To describe the first reported case of non-proliferative Duchenne muscular dystrophy-associated retinopathy manifested as bilateral perifoveal ischemia. This observational case report details a 21-year-old male with genetically confirmed Duchenne muscular dystrophy (DMD) who presented with bilateral visual decline. A comprehensive ophthalmic evaluation was performed including best-correct visual acuity (BCVA) assessment, slit-lamp biomicroscopy, dilated fundus examination, full-field and multifocal electroretinography (ERG) in accordance with ISCEV standards and ERGs to sawtooth modulation, structural spectral-domain optical coherence tomography (OCT) and optical coherence tomography angiography (OCTA) in both eyes. BCVA was 20/40 in both eyes. Anterior segment examination revealed bilateral posterior subcapsular cataracts, while dilated fundoscopic examination was unremarkable. Multifocal ERG demonstrated reduced amplitudes in the central and parafoveal rings, indicating localized retinal dysfunction. OCTA disclosed bilateral, irregular enlargement of the foveal avascular zone consistent with perifoveal ischemia. These vascular abnormalities corresponded to the areas of inner retinal thinning with secondary outer nuclear layer expansion in structural OCT. DMD-associated retinopathy may present with retinal ischemia in the absence of overt fundoscopic abnormalities. Multimodal structural and functional modalities including multifocal ERG, OCT and OCTA may be critical to the early detection of subclinical ischemic changes and for identifying patients at risk of progression to proliferative retinopathy.

Proliferative diabetic retinopathy (PDR) is one of the leading causes of blindness in working-age adults. We have previously shown that the risk of PDR is significantly elevated in individuals with intrauterine exposure to famine. However, the genetic mechanisms mediating this association remain unknown. The aim of the current study was to investigate the molecular underpinnings of famine-related PDR by performing genome-wide association (GWAS) and interaction studies (GWIS). We analysed n = 2925 patients with type 2 diabetes from the DOLCE cohort of Northern Ukraine, of whom n = 1364 were born during historical famine periods (1929-1949, including the Holodomor and World War II). PDR cases were defined as individuals with either diagnosed proliferative retinopathy, laser-treated diabetic retinopathy (DR) or blindness in either eye. GWAS and GWIS were performed using linear mixed model (LMM) adjusted for established risk factors and genetic relationship matrix. GWAS identified rs3795299 in IL22RA1 as the top signal (pLMM = 1.05 × 10-6), which was also the strongest gene in the gene-based analysis (p = 3.19 × 10-5), with suggestive enrichment of response to ketones (GO) and base excision repair (KEGG) pathways. In the GWIS, the strongest signal was rs1506783 in PAPPA2 (pLMM = 1.29 × 10-7). A second biologically credible candidate was rs2230805 in ABCA1 (pLMM = 4.44 × 10-6), reaching borderline genome-wide significance in gene-based analysis (p = 4.31 × 10-6). Interaction analyses showed suggestive enrichment for nucleosomal DNA binding (GO), tryptophan metabolism and glycerolipid metabolism (KEGG) pathways. Furthermore, at nominal significance, we validated variants in previously reported diabetic retinopathy-associated genes, including TCF7L2, SLC2A1, SLC2A11 and VDR in the GWAS, as well as 13 variants in genes including VEGF, VEGFR1, ANGPT1, PLXDC2, SELP and PON2 in the GWIS. Our findings suggest that famine-related PDR susceptibility involves distinct developmental programming mechanisms, including altered insulin-growth signalling (PAPPA2) and lipid metabolism (ABCA1), whereas immune-related pathways (IL22RA1) may contribute to the conventional glycaemia-driven route to PDR through VEGF-mediated angiogenesis. These genes represent potential therapeutic targets and emphasize the importance of the perinatal environment in lifelong vascular health and disease.

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in Type 1 Diabetes (T1D), but a subset of individuals remains free from macrovascular or renal complications despite decades of hyperglycaemia and a significant risk factor burden. We used a targeted proteomic approach (Olink Cardiovascular panel III, targeting 92 proteins) to characterize the proteomic profile of cardiovascular resilience in T1D by comparing 92 patients with long-standing T1D (age 59.8 [53.2, 69.1], duration 40.0 [35.0, 45.2] years) free from macrovascular complications or nephropathy against a reference group of 57 T1D patients with accelerated vascular pathology (age 42.0 [32.0, 56.0], duration 22.0 [18.0, 27.0] years), proliferative retinopathy and/or nephropathy in relation to diabetes duration, termed Rapid Progressors (RP). Twenty proteins differed significantly between RP and Escapers (False Discovery Rate [FDR] < 0.05) after adjustment for age, sex, HbA1c, and eGFR: Caspase-3 was significantly higher in RP (Adjusted difference: +2.12 Normalized Protein eXpression [NPX], p < 0.001). Proteins associated with platelet activation and leukocyte adhesion with increased levels in RP included Junctional Adhesion Molecule A (+ 1.40 NPX), Glycoprotein VI (GP6: + 1.29 NPX), and P-Selectin (+ 0.82 NPX) (all p < 0.001). PECAM-1 (+ 0.55 NPX) and TNFRSF14 (+ 0.43 NPX), were also elevated. RP also showed higher levels of metabolic and tissue-remodelling proteins; Transferrin Receptor (+ 0.53 NPX) and Fatty Acid Binding Protein 4 (+ 0.52 NPX), as well as higher Bleomycin Hydrolase, Trefoil Factor 3, GDF-15, U-PAR, and Cystatin B. Conversely, von Willebrand Factor (vWF) levels (-1.35 NPX, p < 0.001) and Paraoxonase 3 (PON3) was lower in RP (-0.34 NPX, p = 0.003). In conclusion, escaping complications in long-term T1D appears to be associated with active molecular mechanisms. Progression is marked by apoptosis (Caspase-3), fibrosis (CHI3L1) and platelet activation (GP6), whereas resilience is associated with a distinct signature involving higher vWF and PON3. These findings highlight a profound biological divergence between extreme T1D phenotypes and provide a foundation for further research into vascular resilience.

Retinal Pericytes and Their Role in Proliferative Retinopathies.

Retinal angiogenesis relies on a precisely timed interaction between astrocytes and endothelial cells (ECs), yet the transcriptional regulatory program underlying this complex neurovascular crosstalk remains poorly characterized. Here, we define Zeb2 as a pivotal transcriptional modulator of retinal astrocyte function that coordinates developmental and pathological vascular growth. It is transiently expressed in retinal astrocyte progenitor cells during development and re-induced under pathological hypoxia. Conditional ablation of Zeb2 in retinal astrocytes enhanced their proliferation, migration, and maturation by upregulating VEGFA and altering other signalling, leading to excessive superficial vascular growth during development. In oxygen-induced retinopathy, Zeb2 inactivation exacerbated pathological neovascularization while impairing reparative revascularization, which is associated with a transcriptional signature favouring tuft ECs over tip ECs. Mechanistically, it inhibited the neurotoxic A1 astrocyte identity, resulting in dampened inflammatory response and diminished genetic program promoting revascularization and/or preventing neovascularization including Plxnd1, Nrf2, and FGF2 signalling. These findings establish Zeb2 as an oxygen-sensitive regulator of astrocyte function that differentially modulates physiological and pathological angiogenesis, highlighting its potential as a therapeutic target in proliferative retinopathies.

Diabetic retinopathy (DR), the primary driver of preventable vision impairment in the global working-age demographic, arises from chronic hyperglycaemia and manifests as non-proliferative or proliferative retinopathy with or without diabetic macular oedema. Inflammation and macrophage-derived cytokines drive progression, and proteomics can identify proteins that may be associated with DR. Vitamin C has been implicated in diabetic complications, yet its causal impact on DR remains unclear. We performed quantitative proteomics and bioinformatics analyses of peripheral-blood macrophages from patients with proliferative DR (PDR), non-PDR, diabetes without retinopathy and non-diabetic controls. In a series of experiments, we used THP-1 cells exposed to sustained hyperglycemia and retinal lysates from streptozotocin (STZ)-induced mice to quantify TPT1 expression and to investigate its role in modulating autophagy-related mediators and cellular redox homeostasis. Causal inference between circulating vitamin C and DR risk was tested by two-sample Mendelian randomization (MR). Quantitative profiling revealed 265 proteins whose abundance differed significantly between PDR and controls; 145 were up-regulated and 120 down-regulated, with TPT1 emerging as a central hub within the macrophage interactome. TPT1 expression was markedly reduced under hyperglycemic conditions, which was accompanied by impaired autophagic activity and increased reactive oxygen species production. MR analysis revealed that vitamin C levels were negatively correlated with the risk of DR (OR = 0.09, 95% CI: 0.01-0.57, P = 0.01). Deficiency of TPT1 links impaired macrophage autophagy to the progression of diabetic retinopathy, while vitamin C, which restores TPT1 expression, represents a promising therapeutic strategy.

IntroductionDiabetic retinopathy (DR) remains a prevalent cause of preventable blindness and one of the most serious complications of diabetes mellitus globally, which can be minimized by periodic screening and risk factor management. Nonetheless, few studies have assessed its prevalence and predictors among diabetic patients in primary care settings. This study aimed to determine the prevalence and predictors of DR among diabetic patients in primary care in Bahrain.MethodsA cross-sectional study was conducted in October-November 2025 across all primary healthcare centers in Bahrain. All adult patients with diabetes attending diabetic clinics were included. DR was assessed by a specialist optometrist using a non-mydriatic retinal camera (TOPCON NW500). Retina assessment results included normal retina, non-proliferative retinopathy and proliferative retinopathy. Sociodemographic characteristics, comorbidities, and risk factors were collected. Descriptive and inferential analyses were done. A P-value <0.05 was considered statistically significant.ResultsA total of 594 patients were included, with a median age of 61 years. Most participants were male (337, 56.7%), Bahraini (506, 85.2%), and had type 2 diabetes (575, 96.8%). Dyslipidemia (463, 77.9%) and hypertension (397, 66.8%) were the commonest comorbidities. DR was noted in 88 (14.8%) patients; 13% (n=77) had non-proliferative DR and 1.8% (n=11) had proliferative DR. Univariate analysis showed that patients with retinopathy were older (P<0.001), had a longer diabetes duration (P<0.001), and higher rates of hypertension (P=0.001), dyslipidemia (P=0.009), chronic kidney disease (P<0.001), and ischemic heart disease (P=0.042). Additionally, higher glycated hemoglobin (P=0.014), and triglycerides (P=0.022), and lower glomerular filtration rate (P<0.001) were found among patients with retinopathy. Logistic regression identified a longer diabetes duration (OR=1.576, P<0.001), hypertension (OR=1.912, P=0.039), abnormal monofilament test (OR=2.92, P=0.027), and higher HbA1c (OR=1.013, P=0.033) as predictors of DR.ConclusionDR affects one in seven diabetic patients attending primary care in Bahrain, particularly those with a longer disease duration, hypertension, poor glycemic control, and neuropathy. Annual retinal screening, optimal glycemic control, and risk factor management by primary care professionals are essential to reduce its sequelae.

Tetracyclines and Risk of Proliferative Vitreoretinopathy after Rhegmatogenous Retinal Detachment.

Sickle cell retinopathy (SCR) is a well-documented and potentially vision-threatening presentation of sickle cell disease (SCD). In this article, we provide a comprehensive review of the management options for non-proliferative sickle cell retinopathy (NPSR) and proliferative sickle cell retinopathy (PSR) based on the existing ophthalmic literature. The mainstay of NPSR treatment focuses on preventing progression to PSR by identifying and altering modifiable risk factors. Once NPSR progresses to PSR, suppression of vascular endothelial growth factor (VEGF) expression with laser photocoagulation or intravitreal anti-VEGF injections can be considered. While no standard criteria exist for timing and type of intervention, both treatment modalities have been utilized for advanced PSR. In contemporary practice, scatter laser photocoagulation is performed far more commonly than the historically described feeder-vessel photocoagulation. Surgical management typically includes pars plana vitrectomy (PPV), scleral buckle (SB), or combined PPV-SB and are generally indicated in PSR for non-clearing vitreous hemorrhage, tractional or rhegmatogenous retinal detachment (RD), and epiretinal membrane formation. There is currently no consensus on standard guidelines for the management of SCR. Evidence suggests that surgical intervention can improve vision in advanced stages of PSR and that anti-VEGF therapy may have a role in treatment. However, studies in the ophthalmic literature are limited by relatively small sample sizes and difficulty accounting for a patient's prior medical or surgical interventions. Additionally, more robust studies are required to determine the long-term efficacy and safety of anti-VEGF in SCR. A multidisciplinary team approach to SCR and SCD remains the cornerstone of management for this systemic disease.

The aim of this study was to evaluate plasma and aqueous Maresin-1 (MaR1) levels in patients with diabetic retinopathy (DR) and to examine the ability of these levels to distinguish proliferative diabetic retinopathy. The study included three age and gender-matched groups of 25 cataract patients with no diabetes mellitus (DM) or additional disease (C), 25 cataract patients with diabetes and no retinopathy (DM + C), and 25 cataract patients with diabetic proliferative retinopathy (DR + C). All the patients were examined with respect to age, gender, fasting plasma glucose and hemoglobin A1c (HbA1c). Phaco + IOL implantation was applied to all patients in all the groups, and aqueous samples were taken during the operation. The plasma and aqueous MaR1 levels were analyzed using enzyme-linked immunosorbent assays. The diagnostic performance of plasma and aqueous MaR1 levels in distinguishing the DR + C group from the C group was evaluated using receiver operating characteristic (ROC) curve analysis. A statistically significant difference was determined between the groups with respect to fasting plasma glucose, and HbA1c levels (p < 0.0167 for all parameters tested). The plasma MaR1 levels in group DR + C were determined to be statistically significantly lower compared to the C and DM + C groups (p < 0.001). The plasma MaR1 levels in group DM + C were determined to be statistically significantly lower compared to the C group (p < 0.001). The aqueous MaR1 levels in group DR + C were determined to be statistically significantly higher compared to the C and DM + C groups (p < 0.001, p < 0.001, respectively). No statistically significant difference was determined between the DM + C and C groups in respect of the aqueous MaR1 levels (p = 0.590). ROC analysis showed excellent discriminative performance of both plasma and aqueous MaR1 levels in distinguishing the DR + C group from the C group (AUC = 0.968 and 0.974, respectively; both p < 0.001). According to the results of the study, MaR1 levels were significantly lower in plasma and significantly higher in the aqueous humor in the DR + C group. ROC analysis indicated that both plasma and aqueous MaR1 levels showed good discriminative ability in distinguishing the DR + C group from the control group. These findings suggest that alterations in MaR1 levels may be associated with the inflammatory processes involved in diabetic retinopathy and may reflect disease-related biological changes in both systemic circulation and ocular tissues.

To evaluate vitreoretinal interface (VRI) findings and layer-specific macular thickness profiles on optical coherence tomography (OCT) in children with Duchenne muscular dystrophy (DMD). This retrospective case–control study included 26 children with DMD and 28 age- and sex-matched healthy controls. All participants underwent comprehensive ophthalmic examination and Spectralis spectral-domain OCT. Ganglion cell–inner plexiform layer (GCIPL), inner nuclear layer (INL), and outer plexiform layer (OPL) thicknesses were obtained using the ETDRS grid (central 1-mm subfield and quadrants of the 3-mm and 6-mm rings). Between-group comparisons were evaluated using covariate-adjusted models (age, spherical equivalent, and intraocular pressure), with false discovery rate (Benjamini–Hochberg) correction applied within each layer. Only right eyes were analyzed. Best-corrected visual acuity was 0.0 logMAR in both groups, and spherical equivalent and intraocular pressure were comparable. No VRI abnormalities or vascular manifestations, including Duchenne-associated proliferative retinopathy, were detected. After covariate adjustment and FDR correction, GCIPL thickness remained reduced in the 3-mm inferior and 6-mm temporal sectors (both q = 0.0135), and INL thickness remained reduced in the 3-mm inferior sector (q = 0.036). Within the DMD group, age was not significantly correlated with these parameters. Children with DMD and preserved visual acuity showed subtle, sector-specific thinning of inner retinal layers (GCIPL and INL) on OCT, while VRI and vascular abnormalities were absent. Larger longitudinal studies are needed to confirm these findings and clarify their clinical significance.

ObjectivesTo determine the spectrum of ocular complications of sickle cell disease (SCD) and age of onset of proliferative sickle cell retinopathy (PSR) in children attending the pediatric clinic at a tertiary hospital in southern Ghana.MethodsA cross-sectional study of all children with SCD in steady state, ages 2 to 16 years. Demographic and clinical data were recorded using predesigned forms. The ocular manifestations of SCD were classified as either proliferative or non-proliferative based on the presence or absence of neovascularization, respectively.ResultsIncluded in this study were 294 children, (53.4% males), mean age 9.2 ± 3.7 years and majority had HbSS-199 (67.9%) and HbSC-74 (25.3%) genotypes. Comma-shaped conjunctiva vessels were the commonest anterior segment manifestation occurring in 85% of children. Non-proliferative posterior segment signs included: venous tortuosity 69 (23.5%), salmon-patch hemorrhages 4 (1.4%), iridescent spots 38 (12.9%), and black sunburst 24 (8.2%). Prevalence of PSR of any stage among children with HbSS was 2.5% (5/199) and 8.1% (6/74) among those with HbSC (P = .0366). The earliest age PSR was detected in this cohort was 8 years and for PSR stage 3, 13 years. No child was blind from eye complications of SCD or any other cause.ConclusionComma-shaped conjunctiva vessels were the commonest anterior segment manifestation of SCD, and retinal venous tortuosity was the most common posterior segment manifestation. Proliferative retinopathy was more common in HbSC genotype.

Chronic kidney disease (CKD) remains underdiagnosed in people with type 2 diabetes mellitus (T2DM), particularly in early stages, despite its strong association with renal disease progression, cardiovascular outcomes, and current guideline recommendations for early cardio-renal protective interventions. Contemporary, nationally representative primary care data from Spain evaluating CKD underdiagnosis in people with T2DM are limited. This study estimated the prevalence of diagnosed and undiagnosed CKD in adults with T2DM in Spain, described treatment patterns by CKD diagnosis status, and identified factors associated with undiagnosed CKD. A planned secondary analysis of the DIAMOND2 multicentre cross-sectional study was performed in Spanish primary care. Data were retrospectively collected from electronic medical records during the calendar year 2022, and the analysis was performed between January and July 2023. Data from 5009 adults with T2DM randomly selected from 70 centres were analysed. CKD was defined according to KDIGO 2024 criteria as estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m² and/or urine albumin-to-creatinine ratio (uACR) ≥ 30 mg/g. Patients were classified as having diagnosed CKD (recorded), undiagnosed CKD (meeting criteria without record), or no CKD. Descriptive statistics were used, and multivariable Poisson regression models with robust variance were fitted to identify factors associated with undiagnosed CKD. True CKD prevalence was 32.0 %, with 54 % undiagnosed. Undiagnosed CKD was mainly in patients with isolated eGFR or uACR abnormalities and lower KDIGO risk. SGLT2 inhibitors were prescribed to 45.2 % of diagnosed and 40.0 % of undiagnosed CKD, versus 35.4 % without CKD (p < 0.001). In multivariable analysis, undiagnosed CKD was associated with metformin use and higher eGFR, and inversely with diabetes duration, heart failure, and proliferative retinopathy. Over half of CKD cases in Spanish adults with T2DM remain undiagnosed, particularly at early disease stages, limiting risk stratification and optimal cardio-renal management. These findings underscore the need for systematic CKD screening and improved recognition of early kidney disease in primary care.

Epidemiological, clinical, angiographic and therapeutic features of sickle cell retinopathy in Burkina Faso

Proliferative retinopathy (PR), a leading cause of visual impairment, is characterized by pathological retinal neovascularization. As an important methyltransferase, methyltransferase-like 14 (METTL14) plays a key role in the N6-methyladenosine (m6A) modification, which is the most widespread modification in mRNA and has been defined as a critical regulator in retinal diseases. This study aims to clarify the mechanisms by which METTL14 regulates pathological retinal neovascularization in PR. The m6A levels were determined by m6A RNA colorimetric quantification in mice retinas and endothelial cells. The METTL14 levels in mice retinas and endothelial cells were detected by qPCR, western blotting and immunofluorescence assays. Retinal flat mounts from the oxygen-induced retinopathy (OIR) mice were used to assess the effects of METTL14 on retinal neovascularization. The effects of METTL14 on angiogenic functions of endothelial cells were measured by cell counting kit-8 (CCK-8), wound healing and tube formation assays. Mechanistically, we used the sequence-based RNA adenosine methylation site predictor (SRAMP) system to predict the target genes of METTL14 and performed qPCR, western blotting and RNA immunoprecipitation assays to validate their interactions. Statistical analyses were performed using Student's t test or one-way ANOVA. The levels of m6A and METTL14 were reduced in the retinas of OIR mice and in cobalt chloride (CoCl2)-induced endothelial cells. METTL14 overexpression increased the m6A levels in mice retinas and endothelial cells. METTL14 overexpression in the OIR mice decreased the retinal neovascularization and vaso-obliteration. In CoCl2-induced endothelial cells, METTL14 overexpression enhanced cells viability and reduced cells migration and tube formation. Mechanistically, METTL14 bound to hypoxia-inducible factor 1-alpha (HIF-1α) and suppressed HIF-1α levels. This study suggests that METTL14-mediated m6A modification is a pivotal step in regulating the pathogenesis of retinal neovascularization. Therefore, METTL14 might be introduced as a promising therapeutic strategy for the management of PR. However, our findings are limited by the types of clinical samples, and further validation in larger clinical cohorts is required.

Association of neighborhood indices on outcomes of patients with proliferative sickle retinopathy.

Rationale: Proliferative retinopathies are the leading causes of blindness worldwide. Current treatment paradigms rely heavily on intravitreal injections of anti-vascular endothelial growth factor A (anti-VEGFA) agents, which, despite their efficacy, are associated with ocular complications and patient discomfort. To address these challenges, we have developed a novel mixed-layered trehalose-functionalized dendrimer (Tre-D) conjugated with Axitinib, a multi-receptor tyrosine kinase inhibitor, (Tre-D-Axitinib) for systemic delivery to aberrant neovascular tufts in retina.Methods: Tre-D is synthesized through a scalable and convenient synthetic methodology using click chemistry. The in vitro cytocompatibility, uptake and angiogenesis assays are carried out in Human Retinal Microvascular Endothelial Cells (HRMECs), Human umbilical vein endothelial cells (HUVECs) and macrophages (RAW-Blue). The in vivo uptake and efficacy of Tre-D-Axitinib are evaluated in a mouse model of oxygen induced retinopathy (OIR) via intraperitoneal (IP) administration of the treatment.Results: The Tre-D demonstrates inherent targeting to neovascular tufts in an OIR mouse model. Tre-D-Axitinib leads to increased vaso-obliteration in the ischemic retina. The IP administration of Tre-D-Axitinib effectively reduces pathological retinal neovascularization, tuft formation, and vessel anastomoses while showing minimal off-target effects and rapid renal clearance. Mechanistic studies reveal that Tre-D-Axitinib inhibits VEGFA-induced proliferation, migration, and angiogenesis in human retinal endothelial cells.Conclusions: To date, there are no organic nanoparticles that localize selectively in aberrant neovascular tufts at the site of pathology in retina when systemically administered. By eliminating the need for invasive intravitreal injections and addressing systemic toxicities, Tre-D-Axitinib introduces a novel systemic nanotherapeutic strategy with broad implications for treating ischemic retinopathies.

Export Diabetic retinopathy remains a leading cause of vision impairment worldwide, with early stages characterized by endothelial dysfunction and later stages marked by pathological neovascularization. Although intravitreal antivascular endothelial growth factor (VEGF) therapies are effective in advanced stages, they show limited efficacy in correcting early vascular dysfunction and macular edema. This study explores the therapeutic potential of GYT-088, a metabolite derived from medicinal fungi, in restoring retinal vascular function at noncytotoxic concentrations. In a type 2 diabetic rhesus monkey model that closely resembles human disease, systemic GYT-088 (6 mg/kg) improved macular edema in two of three animals without altering glucose metabolism. Retinal vessel tortuosity and perivascular changes were also reduced. In a murine model of laser-induced neovascularization, intravitreal GYT-088 suppressed pathological angiogenesis in a dose- and time-dependent manner, showing efficacy comparable to the anti-VEGF agent Eylea. Optical coherence tomography imaging further confirmed preservation of retinal layer structure and reduction of hyperreflective foci. In vitro studies revealed that GYT-088 upregulated endothelial nitric oxide (NO) synthase and claudin-5, while suppressing caveolin-1 (CAV1) expression – leading to increase NO production and reinforced endothelial barrier function. Mechanistic experiments confirmed CAV1 as a negative regulator of GYT-088-mediated vascular protection. Together, these findings support GYT-088 as a promising therapeutic candidate for improving nonproliferative and proliferative diabetic retinopathies.

ResumenIntroducción:la retinopatía diabética es una complicación de la diabetes mellitus tipo 2. Un inadecuado control glucémico puede favorecer un estado inflamatorio crónico. El índice neutrófilo-linfocito se ha utilizado como marcador de inflamación sistémica.Objetivo:correlacionar el índice neutrófilo-linfocito con el grado de retinopatía en pacientes con diabetes mellitus tipo 2.Material y métodos:estudio transversal y analítico. Se incluyeron pacientes con diabetes mellitus tipo 2. Se investigó el grado de retinopatía, la cifra de glucosa, la HbA1C y el recuento de neutrófilos y linfocitos para calcular el índice neutrófilo-linfocito. Para comprobar la hipótesis, en el análisis estadístico se utilizaron la prueba exacta de Fisher, U de Mann-Whitney, Kruskal-Wallis y Rho de Spearman. Se consideró significación estadística con una p < 0.05.Resultados:se incluyeron 50 pacientes, con edad de 65 ± 10 años. La media del índice neutrófilo-linfocito fue de 2.5 ± 1.1. El 56% de los pacientes presentó retinopatía no proliferativa leve, el 14% retinopatía no proliferativa moderada y el 30% retinopatía proliferativa de alto riesgo. Se encontró correlación positiva entre el índice neutrófilo-linfocito y el grado de retinopatía, r = 0.532 (p = 0.000).Conclusiones:los pacientes con diabetes mellitus tipo 2 con mayor grado de retinopatía diabética presentaron un índice neutrófilo-linfocito más elevado. Se encontró correlación positiva entre el índice neutrófilo-linfocito y el grado de retinopatía diabética.

To describe the risk management at a university eye hospital after two outbreaks of nosocomial endophthalmitis cases after pars plana vitrectomy. In two series of postoperative endophthalmitis cases after in-house vitrectomy, the basic workflows in direct patient care were evaluated with regard to patient safety. Hygienic microbiological environmental examinations were performed on relevant materials and surfaces. In particular, the direct surgical utensils were inspected with regard to possible bacterial colonisation. Pathogens (Staphylococcus aureus) were detected in 2 of 7 endophthalmitis cases. The S. aureus strains showed no clonality. The procedures were 23 G and 25 G vitrectomies for retinal detachment (3× rhegmatogenous, 1× PVR), subretinal macular hemorrhage (1×) and vitreous haemorrhage for proliferative retinopathy (2×). The duration of surgery was between 20 min and 65 min; the time between initial vitrectomy and the surgery for endophthalmitis was between 2 and 5 days (mean 3.6 days). A silicone oil filling was instilled once during the first operation and otherwise the eye was tamponaded with gas (4×) or air (2×). The surgical teams were heterogeneous; n = 5 surgeons were involved and the initial procedures took place in n = 4 different operating theatres. In all cases, general anaesthesia was applied (6× laryngeal mask, 1× endotracheal intubation). No definitive source of infection was found. The interventions with regard to patient safety were therefore aimed at strengthening compliance with existing measures for preventing infection and adapting work processes. In the acute phase, antibiotics were instilled intraoperatively into the anterior chamber after vitrectomy, contrary to the usual in-house procedure. Other types of intraocular surgery were not affected. The accumulation of in-house endophthalmitis cases is a catastrophic event in an eye clinic and stringent risk management is required to identify the causes. Openness and transparency are essential factors for an adequate workup. This manuscript shows what the individual steps could look like and how the results can be dealt with. The problem of not having found a clear point source for the infections is discussed.