This study is a retrospective, nationwide, matched cohort study to investigate the risk of band keratopathy following end-stage renal disease (ESRD). The study cohort included 94,039 ESRD on-dialysis patients identified by the International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM), code 585 and registered between January 2000 to December 2009 at the Taiwan National Health Insurance Research Database. An age- and sex-matched control group comprised 94,039 patients selected from the Taiwan Longitudinal Health Insurance Database 2000. Information for each patient was collected from the index date until December 2011. In total, 230 ESRD patients and 26 controls had band keratopathy (P < 0.0001) during the follow-up period, indicating a significantly elevated risk of band keratopathy in the ESRD patients compared with controls (incidence rate ratio = 12.21, 95% confidence interval [CI] = 8.14–18.32). After adjustment for potential confounders including sarcoidosis, hyperparathyroidism, iridocyclitis and phthisis bulbi, ESRD patients were 11.56 times more likely to develop band keratopathy in the full cohort (adjusted HR = 11.56, 95% CI = 7.70–17.35). In conclusion, ESRD increases the risk of band keratopathy. Close interdisciplinary collaboration between nephrologists and ophthalmologists is important to deal with band keratopathy following ESRD and prevent visual acuity impairments.

Objective To investigate the risk of recurrent corneal erosion (RCE) in patients with diabetes mellitus (DM). Design, setting and participants This retrospective, nationwide, matched cohort study included 239 854 patients with DM recruited between 2003 and 2005 from the Longitudinal Cohort of Diabetes Patients database. The control group included the same number of age-matched and sex-matched patients without DM selected from the Taiwan Longitudinal Health Insurance Database, 2000. Data for each patient were collected from the index date until December 2013. Main outcomes and measures The incidence and risk of RCE were compared between the two groups. Cox proportional hazards regression was used to calculate the HR for RCE after adjustment for potential confounders. The cumulative RCE incidence rate was calculated using Kaplan–Meier analysis. Results In total, 1236 patients with DM and 884 controls developed RCE during the follow-up period, resulting in an incidence rate of RCE in patients with DM (5.87/10 000 person-years (PY)) higher than that in the controls (4.23/10 000 PY). After adjustment for potential confounders, including hypertension, hyperlipidaemia, chronic renal disease and keratoconjunctivitis sicca, patients with DM were 1.35 times (95% CI, 1.24 to 1.48) more likely to develop RCE than the total sample cohort. Conclusions DM increases the risk of RCE, which is an interdisciplinary issue. Therefore, close collaboration between endocrinologists and ophthalmologists is important in managing RCE following DM.

This study investigated the regulatory role of microRNA 100 (miR-100) in hydrogen peroxide (H₂O₂)-induced apoptosis of human retinal pigment epithelial ARPE-19 cells. H₂O₂ induced oxidative cell death of cultured ARPE-19 cells was measured by cytotoxicity assay. qRT-PCR was used to quantify cytosolic and extracellular contents of miR-100. Kinase and miR-100 inhibition treatments were applied to determine the regulatory signaling pathways involved in cell death regulation. H₂O₂ dose-dependently reduced viability of ARPE-19 cells and simultaneously upregulated miR-100 levels in both cytosolic and extracellular compartments. Western blotting detection indicated that H₂O₂ elicited hyperphosphorylation of PI3K/Akt, ERK1/2, JNK, p38 MAPK, and p65 NF-κB. Further kinase inhibition experiments demonstrated that PI3K, p38 MAPK, and NF-κB activities were involved in oxidative-stress-induced miR-100 upregulation in ARPE-19 cells, while blockade of PI3K, JNK, and NF-κB signaling significantly attenuated the oxidative cell death. Intriguingly, MiR-100 antagomir treatment exerted a cytoprotective effect against the H₂O₂-induced oxidative cell death through attenuating the oxidation-induced AMPK hyperphosphorylation, restoring cellular mTOR and p62/SQSTM1 levels and upregulating heme oxygenase-1 expression. These findings support that miR-100 at least in part mediates H₂O₂-induced cell death of ARPE-19 cells and can be regarded as a preventive and therapeutic target for retinal degenerative disease.

This retrospective, nationwide, matched cohort study investigated the temporal relationship of central serous chorioretinopathy (CSCR) following topical ophthalmic corticosteroid (TOC) use. Using the Longitudinal Health Insurance Database 2000 (LHID2000), we collected patients diagnosed with CSCR between January 2001 and December 2010 (n = 2921) and a control group (n = 17,526). Information for each patient was collected and tracked from the index date until December 2011. TOC users were classified based on (i) the date of the last prescription before diagnosis: current users (≤30 days) and former users (31–182 days and ≥183 days) and (ii) the prescription refill intervals: persistent users (interval ≤90 days) and non-persistent users (interval >90 days). The odds ratio (OR) was estimated from multivariate conditional logistic regression after adjusting for relevant confounders. After adjusting for age, sex, geographic region, index date, previously known comorbidities, the date of last TOC prescription before diagnosis, or prescription refilling intervals, the results revealed that patients were likely to have developed CSCR while using TOCs currently (OR = 30.42, 95% CI = 25.95–35.66, p < 0.001) and persistently (OR = 7.30, 95% CI = 6.13–8.69, p < 0.001) as compared to the controls. Our results indicate that current or persistent TOCs use increases the risk of CSCR. Thus, patients requiring TOCs should be advised of this risk, particularly in current or persistent use conditions.

Aims To investigate the risk of corneal ulcer in patients with atopic keratoconjunctivitis (AKC). Methods The nationwide, population-based, retrospective, matched cohort study included 171 019 newly diagnosed patients with AKC who were identified by the International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM), code 372.05, and selected from the Taiwan National Health Insurance Research Database. The age-, sex- and potential comorbidities-matched control group included 171 019 patients with non-AKC selected from the Taiwan Longitudinal Health Insurance Database 2000. Patient information was collected between 1 January 2004 and 31 December 2011, and both groups of patients were tracked from the index date until December 2013. The incidence and risk of corneal ulcer (ICD-9-CM code 370.0 except for 370.07) was compared between the groups. A Cox proportional hazard regression analysis was performed to obtain the adjusted HR for corneal ulcer. The cumulative corneal ulcer incidence rate was calculated with the Kaplan-Meier analysis. Results In total, 2018 patients with AKC and 1481 controls developed a corneal ulcer during the follow-up period. The incidence rate of corneal ulcer was 1.42 times (95% CI1.33 to 1.52; p<0.0001) higher in patients with AKC than in controls. After adjusting for potential confounders, including diabetes mellitus, chronic renal disease, topical steroid ophthalmic agent use, lid margin disease, keratoconjunctivitis sicca, ocular blunt trauma and post-corneal transplantation, patients with AKC were 1.26 times more likely to develop a corneal ulcer than controls (adjusted HR, 1.26; 95% CI 1.14 to 1.39; p<0.05). Conclusions Patients with AKC had an increased risk of developing a corneal ulcer and should be advised of this risk.