induced secretion of IL-8 in cultured UM via JNK and NF-κB signal pathways. The anti-inflammatory effects of lutein and zeaxanthin might be explored as a therapeutic approach in the management of uveitis and other inflammatory diseases of the eye.

Dry eye is a common disorder characterized by deficiency of tear. Hyperosmoticity of tear stimulates inflammation and damage of ocular surface tissues and plays an essential role in the pathogenesis of dry eye. Cultured human corneal epithelial (CE) cells were used for the study of effects of lutein and hyperosmoticity on the secretion of IL-6 by CE cells. Cell viability of CE cells was not affected by lutein at 1–10 μM as determined by MTT assay. Hyperosmoticity significantly elevated the secretion of IL-6 by CE cells as measured by ELISA analysis. The constitutive secretion of IL-6 was not affected by lutein. Lutein significantly and dose-dependently inhibited hyperosmoticity-induced secretion of IL-6. Phosphorylated- (p)- p38 MAPK, p-JNK levels in cell lysates and NF-κB levels in cell nuclear extracts were increased by being exposed to hyperosmotic medium. JNK, p38, and NF-κB inhibitors decreased hyperosmoticity-induced secretion of IL-6. Lutein significantly inhibited hyperosmoticity-induced elevation of NF-κB, p38, and p-JNK levels. We demonstrated that lutein inhibited hyperosmoticity-induced secretion of IL-6 in CE cells through the deactivation of p38, JNK, and NF-κB pathways. Lutein may be a promising agent to be explored for the treatment of dry eye.

The effects of apigenin on the expression of VEGF in uveal melanoma cells have not been reported. We studied this effect and relevant signaling pathways in two human uveal melanoma cell lines (SP6.5 and C918). ELISA assay revealed that the constitutive secretion of VEGF by uveal melanoma cells was 21-fold higher than that in normal uveal melanocytes. Apigenin at subtoxic levels (1–5 μM) significantly suppressed the secretion of VEGF in a dose- and time-dependent manner in melanoma cells. VEGF levels in the conditioned culture media from SP6.5 and C918 cell lines treated with 5 μM apigenin for 24 h reduced to 29% and 21% of those in cells not treated with apigenin, respectively. RT-PCR analysis found that apigenin also decreased the expression of VEGF mRNA in melanoma cells. ELISA study of various signal pathways showed that apigenin significantly decreased phosphorylated Akt and ERK1/2 but increased phosphorylated JNK1/2 and p38 MAPK levels in melanoma cells. PI3K/Akt or ERK1/2 inhibitors significantly decreased, but JNK1/2 and p38 MAPK inhibitors did not influence the secretion of VEGF by melanoma cells, suggesting that apigenin suppresses the secretion of VEGF mainly through the inhibition of PI3K/Akt and ERK1/2 pathways.

To evaluate whether the presence of psoriasis increases the risk of keratopathy incidence by using Taiwan’s National Health Insurance Research Database (NHIRD). This retrospective cohort study used data from the NHIRD for the 2009 to 2012 period. A total of 3,648 patients diagnosed with psoriasis were enrolled in the study group while another 14,592 individuals were selected as the control group. The study group was propensity score-matched with a group of controls who had not received a diagnosis of psoriasis. Multivariate Cox regression analysis was performed to estimate the adjusted hazard ratio (aHR) of keratopathy. For the events of keratopathy, 71 patients in the study group and 208 patients in the control group developed keratopathy with a attributable risk of 23.43 per 100,000 person-months (incidence rate ratio = 1.40; P = 0.01) which correlated to the elevated cumulative probability (P = 0.03). The multivariate analysis revealed that the risk of keratopathy was higher in patients who had psoriasis (aHR = 1.31, P = 0.04). In addition, age older than 60 years (aHR = 2.10, P<0.01) and dry eye disease (aHR = 2.79, P<0.01) would also increase the risk of developing keratopathy. Psoriasis was associated with an increased risk of keratopathy in patients without preexisting prominent corneal disease. Moreover, the risk of incident keratopathy increases with exposure to psoriasis.

Glaucoma is the leading cause of irreversible blindness worldwide, with primary open angle glaucoma (POAG) accounting for the greatest number of total glaucoma cases. This study aimed to evaluate the efficacy and safety of micropulse transscleral cyclophotocoagulation (MP-TSCPC) as a primary procedure in POAG during the COVID-19 pandemic. We retrospectively analyzed 60 eyes of 52 patients, who were diagnosed with mild-to-end-stage POAG without previous glaucoma surgery and received MP-TSCPC between 1 January 2020 and 31 August 2020. The mean preoperative intraocular pressure (IOP) significantly decreased from 27.8 mm Hg to 19.8, 20.1, 20.3, 20.4, and 20.2 mm Hg at 1, 3, 6, 9, and 12 months, respectively (all p < 0.05). The mean number of IOP-lowering medications used significantly decreased from 3.3 at the baseline to 1.6, 1.8, 1.8, 1.9, and 1.9 at 1, 3, 6, 9, and 12 months, respectively (all p < 0.001). Total withdrawal of antiglaucoma medications was fulfilled in five patients. The main outcome was achieved in 81.7% at postoperative month 12. The most common adverse effect was transient mydriasis (28.3%). No major complications were encountered. MP-TSCPC seems to be an effective and safe treatment to reduce IOP and the medication burden with minimal vision-threatening complications in mild-to-end-stage POAG patients without previous glaucoma surgery.