Search

Meibomian gland dysfunction and dry eye disease are closely related conditions that often coexist and can contribute to the development of each other. Understanding the similarities and differences between these diseases can assist clinicians in implementing effective treatments for both conditions in a clinical setting. Dry eye disease is a multifactorial disease of the tears and ocular surface. This study aimed to evaluate the demographic characteristics of patients with meibomian gland dysfunction in Taiwan, investigate the association between meibomian gland dysfunction and dry eye parameters, and estimate the prevalence of meibomian gland dysfunction among patients with dry eye symptoms at a tertiary referral centre. This cross-sectional study enrolled patients aged ≥20 years who complained of dry eye symptoms and visited a tertiary centre between September 2019 and March 2020. The patients completed the Ocular Surface Disease Index and Standard Patient Evaluation of Eye Dryness questionnaires before undergoing ocular examination. The lipid layer thickness and meiboscale scores were recorded. In addition, the study measured tear film break-up time, examined corneal staining, and evaluated the number of meibomian glands yielding liquid secretions using a slit lamp. The study evaluated 202 eyes of 202 patients with a mean age of 58.05 ± 13.34 years. The prevalence of meibomian gland dysfunction was 93%. Mean meiboscale score and age were negatively associated, and tear film break-up time was positively associated with the mean number of meibomian glands yielding liquid secretions. Hyperlipidaemia and smoking were the main risk factors for Meibomian gland dysfunction. The prevalence of meibomian gland dysfunction among patients with dry eye symptoms was extremely high at the tertiary centre, highlighting the strong relationship between Meibomian gland dysfunction and dry eye disease. Clinicians should consider meibomian gland dysfunction as a possible cause of dry eye. [ABSTRACT FROM AUTHOR]

Corneal epithelial healing after refractive surgery is a clinically significant issue, especially for surface ablation procedures, and this can be monitored using optical coherence tomography (OCT). The aim of this work is to investigate the corneal epithelial thickness and irregularity by OCT after transepithelial photorefractive keratectomy (t-PRK) and analyse its correlation with visual and refractive outcomes. Patients aged ≥18 years with myopia, with or without astigmatism, who underwent t-PRK between May 2020 and August 2021 were included. All participants were subjected to complete ophthalmic examinations and OCT pachymetry at every follow-up visit. Patients were followed up at 1 week and 1, 3, and 6 months postoperatively. A total of 67 patients (126 eyes) were enrolled in this study. One month postoperatively, spherical equivalent refraction and visual acuity achieved preliminary stability. However, central corneal epithelial thickness (CCET) and standard deviation of the corneal epithelial thickness (SDcet) took 3–6 months to progressive recovery. Patients with higher baseline spherical equivalent refraction were associated with slower epithelial recovery. At every follow-up time point, a significant superior-inferior difference in the minimum corneal epithelial thickness area was observed. Higher stromal haze was correlated with higher spherical equivalent refraction (both baseline and residual) but had no relation with visual outcomes. There was a significant correlation between higher CCET with a better uncorrected distance visual acuity and lower corneal epithelial thickness irregularity. CCET and SDcet measured by OCT seem to be a good auxiliary indicator for reflecting the status of corneal wound recovery after t-PRK surgery. However, a well-designed randomised control study is needed to confirm the study results. [ABSTRACT FROM AUTHOR]

Purpose: To evaluate the anti‐haze effect and visual outcome after intraoperative mitomycin C (MMC) use during photorefractive keratectomy (PRK) in myopia or myopic astigmatism patients. Methods: We searched in PubMed, EMBASE, Cochrane Library and Google Scholar comprehensively to obtain studies comparing the clinical effects after PRK with and without MMC published until February 2020. Meta‐analysis of primary outcome (corneal haze rate) and secondary outcomes [predictability, efficacy, safety and corneal endothelial cell density (ECD)] were conducted. We used trial sequential analysis (TSA) in an effort to collect firm evidence supporting our conclusion. Results: Of the included 11 randomized controlled trials, five cohort and one case–control studies, 3536 eyes (2232 and 1304 in the MMC and control groups, respectively) were enrolled for meta‐analysis. The TSA disclosed strong evidence of decline in corneal haze rate in the MMC group compared with that of the control group. In the subgroup analysis of duration, MMC seemed to reduce corneal haze rate in early‐onset and late‐onset haze. Predictability of refraction and visual acuity were greater in the MMC groups, not significantly though. The proportion of patients losing at least two lines of best corrected visual acuity postoperatively in the MMC groups was lower than that in the control groups. The corneal postoperative ECD showed no significant difference between the MMC and control groups. Conclusion: Our meta‐analysis revealed that MMC is an important anti‐haze agent in PRK for reducing both early‐ and late‐onset haze and can also help improving predictability of refraction and subjective postoperative visual acuity. [ABSTRACT FROM AUTHOR]

Corneal scarring is a common poor outcome of corneal trauma. Transforming growth factor β-1 plays a vital role in corneal fibrosis, inducing keratocyte transformation to myofibroblasts. Other than corneal transplantation, no other curative treatment methods for corneal scarring are currently available. Hypercapnic acidosis exerts anti-inflammatory and anti-migratory effects on numerous organs; however, its effect on corneal fibroblasts remains unknown. Hence, this study aimed to evaluate the effect of hypercapnic acidosis on transforming growth factor β-1-induced fibrosis in corneal fibroblasts and to elucidate the underlying mechanisms. Corneal fibroblasts were obtained from human limbal tissue and cultured with or without transforming growth factor β-1 under hypercapnic acidosis or no-hypercapnic acidosis conditions, and subjected to scratch wound, cell migration, and collagen matrix contraction assays. Furthermore, immunocytochemistry was performed to evaluate the alpha-smooth muscle actin stress fiber. Finally, western blotting was performed to assess the expression of proteins in the NF-κB and Smad pathways. Hypercapnic acidosis suppressed collagen gel contraction capacity in transforming growth factor β-1-treated corneal fibroblasts and inhibited transforming growth factor β-1-induced cell migration. Moreover, hypercapnic acidosis downregulated corneal fibrosis marker alpha-smooth muscle actin in transforming growth factor β-1-treated corneal fibroblasts. Furthermore, hypercapnic acidosis suppressed transforming growth factor β-1-induced fibrosis, at least partly, by inhibiting Smad2/3 phosphorylation and down-regulating p-IκB-dependent and RelB signaling transduction. Hypercapnic acidosis inhibits transforming growth factor β-1-induced corneal fibroblast migration, collagen gel contraction capacity, and alpha smooth muscle actin expression, potentially through the Smad and NF-κB pathways. Therefore, hypercapnic acidosis may be a potentially useful anti-fibrotic therapy for corneal scarring. [ABSTRACT FROM AUTHOR]