Anti-fibrotic, anti-VEGF (vascular endothelial growth factor) medications, or radiotherapy, as adjuvant for pterygium surgical procedure, has been suggested for reducing recurrence, but difficulties may be experienced in deciding which treatment to use. The purpose of this study was to compare the efficacies of these different adjuvants for preventing recurrence following pterygium surgery. We conducted a systematic review to identify randomized controlled trials of patients with primary or recurrent pterygium who received anti-fibrotic, anti-VEGF medication, or radiotherapy as adjuvants in combination with surgical procedure. The surgical procedure contained bare sclera technique or petrygium excision combination with tissue grafting. The primary outcome of this study was recurrence. Direct-comparison and Bayesian network meta-analyses were performed to assess direct and indirect evidence of efficacy. We obtained data from 34 randomized controlled trials, representing a total of 2483 patients. Adjuvants included bevacizumab, 5-FU (5-fluorouracil), MMC (mitomycin C), and β-RT (beta-radiotherapy). Compared with placebo, we found distinguishable improvement in recurrence with bevacizumab (odds ratio [OR] 0.38, 95% confidence interval [CI] 0.18–0.80), MMC (0.12, 95% CI 0.06–0.21), and β-RT (0.17, 95% CI 0.04–0.69), but not with 5-FU (0.41, 95% CI 0.12–1.39). MMC significantly reduced recurrence when compared to bevacizumab (0.31, 95% CI 0.13–0.77) and 5-FU (0.28, 95% CI 0.08–0.99). The probability of having the most recurrences after excision was lowest for MMC, followed by bevacizumab and β-RT. Similar results were found in subgroup analyses, including for primary pterygium, and the patients receiving bare sclera technique or conjunctival autograft. Adjuvants such as MMC, bevacizumab, and β-RT could effectively prevent recurrence following pterygium excision. However, their efficacy and acceptability require further clarification in future randomized controlled trials.

Purpose: This study is aimed to investigate the effects of periocular steroids induction on intraocular pressure (IOP), retinal ganglion cells (RGCs) and trabecular meshwork (TM) ultrastructure in glucocorticoid-induced ocular hypertension mice model. Materials and Methods: Dexamethasone-21-acetate (Dex-Ace) was administered through periocular conjunctival fornix injection every 3 days in C57BL/6J mice. Intraocular pressure was measured weekly by rebound tonometry. RGCs were examined with immunofluorescent staining of BRN3a at week 1, 4, and 8. TM morphology was visualized with electron microscopy. Autophagy was evaluated with immunoblotting in TM tissues. Results: Dex-Ace rapidly and significantly induced IOP, which peaked at week 4. The absolute increase in IOP in the Dex-Ace-treated mice was 8.1 ± 1.4 mmHg, a 60% induction (p < 0.0001) compared with that in the vehicle-treated mice. The IOP sustained a higher level in the Dex-Ace group from week 4 to week 8. Dex-Ace treatment decreased the number of RGCs in a time-dependent manner, suggesting that high IOP resulted in optic neuropathy. In addition, Dex-Ace thickened trabecular beams and decreased intertrabecular spaces, with marked accumulation of fibrillar and amorphous granular extracellular material. Moreover, Dex-Ace induced swollen and elongated mitochondria in TM cells. The average mitochondria area was 0.090 ± 0.044 µm² in the vehicle-treated mice, and increased to 0.161 ± 0.094 µm² (p < 0.0001), 0.121 ± 0.029 µm² (p = 0.0223) and 0.171 ± 0.076 µm² (p < 0.0001) in the Dex-Ace-treated mice at weeks 1, 4 and 8, respectively. Autophagy was also increased by Dex-Ace treatment, indicating by the upregulation of LC3-I, LC3-II and beclin-1, and downregulation of p62. Conclusion: Dex-Ace administration decreased RGCs and changed TM ultrastructure, mimicking hallmarks of human glucocorticoid-induced glaucoma (GIG). In addition, mitochondria and autophagy dysfunction suggested abnormal energy metabolism in TM cells, which warranted further study to fully elucidate the pathogenesis of GIG.

We performed a meta-analysis to determine the impact of mild, moderate, and severe visual field loss on quality of life (QoL) in patients with glaucoma. A comprehensive literature search was performed using the PubMed, Excerpta Medica dateBASE and China National Knowledge Infrastructure databases to identify relevant articles published before June 30, 2016. Patients’ QoL was measured using the Glaucoma Quality of Life-15 Questionnaire (GQL-15). In total, 401 patients with glaucoma and 205 patients without glaucoma participated in 4 experiments. The GQL-15 summary scores are statistically different between patients with and without glaucoma (standard mean difference [SMD] = 0.94, 95% confidence interval [CI]: 0.73–1.16, P < .01). GQL-15 summary scores for patients with mild, moderate, and severe visual field loss all differed significantly from those of patients without glaucoma; the SMDs for their summary scores were as follows: mild: 1.24, 95% CI: 0.26 to 2.22, P = .01; moderate: 2.05, 95% CI: 0.91 to 3.19, P < .001; and severe: 2.57, 95% CI: 1.44 to 3.71, P < .001. Two factor scores for central and near vision (SMD = −0.35, 95% CI: −1.01 to 0.30, P = .29) and glare and dark adaptation (SMD = −0.36, 95% CI: −1.01 to 0.30, P = .28) did not differ significantly between patients with mild and moderate visual field loss. However, summary scores and 2 factor scores (peripheral vision and outdoor mobility) differed significantly between patients with mild and moderate glaucoma. In addition, summary scores and all 4 factor scores differed significantly between patients with mild and severe glaucoma. Moreover, summary scores and 3 factor scores (peripheral vision, glare and dark adaptation, and outdoor mobility) differed significantly between patients with moderate and severe glaucoma. However, scores for 1 factor (central and near vision) did not differ significantly between any of the patient groups (SDM = −0.53, 95% CI = −1.33 to 0.27, P = .19). Glaucoma patients with visual field loss showed significantly poorer QoL relative to that of patients without glaucoma. Patients’ QoL decreased as their glaucoma severity increased.

Glucocorticoid-induced glaucoma (GIG) is a chronic optic neuropathy caused by systemic or topical glucocorticoid (GC) treatment, which could eventually lead to permanent vision loss. To investigate the protective effects of rapamycin (RAP) on the trabecular cells during the development of GIG in mice, the effects of RAP on intraocular pressure (IOP), trabecular ultrastructure, and retinal ganglion cells (RGCs) were examined in C57BL/6J female mice treated with dexamethasone acetate (Dex-Ace). The expression of α-actin in trabecular tissue was detected by immunofluorescence, and the autophagic activity of trabecular cells and the expression of GIG-related myocilin and α-actin were detected by immunoblotting. Our results indicated that Dex-Ace significantly increased IOP at the end of the third week (p < 0.05), while RAP treatment neutralized this elevation of IOP by Dex-Ace. Dex-Ace treatment significantly decreased the RGC numbers (p < 0.05), while synchronous RAP treatment kept the number comparable to control. The outer sheath of elastic fibers became thicker and denser, and the mitochondria of lesions increased in Dex-Ace-treated groups at 4 weeks, while no significant change was observed in the RAP-treated trabecular tissues. Dex-Ace induced myocilin, α-actin, Beclin-1, and LC3-II/LC-I ratio, and lowered p62, while synchronous RAP treatment further activated autophagy and neutralized the induction of myocilin and α-actin. Our studies suggested that RAP protected trabecular meshwork cells by further inducing autophagy way from damages of GC treatment.

The oxidative stress‐induced premature senescence of trabecular meshwork (TM) represents a pivotal risk factor for the development of glucocorticoid‐induced glaucoma (GIG). This study aimed to elucidate the pathogenesis of TM senescence in GIG. MethodsIntraocular pressure (IOP), transmission electron microscopy and senescence‐associated protein expression in TM were evaluated in GIG mice. Protein expression of phosphoinositide‐3‐kinase regulatory subunit 1 (PIK3R1) and monoamine oxidase A (MAOA), phosphorylation of AKT were quantified. ROS and mitochondrial superoxide levels were measured to evaluate cellular oxidative stress. Cell cycle analysis, β‐galactosidase staining, senescence‐associated protein expression were employed to assess the aging status of primary human trabecular meshwork cells (pHTMs). ResultsmRNA‐seq and KEGG analysis indicating PI3K/AKT pathway as a key regulator in TM of GIG. PI3K inhibitor significantly prevented IOP elevation and abnormal mitochondrial morphology of TM in the GIG mouse model. PI3K inhibitor or selective silencing of PIK3R1 alleviated dexamethasone (DEX)‐induced oxidative stress, also mitochondrial dysfunction, inhibiting MAOA expression in pHTMs. The same phenomenon was observed in the GIG models with inhibition of MAOA. Further KEGG analysis indicates that cellular senescence is the key factor in the pathogenesis of GIG. TM senescence was observed in both GIG mouse and cell models. Inhibition of the PI3K/AKT/MAOA pathway significantly alleviated DEX‐induced premature cellular senescence of TM in GIG models. Glucocorticoids activated the PI3K/AKT/MAOA pathway, leading to mitochondrial dysfunction, oxidative stress, and premature aging in TM, elevating IOP. This mechanism could be associated with the onset and progression of GIG, providing a potential approach for its treatment.