Introduction: In the absence of capsular support, anterior chamber intraocular lens (IOL), iris fixated IOL and sutured scleral fixated intraocular lens (SFIOL) implantation have been performed for many years. Recently sutureless glued SFIOL have been used as a primary or secondary procedure to correct aphakia. In this study we have used sutureless and glueless technique of SFIOL implantation. Methodology: An interventional case series was conducted. Aphakic patients without capsular support, sub-luxated lens (>180˚), dislocated lens and dislocated IOL were the inclusion criteria. The patients with hazy cornea, non-dilating pupil, macular scar and glaucoma were not enrolled in the study. Results: Of 62 eyes who completed 1 month followup, 48 were men and 14 women. There was a significant improvement in uncorrected distance visual acuity after surgery (p<0.001). One month postoperative best corrected distance visual acuity was 6/18 or better in 45 eyes (72.6%). The common early postoperative complications were hypotony, corneal edema. No serious complications such as endophthalmitis and retinal detachment were seen. Conclusion: Our technique of sutureless and glueless SFIOL implantation showed good visual outcome in the absence of serious complications. SFIOL will be the only choice in eyes that have anatomic contraindications like non constricting pupil, large sectoral iridectomy and peripheral anterior synechia in which other types of lens are not suitable.

Valsalva retinopathy is a common condition but retinal holes secondary to Valsalva retinopathy are rarely reported. The author believes this to be the first report to describe multiple retinal holes after hyaloidotomy for Valsalva retinopathy.

Diabetic retinopathy (DR) is the most common microvascular complication of diabetes mellitus (DM). DR is complex and the term encompasses several clinical subtypes of diabetic eye disease, including diabetic macular edema (DME), the most frequent cause of central vision loss in DR patients. Both genetic and environmental factors contribute to the pathophysiology of DR and its subtypes. While numerous studies have identified several susceptibility genes for DR, few have investigated the impact of genetics on DME susceptibility. This review will focus on the current literature surrounding genetic risk factors associated with DME. We will also highlight the small number of studies investigating the genetics of response to antivascular endothelial growth factor (anti-VEGF) injection, which is used to treat DME.

Objectives To assess whether insulin therapy impacts the effectiveness of anti-vascular endothelial growth factor (anti-VEGF) injection for the treatment of diabetic macular edema (DME) in type 2 diabetes mellitus. Methods This was a retrospective multi-center analysis. The best-corrected visual acuity (BCVA) at 12 months, BCVA change, central macular thickness (CMT), CMT change, and cumulative injection number were compared between the insulin and the oral hypoglycemic agent (OHA) groups. Results The mean final BCVA and CMT improved in both the insulin (N = 137; p < 0.001; p < 0.001, respectively) and the OHA group (N = 61; p = 0.199; p < 0.001, respectively). The two treatment groups were comparable for final BCVA (p = 0.263), BCVA change (p = 0.184), final CMT (p = 0.741), CMT change (p = 0.458), and the cumulative injections received (p = 0.594). The results were comparable between the two groups when stratified by baseline vision (p > 0.05) and baseline HbA1c (p > 0.05). Conclusion Insulin therapy does not alter treatment outcomes for anti-VEGF therapy in DME.

Intraocular anti-vascular endothelial growth factor (VEGF) therapies are the front-line treatment for diabetic macular edema (DME); however, treatment response varies widely. This study aimed to identify genetic determinants associated with anti-VEGF treatment response in DME. We performed a genome-wide association study on 220 Australian patients with DME treated with anti-VEGF therapy, genotyped on the Illumina Global Screening Array, and imputed to the Haplotype Reference Consortium panel. The primary outcome measures were changes in central macular thickness (CMT in microns) and best-corrected visual acuity (BCVA in ETDRS letters) after 12 months. Association between single nucleotide polymorphism (SNP) genotypes and DME outcomes were evaluated by linear regression, adjusting for the first three principal components, age, baseline CMT/BCVA, duration of diabetic retinopathy, and HbA1c. Two loci reached genome-wide significance (p < 5 × 10−8) for association with increased CMT: a single SNP on chromosome 6 near CASC15 (rs78466540, p = 1.16 × 10−9) and a locus on chromosome 12 near RP11-116D17.1 (top SNP rs11614480, p = 2.69 × 10−8). Four loci were significantly associated with reduction in BCVA: two loci on chromosome 11, downstream of NTM (top SNP rs148980760, p = 5.30 × 10−9) and intronic in RP11-744N12.3 (top SNP rs57801753, p = 1.71 × 10−8); one near PGAM1P1 on chromosome 5 (rs187876551, p = 1.52 × 10−8); and one near TBC1D32 on chromosome 6 (rs118074968, p = 4.94 × 10−8). In silico investigations of each locus identified multiple expression quantitative trait loci and potentially relevant candidate genes warranting further analysis. Thus, we identified multiple genetic loci predicting treatment outcomes for anti-VEGF therapies in DME. This work may potentially lead to managing DME using personalized treatment approaches.