Plasma levels of E-selectin are associated with retinopathy in sickle cell disease.

BACKGROUND: The vascular endothelium is markedly disrupted in sickle cell disease (SCD) and is the converging cascade of the complex pathophysiologic processes linked to sickle cell vasculopathy. Circulating endothelial activation and/or apoptotic markers may reflect this endothelial activation/damage that contributes to the pathophysiology of the SCD vascular complications. METHODS: Plasmatic levels of circulating endothelial cells (CECs), E-selectin, progenitor's endothelial cells (EPCs), and circulating extracellular vesicles (EVs) were evaluated in 50 SCD patients, 16 with vasculopathy. The association between these markers and the occurrence of disease-related microvascular injuries of the eye (retinopathy), kidney (nephropathy), and skin (chronic active ulcers) was explored. RESULTS: Among the endothelial activation markers studied, only higher plasma levels of E-selectin were found in SCD patients with vasculopathy (p = .015). Increased E-selectin levels were associated with retinopathy (p < .001) but not with nephropathy or leg ulcers. All patients, at steady state, with or without vasculopathy, did not display a high count of CEC and EPC, markers of endothelial injury and repair. We did not show any significant differences in EVs levels between vasculopathy and not vasculopathy SCD patients. CONCLUSIONS: Further studies will be required to determine whether the E-selectin could be used as an early biomarker of retinopathy sickle cell development.

Plasma lipid levels and risk of retinal vascular occlusion: A genetic study using Mendelian randomization.

The causal effects of plasma lipid levels and the risk of retinal vascular occlusion (RVO) have not been clearly identified, especially for high-density lipoprotein-cholesterol (HDL-C) and low-density lipoprotein-cholesterol (LDL-C). Here, we try to identify these causal risk factors using a two-sample Mendelian randomization (MR) analysis. Single nucleotide polymorphisms (SNPs) were chosen as instrumental variables (IVs). We obtained genetic variants associated with lipid exposure at the genome-wide significance (P<5×10-8) level from a meta-analysis of GWAS from the Global Lipids Genetics Consortium (GLGC) based on 188,577 individuals of mostly European ancestry for MR analyses. Meanwhile, we used lipid GWAS from UK Biobank (UKB) with a sample size of 115,078 individuals as a supplement. We obtained genetic predictors of RVO from a FinnGen biobank study. We conducted both univariable and multivariable MR (MVMR) analyses to identify the causal effects of RVO. Although inverse variance weighted (IVW) was the primary method used for MR analyses, MR-Egger and weighted-median methods were used as supplements to IVW. We determined the heterogeneity of IVs using Cochrane's Q test and I2 , and used the MR-Egger intercept and MR-PRESSO Global test to detect horizontal pleiotropy. A leave-one-out sensitivity analysis was conducted by removing a single variant from the analysis. Genetically predicted increased HDL-C level was associated with decreased risk of RVO from GLGC [OR=0.806; 95% CI=(0.659, 0.986); P=0.036], which was consistent with UKB results [OR=0.766; 95% CI=(0.635, 0.925); P=0.005]. MVMR analysis for plasma lipids [adjusted OR=0.639; 95% CI=(0.411, 0.992); P=0.046] or diabetes [adjusted OR=0.81; 95% CI=(0.67, 0.979); P=0.029] suggested that low HDL-C may be an independent risk factor for RVO. However, there was no evidence to support a causal association between LDL-C {GLGC [adjusted OR=1.015; 95% CI=(0.408, 2.523); P=0.975], UKB [OR=1.115; 95% CI=(0.884, 1.407); P=0.359]}, total cholesterol {GLGC [adjusted OR=0.904; 95% CI=(0.307, 2.659); P=0.854], UKB [OR=1.047; 95% CI=(0.816, 1.344); P=0.716]} or triglycerides {GLGC [OR=1.103; 95% CI=(0.883, 1.378); P=0.385], UKB [OR=1.003; 95% CI=(0.827, 1.217); P=0.098]} and RVO. Using two-sample MR analysis, our study suggested that dyslipidemia was a risk factor for RVO. Furthermore, our results indicated that a low HDL-C level may be an independent risk factor for RVO, suggesting that controlling HDL-C level may be effective in RVO development.

Retinal oxygen saturation is associated with HbA1c but not with short-term diabetes control, internal environment, smoking and mild retinopathy - ROXINEGLYD study.

PURPOSE: Purpose of this prospective uncontrolled single-centre pilot study was to find an association of retinal oxygen saturation (SatO2 ) with acid-base balance (ABB), carboxyhaemoglobin concentration, current plasma glucose concentration (PG), mean PG and PG variability over the last 72 hr, haemoglobin A1c (HbA1c), and other conditions. METHODS: Forty-one adults (17 men) with type 1 (N = 14) or type 2 (N = 27) diabetes mellitus, age 48.6 ± 13.5 years, diabetes duration 9 (0.1-36) years, BMI 29.4 ± 6.3 kg/m2 , and HbA1c 52 ± 12.7 mmol/mol completed the study. The 4-day study comprised two visits (Day l, Day 4) including 72 hr of continuous glucose monitoring (CGM) by iPro® 2 Professional CGM (Medtronic, MiniMed, Inc., Northridge, CA, USA). Retinal oximeter Oxymap T1 (Oxymap ehf., Reykjavik, Iceland) was used to assess SatO2 . RESULTS: Wilcoxon signed-rank test showed no SatO2 difference between eyes and visits. Spearman's correlation analysis revealed a significant correlation between arterial SatO2 and PG variability in type 2 diabetes mellitus, a positive correlation of venous SatO2 with HbA1c and with finger pulse oximetry. However, no correlation of SatO2 with ABB, carboxyhaemoglobin, current PG, mean PG over the 72 hr, age, diabetes duration, BMI, lipoproteinaemia, body temperature, systolic and diastolic blood pressure, heart rate, central retinal thickness and retinal nerve fibre layer thickness was found. CONCLUSION: This study confirmed the association of venous SatO2 with long-term but not with short-term diabetes control, ABB and other conditions. The increased SatO2 and questionable impact of PG variability on retinal SatO2 is a research challenge.

Carotenoid status in type 2 diabetes patients with and without retinopathy.

Diabetic retinopathy (DR) is one of the leading causes of blindness. Carotenoids are plant-derived pigments required for general health and particularly for vision. In this study, we evaluated the dietary intake and blood carotenoid levels of type 2 diabetes (T2D) patients with and without DR. A cross-sectional case-control study was conducted among 151 age-matched controls and 344 T2D patients, of which 194 had DR and 150 had no DR (NDR). After a complete ophthalmic examination, the demographic, anthropometric and clinical profiles were obtained. Carotenoids in the plasma were measured by HPLC and dietary intakes were obtained using a food frequency questionnaire. The mean plasma levels of carotenoids (except γ-carotene) were significantly lower in the DR group compared to the Control and NDR groups. The dietary intakes of zeaxanthin, lycopene, α-carotene and ß-carotene were significantly lower in the NDR group compared to the Control group, and were further lower in the DR group compared to the NDR group. Plasma carotenoid levels were significantly inversely associated with the duration of diabetes, RBS and HbA1c but positively associated with HDL. This study demonstrated decreased plasma levels and lower dietary intakes of carotenoids in DR subjects.

Ocular Findings Associated with Hypoparathyroidism.

Purpose: To determine the corneal and retinal changes associated with serum calcium, phosphorus and parathyroid hormone (PTH) levels in patients with hypoparathyroidism.Methods: Patients who were under follow-up for hypoparathyroidism in the endocrinology department were included in the study. All participants underwent a complete ophthalmological examination. Moreover, central corneal thickness (CCT), anterior chamber depth (ACD), retinal nerve fiber layer (RNFL) thickness, ganglion cell layer (GCL) thickness were recorded. Serum biochemical parameters were recorded.Results: In a total of 75 patients (35 in the hypoparathyroidism group and 40 in the healthy control group) were included in this study. Central corneal thickness (519.95 ± 33.21 vs. 539.10 ± 32.96, p: 0.001) and RNFL (105.10 ± 11.89 vs. 113.56 ± 9.54, p: 0.005) were significantly thinner and ACD was significantly deeper in the hypoparathyroidism group.Conclusion: We determined thinner CCT and RNFL values in patients with hypoparathyroidism related to serum calcium levels together with a significant deepness in ACD.

Circulating MicroRNA-15a Associates With Retinal Damage in Patients With Early Stage Type 2 Diabetes.

Circulating microRNAs are potential biomarkers of type 2 diabetes mellitus (T2DM) and related complications. Here, we investigated the association of microRNA-15a with early retinal damage in T2DM. A cohort of untreated subjects screened for intermediate/high risk of T2DM, according to a score assessment questionnaire, and then recognized to have a normal (NGT) or impaired (IGT) glucose tolerance or T2DM was studied. The thickness of the ganglion cell complex (GCC), an early marker of retinal degeneration anteceding overt retinopathy was assessed by Optical Coherence Tomography. Total and extracellular vesicles (EV)-associated microRNA-15a quantity was measured in plasma by real time PCR. MicroRNA-15a level was significantly higher in subjects with IGT and T2DM compared with NGT. MicroRNA-15a abundance was correlated to body mass index and classical diabetes biomarkers, including fasting glucose, HbA1c, insulinemia, and HOMA-IR. Moreover, GCC thickness was significantly reduced in IGT and T2DM subjects compared with NGT controls. Importantly, total microRNA-15a correlated with GCC in IGT subjects, while in T2DM subjects, EV-microRNA-15a negatively correlated with GCC, suggesting that microRNA-15a may monitor initial retinal damage. The assessment of plasma microRNA-15a may help refining risk assessment and secondary prevention in patients with preclinical T2DM.

Impact of Glucose Level on Micro- and Macrovascular Disease in the General Population: A Mendelian Randomization Study.

OBJECTIVE: To evaluate whether high glucose levels in the normoglycemic range and higher have a causal genetic effect on risk of retinopathy, neuropathy, nephropathy, chronic kidney disease (CKD), peripheral arterial disease (PAD), and myocardial infarction (MI; positive control) in the general population. RESEARCH DESIGN AND METHODS: This study applied observational and one-sample Mendelian randomization (MR) analyses to individual-level data from 117,193 Danish individuals, and validation by two-sample MR analyses on summary-level data from 133,010 individuals from the Meta-Analyses of Glucose and Insulin-Related Traits Consortium (MAGIC), 117,165 from the CKDGen Consortium, and 452,264 from the UK Biobank. RESULTS: Observationally, glucose levels in the normoglycemic range and higher were associated with high risks of retinopathy, neuropathy, diabetic nephropathy, PAD, and MI (all P for trend <0.001). In genetic causal analyses, the risk ratio for a 1 mmol/L higher glucose level was 2.01 (95% CI 1.18-3.41) for retinopathy, 2.15 (1.38-3.35) for neuropathy, 1.58 (1.04-2.40) for diabetic nephropathy, 0.97 (0.84-1.12) for estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2, 1.19 (0.90-1.58) for PAD, and 1.49 (1.02-2.17) for MI. Summary-level data from the MAGIC, the CKDGen Consortium, and the UK Biobank gave a genetic risk ratio of 4.55 (95% CI 2.26-9.15) for retinopathy, 1.48 (0.83-2.66) for peripheral neuropathy, 0.98 (0.94-1.01) for eGFR <60 mL/min/1.73 m2, and 1.23 (0.57-2.67) for PAD per 1 mmol/L higher glucose level. CONCLUSIONS: Glucose levels in the normoglycemic range and higher were prospectively associated with a high risk of retinopathy, neuropathy, diabetic nephropathy, eGFR <60 mL/min/1.73 m2, PAD, and MI. These associations were confirmed in genetic causal analyses for retinopathy, neuropathy, diabetic nephropathy, and MI, but they could not be confirmed for PAD and seemed to be refuted for eGFR <60 mL/min/1.73 m2.

Retinopathy in patient with AC hemoglobinopathy / Retinopatia em pacientes com hemoglobinopatia AC

Abstract Hemoglobin C is the second most frequent Hb variant in Brazil and the world. Hemoglobin C trait is described as a benign and asymptomatic condition. There is little information in the literature about the association of retinal vascular disease and the presence of hemoglobin AC, being this information restricted to a few case reports. This case report describes a 26-year-old female patient with hemoglobin C trait. She presents areas of non-perfusion and arteriovenous shunts in the retinal temporal periphery of the left eye, like changes in Goldberg's stage II of proliferative sickle retinopathy. After three years of follow-up, the patient exhibits the same the alteration in right eye as well.

Resumo A hemoglobina C é a segunda variante de hemoglobina mais comum no Brasil e no mundo. O traço C é descrito como uma condição benigna e assintomática. Há pouca informação na literatura sobre a associação de doença vascular retiniana e a presença de hemoglobina AC, sendo esta informação restrita a alguns poucos relatos de casos. Este relato de caso descreve uma paciente do gênero feminino de 26 anos de idade com traço C. Ela apresenta áreas de não perfusão e shunts artério-venosos na periferia temporal da retina do olho esquerdo, similar ao estágio II de Goldberg de retinopatia proliferativa falciforme. Após três anos de acompanhamento, a paciente apresentou a mesma alteração também em olho direito.

Life Style Intervention Improves Retinopathy Status-The Finnish Diabetes Prevention Study.

The aim of the study was to find out whether participation in earlier intervention had an effect on the occurrence of retinopathy in study participants. We also examined risk factors (age, sex, weight, fasting and 2 h glucose, fasting insulin, blood pressure, serum lipids) for early retinal changes. The study included 522 individuals (mean 55 years old, range 40-64 years) with impaired glucose tolerance who were randomized into intervention (weight loss, healthy diet, and physical activity, N = 265) and control groups (N = 257). Intervention lasted for median of four years in 1993-2000, after which annual follow-up visits at study clinics were conducted. In the years 2002-2006 (at least five years after stopping intervention), fundus photography was offered for all study participants in four of five study clinics. Photographs were assessed by two experienced ophthalmologists (A.A. and K.K.), masked for the group assignment. After exclusion of poor quality photographs, the data of 211 individuals (N = 113 for intervention and N = 98 for control group) were included in the present study. The occurrence of microaneurysms was significantly higher in the control (37/98, 38%) than in the intervention group (27/113, 24%; p = 0.029). In the model, including age, sex, diabetes diagnosis before the retinal assessment, body mass index (BMI), and treatment group, the odds ratio for microaneurysms was markedly lower in intervention group (OR 0.52; 0.28-0.97, p = 0.039). The only risk factor that predicted the occurrence of microaneurysms was serum triglycerides at baseline (mean ± SD 1.9 ± 0.9 vs. 1.6 ± 0.7, mmol/L, with and without microaneurysms, respectively, p = 0.003). Triglycerides associated with decreased microaneurysms in regression analysis for age, sex, fasting glucose, and intervention group (OR 1.92, p = 0.018). Lifestyle intervention in overweight and obese individuals with impaired glucose tolerance showed decreased occurrence of retinal microaneurysms. Elevated serum triglycerides were associated to the development of early diabetic microangiopathy.

Detection of serum anti-retinal antibodies in the Chinese patients with presumed autoimmune retinopathy.

PURPOSE: To explore the presence of serum anti-retinal antibodies (ARAs) in the Chinese patients with presumed autoimmune retinopathy (AIR). METHODS: Twenty-three Chinese patients with presumed AIR, disease controls including 40 RP patients, 22 bilateral uveitis patients, 18 acute zonal outer occult retinopathy (AZOOR) patients, and 30 healthy donors were included. Serum samples of all the subjects were obtained and analyzed for the presence of four ARAs including recoverin, α-enolase, carbonic anhydraseII (CAII), and collapsin response-mediated protein (CRMP)-5 by Western bolt assay. RESULTS: ARAs were present in the serum of either presumed AIR patients, disease control, or healthy donors. One or more ARAs were present in the 78.2% of presumed AIR while they were indicated in the 35.0% of RP patients (p < 0.01) and 33.3% of healthy donors (p < 0.01). The prevalence of ARAs in the bilateral uveitis and AZOOR was 63.3% and 100% respectively. Positive rate of α-enolase antibody present in the presumed AIR, disease control, and healthy donors was 73.9%, 47.5%, and 33.3% respectively. Positive rate of CAII antibody present above groups was 52.1%, 50%, and 33.3% respectively. Recoverin antibody seemed to be specifically present in the serum of patients with cancer-associated retinopathy. CONCLUSION: Presence of serum ARAs including recoverin, α-enolase, CAII, or CRMP-5 in the Chinese patients with presumed AIR occurred significantly more often than RP patients and healthy donors. Seropositivity of ARAs had diagnostic value for the presumed AIR but mere presence was not sufficient for the diagnosis due to identification of them in the healthy controls and other retinal diseases.

Lipemia retinalis in a 27 day old neonate: A case report.

Familial combined hyperlipidemia, which presents as hypercholesterolemia or hypertriglyceridemia, is the commonest form of genetic hyperlipidemia and is associated with premature coronary artery disease. This is a rare case report of a 27 day-old neonate born out of a third-degree consanguineous marriage, with grade III lipemia retinalis secondary to familial-combined hyperlipidemia.

The impact of IGF-I, puberty and obesity on early retinopathy in children: a cross-sectional study.

BACKGROUND: Childhood obesity has been correlated with coronary heart disease, but the correlation with microvascular disease remains unclear. The retinal microcirculation is affected early in the process of atherosclerosis and it offers the opportunity to indirectly study the effects of obesity on small brain vessels. Insulin-like growth factor 1 (IGF-I) is involved in angiogenesis and it has a crucial role in retinal vascularization. METHODS: A single-centre cross-sectional study was performed in 268 children and adolescents (116 males; mean age 13.03 ± 1.9 years,) with overweight/obesity, in order to identify risk factors for early retinopathy. RESULTS: Nine patients (3.3%) showed signs of retinopathy, defined as arteriovenous crossings and/or papilledema. Body mass index and fat mass, analysed by Dual X-ray Absorptiometry, were not different in patients with or without retinopathy. Patients with retinopathy were pubertal and showed higher waist circumference (107.78 ± 15.83 versus 99.46 ± 10.85 cm; p: 0.027), waist circumference/height ratio (0.66 ± 0.07 versus 0.62 ± 0.05; p: 0.04) and IGF-I SDS (0.03 ± 1.3 versus - 0.66 ± 0.9; p: 0.04). Multivariate analysis (after correction for sex, age, family history of type 2 diabetes mellitus, obesity, cardiovascular disease, hypertension and dyslipidaemia) showed that waist circumference/height ratio and IGF-I SDS were the only variables independently correlated with the presence of retinopathy. CONCLUSIONS: Retinal vascular changes may become evident as an early complication of overweight and obesity, even during childhood and adolescence. Relatively high levels of IGF-I during this phase may act as an additional risk factor for microvascular damage. The screening for retinopathy should be proposed to all children and adolescents with overweight/obesity.

Combination of circulating microRNAs as indicators of specific targets of retinal toxicity in rats.

Circulating miR-96-5p, -124-3p, and 183-5p have been reported as safety biomarkers for retinal toxicity. In the present research, 5 serum microRNAs (miRNAs), which are highly specific to and abundant in the retina, including the 3 miRNAs previously mentioned, were assessed in 3 different models of retinal toxicity. Distinct types of retinal lesions were induced in rats by a single dose of N-methyl-N-nitrosourea (MNU: 10, 30, and 50 mg/kg, i.p.), N-methyl-d-aspartate (NMDA: 200 nmol/eye, intravitreal injection), or sodium iodate (NaIO3: 30 mg/kg, i.v.). Time-course change of serum miRNAs was evaluated by RT-PCR for up to 1 week after administration. Ophthalmologic and histologic examinations and electroretinogram recording were also performed. MNU at 50 mg/kg induced photoreceptor cell death, with elevation in serum miR-96-5p, -124-3p, and -183-5p levels. NMDA induced retinal ganglion and inner nuclear layer cell death, with elevation in serum miR-124-3p. In both models, serum miRNA elevations occurred in parallel with the onset of neuroretinal cell death and retinal dysfunction. NaIO3 induced retinal pigment epithelial cell death without changes in neuroretinal cell or serum miRNAs. In the present research, circulating miR-124-3p was elevated in a case of retinal ganglion and inner nuclear layer cell death as well as photoreceptor cell death. Our data suggest that different patterns of circulating miRNA elevations correspond to death of a specific neuroretinal cell. A miRNA panel consisting of miR-96-5p, -124-3p, and -183-5p may be used as a biomarker to detect neuroretinal cell death and identify the specific target cell.

Elevated fetal haemoglobin levels are associated with decreased incidence of retinopathy in adults with sickle cell disease.

Among the many vascular complications of sickle cell disease (SCD), retinopathy is the most prevalent and represents a leading cause of blindness. Hydroxycarbamide therapy ameliorates many symptoms of SCD, and high fetal haemoglobin (HbF) levels have been shown to protect against the development of retinopathy in children with HbSS. Its effect on adults with SCD, who are at a much higher risk of developing retinopathy, has not been studied. We aimed to investigate the effect of hydroxycarbamide use and HbF level on sickle cell retinopathy development in adults. We performed a retrospective cross-sectional study and collected demographics, comorbidities, and ocular and haematological data from 300 adult sickle cell subjects examined at the Henkind Eye Institute at Montefiore Medical Center during a 5-year period, from October 2012 to November 2017. The cohort was comprised mainly of Black and Hispanic subjects with all SCD genotypes, aged 18-71 years. Results show that in HbSS patients treated with hydroxycarbamide, those with retinopathy had significantly lower HbF levels compared to patients without retinopathy (P = 0·018). Our study identified the optimal HbF cut-off point for retinopathy protection to be 14·87%. Thus, a HbF level of 15% appears to be the threshold above which the odds for developing retinopathy in SS patients are reduced by 50%.

Anti-angiogenic effects of valproic acid in a mouse model of oxygen-induced retinopathy.

Pathological retinal angiogenesis contributes to the pathogenesis of several ocular diseases. Valproic acid, a widely used antiepileptic drug, exerts anti-angiogenic effects by inhibiting histone deacetylase (HDAC). Herein, we investigated the effects of valproic acid and vorinostat, a HDAC inhibitor, on pathological retinal angiogenesis in mice with oxygen-induced retinopathy (OIR). OIR was induced in neonatal mice by exposure to 80% oxygen from postnatal day (P) 7 to P10 and to atmospheric oxygen from P10 to P15. Mice were subcutaneously injected with valproic acid, vorinostat, or vehicle once a day from P10 to P14. At P15, retinal neovascular tufts and vascular growth in the central avascular zone were observed in mice with OIR. Additionally, immunoreactivity for phosphorylated ribosomal protein S6 (pS6), an indicator of mammalian target of rapamycin (mTOR) activity, was detected in the neovascular tufts. Both valproic acid and vorinostat reduced the formation of retinal neovascular tuft without affecting vascular growth in the central avascular zone. Valproic acid reduced the pS6 immunoreactivity in neovascular tufts. Given that vascular endothelial growth factor (VEGF) activates mTOR-dependent pathways in proliferating endothelial cells of the neonatal mouse retina, these results suggest that valproic acid suppresses pathological retinal angiogenesis by interrupting VEGF-mTOR pathways.

Anomalous coagulation factors in non-arteritic anterior ischemic optic neuropathy with central retinal vein occlusion: A case report.

RATIONALE: Non-arteritic anterior ischemic optic neuropathy (NAION) is characterized by sudden, painless visual loss and optic disc edema. NAION occurs mainly in the presence of cardiovascular disease and hypercoagulability, mainly in patients over 50 years of age. We experienced a case of NAION associated with central retinal vein occlusion (CRVO) in a young man with no underlying disease. PATIENT CONCERNS: A 46-year-old man was referred to our clinic following a sudden loss of vision in his right eye. The patient exhibited no underlying disease and reported no ongoing medication. Significant visual loss and visual disturbance of the right eye were observed. The pupil of the right eye was enlarged and an afferent pupillary defect was observed. On fundus examination, retinal hemorrhage was observed in the peripheral retina; macular edema was observed in optical coherence tomography analysis. However, optic disc edema was not evident. No abnormal findings were found in routine blood tests for hypercoagulability. After 3 days of steroid intravenous injection, macular edema disappeared and visual acuity was improved, but optic disc edema began to appear. One week later, optic disc edema was evident and visual acuity was significantly reduced; thus, the patient was diagnosed with NAION. In fluorescein angiography, peripheral retinal ischemia was observed, suggesting that CRVO was complicated. Blood tests, including analysis of coagulation factors, were performed again, showing that coagulation factors IX and XI were increased. DIAGNOSES: Anomalous coagulation factors in non-arteritic anterior ischemic optic neuropathy with central retinal vein occlusion. INTERVENTIONS: Systemic steroids were administered. OUTCOMES: One month later, optic disc edema and retinal hemorrhage gradually diminished and eventually disappeared; however, visual acuity did not recover. CONCLUSION: In young patients without underlying disease, cases of NAION require careful screening for coagulation disorders. Even if there is no abnormality in the test for routine coagulation status, it may be necessary to confirm a coagulation defect through an additional coagulation factor assay.

Quantitative evaluation of early retinal changes in children with type 1 diabetes mellitus without retinopathy.

BACKGROUND: To investigate whether abnormal glucose metabolism and duration of diabetes mellitus (DM) caused the thinning in retinal layers in children with type 1 DM without retinopathy by using spectral domain optical coherence tomography (SD-OCT) and to compare the results obtained with those in healthy children. METHODS: This cross-sectional prospective study included 73 patients with type 1 DM (DM group) and 62 age-matched control subjects (control group). The duration of DM and the glycosylated haemoglobin (HbA1c) levels of the diabetic children were recorded. Macular and peripapillary retinal nerve fibre layer (RNFL) thickness measurements obtained by SD-OCT were compared. RESULTS: There were significant differences in the mean values of the temporal inner, temporal outer and inferior outer macular thickness measurements between the groups (p = 0.031, p = 0.028 and p = 0.039, respectively). Moreover, the children with type 1 DM showed significantly thinner global, temporal superior and nasal inferior RNFL thickness measurements compared to the controls (p = 0.035, p = 0.022 and p = 0.034, respectively). Additionally, both the mean duration of DM and the mean HbA1c values were inversely and statistically significantly correlated with the mean temporal outer macular thickness and global RNFL thickness measurements in the DM group. CONCLUSIONS: Retinal neural changes, which can be shown by SD-OCT, may be present in diabetic eyes even before clinically detectable retinal vasculopathy. Macular and RNFL thickness measurements might be useful indicators for early detection of diabetic retinopathy in the future.