• Diabetic retinopathy
• Glucose transporter-1
• Myelin transcription factor 1
• Parkin
• Synaptotagmin 4

• low vision
• nomogram
• proliferative diabetic retinopathy
• risk prediction model
• vitrectomy

• Humans
• Nomograms
• Prognosis
• Vision, Low
• Vitrectomy
• Retrospective Studies
• Diabetic Retinopathy/diagnosis
• Diabetic Retinopathy/surgery
• Diabetes Mellitus

• Natural Science Foundation of Tianjin City

Diabetes mellitus is a chronic metabolic disorder with increasing prevalence per hour. Cataracts are one of the most common eye complications, and they affect all structures of the eye. The incidence of cataracts is increasing in patients with diabetes by several mechanisms. With the advancement of technology, cataract surgery is now a necessary procedure for diabetic patients. High-risk complications, like diabetic macular oedema, diabetic retinopathy (DR), phakic, postoperative cyst, and postoperative macular oedema, and macular oedema and endophthalmitis following surgery for a pseudocyst, could result in blindness. The importance of preoperative, intraoperative, and postoperative factors cannot be overestimated in managing complications and improving visual outcomes. DR can be a severe problem if it worsens and causes non-proliferative or proliferative DR or if fluid accumulation in the eye is diagnosed as macular oedema. A woman progressing to sight-threatening DR during childbearing age experiences distress and often requires ocular treatment. Diabetes that has been present for a more extended period, as well as more significant hyperglycaemia, hypertension, cardiovascular diseases, and elevated blood pressure, substantially predict the development of DR. Oxidative stress can be caused by hyperglycaemia, irregular metabolic processes, and people with DR developing neurodegeneration. Therefore, controlling postprandial hyperglycaemia is crucial for preventing DR. Femtosecond laser technology, multifocal intraocular lenses, and other surgical innovations are popularly referred to as surgical management; it will be engaged in the coming era to determine whether there will be a continued reduction in the complication of cataract surgery. This article aims to review the correlation of DR with stroke and its screening and to outline the critical management strategies. 

Background: Diabetic retinopathy (DR) is a complication associated with uncontrolled DM. It is a leading preventable cause of visual impairment in the world and a cause of blindness in those under 75 years old in developing countries. We aimed to explore the prevalence and associated risk factors of DR among diabetic patients in the West Bank. Materials and Methods:A quantitative multicenter cross-sectional study was conducted in all West Bank cities. Nearly, 385 patients underwent a comprehensive eye examination in addition to blood and urine tests. A previously validated questionnaire for ocular examination classification was used together with a socio-demographic and past medical history information sheet. Results: The prevalence of all DR in the West Bank was 41.8%. The prevalence of non-proliferative diabetic retinopathy (NPDR) was 50.3% (38.5% for mild NPDR, 10.6% for moderate NPDR and 1.2% for severe NPDR). The prevalence of proliferative diabetic retinopathy (PDR) was 9.9% and 39.7% for diabetic macular edema (DME) (17.4% for mild, 15.5% for moderate and 6.8% for severe DME). The prevalence of vision-threatening PDR and DME was 49.7% for both. In a univariate analysis, DR was significantly associated with body mass index; BMI (p = 0.035), DM duration (p = 0.002), Low-density lipoprotein (LDL) (p = 0.034), glutamic-oxaloacetic transaminase (GOT) level (p = 0.016) andblood urea (BU) (p = 0.044). A multivariate analysis showed a strong significant association between DR andpatients who had DM for 10-19years (adjusted odds ratio; AOR (95%CI); 1.843 (1.05–3.22)), abnormal levels of LDL (AOR (95%CI); 0.50 (0.30–0.83)), abnormal levels of GOT (AOR (95%CI); 0.49 (0.27–0.89)), and overweight (AOR (95%CI); 0.39 (0.19–0.80)). Conclusions: We found that the prevalence of DR in Palestine was higher than the global prevalence. Referral coordination between ophthalmologists and internal physicians is necessary to better follow up with DR patients. An interventional educational program by clinicians and public health professionals is recommended.

Diabetic retinal disease remains one of the most common complications of diabetes mellitus (DM) and a leading cause of preventable blindness. The mainstay of management involves glycemic control, intravitreal, and laser therapy. However, intravitreal therapy commonly requires frequent hospital visits and some patients fail to achieve a significant improvement in vision. Novel and long-acting therapies targeting a range of pathways are warranted, while evidence to support optimal combinations of treatments is currently insufficient. Improved understanding of the molecular pathways involved in pathogenesis is driving the development of therapeutic agents not only targeting visible microvascular disease and metabolic derangements, but also inflammation and accelerated retinal neurodegeneration. This review summarizes the current and emerging treatments of diabetic retinal diseases and provides an insight into the future of managing this important condition.

• angiogenesis
• anti-VEGF
• corticosteroids
• diabetic macular edema
• diabetic retinopathy
• glycemic control
• inflammation
• islet cell transplantation
• pancreatic transplantation

• Angiogenesis Inhibitors/therapeutic use
• Diabetes Complications/drug therapy
• Diabetes Complications/therapy
• Diabetes Mellitus/drug therapy
• Diabetes Mellitus/physiopathology
• Diabetic Retinopathy/drug therapy
• Diabetic Retinopathy/therapy
• Glucocorticoids/therapeutic use
• Glycemic Control/trends
• Humans
• Inflammation/drug therapy
• Intravitreal Injections
• Macular Edema/therapy
• Retina/physiopathology
• Vascular Endothelial Growth Factor A/antagonists & inhibitors

Diabetic retinopathy (DR) is an eye condition that develops after chronically poorly-managed diabetes, and is presently the main cause for blindness on a global scale. Current treatments for DR such as laser photocoagulation, topical injection of corticosteroids, intravitreal injection of anti-vascular endothelial growth factor (VEGF) agents and vitreoretinal surgery are only applicable at the late stages of DR and there are possibilities of significant adverse effects. Moreover, the forms of treatment available for DR are highly invasive to the eyes. Safer and more effective pharmacological treatments are required for DR treatment, in particular at an early stage. In this review, we cover recently investigated promising oral pharmacotherapies, the methods of which are safer, easier to use, patient-friendly and pain-free, in clinical studies. We especially focus on peroxisome proliferator-activator receptor alpha (PPARα) agonists in which experimental evidence suggests PPARα activation may be closely related to the attenuation of vascular damages, including lipid-induced toxicity, inflammation, an excess of free radical generation, endothelial dysfunction and angiogenesis. Furthermore, oral administration of selective peroxisome proliferator-activated receptor alpha modulator (SPPARMα) agonists may induce hepatic fibroblast growth factor 21 expression, indirectly resulting in retinal protection in animal studies. Our review will enable more comprehensive approaches for understanding protective roles of PPARα for the prevention of DR development.

• advanced glycation end products (AGEs)
• antioxidants
• diabetes retinopathy (DR)
• fenofibrate
• fibroblast growth factor 21 (FGF21)
• microglial activation inhibitor
• pemafibrate
• selective peroxisome proliferator-activated receptor alpha modulator (SPPARMα)
• vascular adhesion protein-1 (VAP-1)

Diabetic retinopathy (DR), a major microvascular complication of diabetes, leads to retinal vascular leakage, neuronal dysfunction, and apoptosis within the retina. In this study, we combined STZ with whole-body hypoxia (10% O₂) for quicker induction of early-stage retinopathy in C57BL/6 mice. We also compared the effects of a high glucose condition combined with hypoxia (1% O₂) to a low glucose condition by using retinal pigment epithelial (RPE) cells, which are a crucial component of the outer blood-retinal barrier and the damage is related to retinopathy. In the retina of DM/hypoxic C57BL/6 mice, abnormal a-wave and b-wave activity, yellowish-white spots, hyperfluorescence, and reduced retinal thickness were found using electroretinography (ERG), fundus photography (FP), fundus fluorescein angiography (FFA), and optical coherence tomography (OCT). Shikonin dose-dependently (0.5–50 mg/kg, per os) prevented DM/hypoxia-induced lesions. In eye tissue, administration of shikonin also attenuated DM/hypoxia-induced pre-apoptotic protein BAX expression as well as the production of inflammatory proteins cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS). We also demonstrated that shikonin administration rescues high glucose/hypoxia (1% O₂)-induced inflammation, decreased junction protein expression, and permeability in RPE cells. These results indicate that shikonin treatment may prevent the loss of vision associated with DR.

• cognitive impairment
• renin–angiotensin system
• retinopathy
• stroke
• traumatic brain injury

Diabetic retinopathy, an oculardisease, is governed by systemic as well as local ocular factors. These include primarily chronic levels of blood glucose. Individuals with chronically elevated blood glucose levels have substantially more, and more severe, retinopathy than those with lower blood glucose levels. The relationship of blood glucose to retinopathy is continuous, with no threshold although individuals with hemoglobin A1c levels (a measure of chronic glycemia) <6.5%, generally develop little or no retinopathy. Blood pressure levels have been claimed to influence retinopathy development and progression, but multiple controlled clinical trials of antihypertensive agents in diabetic subjects have produced only weak evidence of benefit from blood pressure lowering on the incidence and progression of diabetic retinopathy. Elevated blood lipids seem to play a role in the progression of retinopathy, and two trials of fenofibrate, a lipid-lowering agent that has not proved effective in preventing cardiovascular disease, have shown benefit in preventing retinopathy progression. The mechanism of this effect may not, however, be directly related to the reduction in blood lipids. Finally, there is strong, but only circumstantial, evidence for a genetic or epigenetic influence on the pathogenesis of diabetic retinopathy. Despite the power of large-scale epidemiologic studies and modern molecular biological and computational techniques, the gene or genes, which predispose or protect against the development and progression of diabetic retinopathy remain elusive.

• Blood Lipids
• Blood Pressure
• Diabetic Retinopathy
• Fenofibrate
• Genetics
• Hemoglobin A1c
• Macular Edema

This work comprehensively reviews the latest treatment options for diabetic macular edema (DME) used in its management and presents further work on the topic. Diabetic retinopathy is an important and increasingly prevalent cause of preventable blindness worldwide. To meet this increasing burden there has recently been a proliferation of pharmacological therapies being used in clinical practice. A variety of medical treatment options now exist for DME. These include non-steroidal anti-inflammatory drugs such as nepafenac, as well as intravitreal steroids like triamcinolone (kenalog). Long-term results up to 7 years after commencing treatment are presented for triamcinolone. Studies are reviewed on the use of dexamethasone (ozurdex) and fluocinolone (Retisert and Iluvien implants) including the FAME studies. A variety of anti-vascular endothelial growth factor (anti-VEGF) agents used in DME are considered in detail including ranibizumab (lucentis) and the RESTORE, RIDE, RISE and Diabetic Retinopathy Clinical Research Network (DRCR.net) studies. Bevacizumab (avastin) and pegaptinib (macugen) are also considered. The use of aflibercept (eylea) is reviewed including the significance of the DA VINCI, VISTA-DME, VIVID-DME and the DRCR.net studies which have recently suggested potentially greater efficacy when treating DME for aflibercept in patients with more severely reduced visual acuity at baseline. Evidence for the anti-VEGF agent bevasiranib is also considered. Studies of anti-tumour necrosis factor agents like infliximab are reviewed. So are studies of other agents targeting inflammation including minocycline, rapamycin (sirolimus) and protein kinase C inhibitors such as midostaurin and ruboxistaurin. The protein kinase C β inhibitor Diabetic Macular Edema Study is considered. Other agents which have been suggested for DME are discussed including cyclo-oxygenase-2 inhibitors like celecoxib, phospholipase A2 inhibitors, recombinant erythropoietin, and monoclonal anti-interleukin antibodies such as canakinumab. The management of DME in a variety of clinical scenarios is also discussed - in newly diagnosed DME, refractory DME including after macular laser, and postoperatively after intraocular surgery. Results of long-term intravitreal triamcinolone for DME administered up to seven years after commencing treatment are considered in the context of the niche roles available for such agents in modern management of DME. This is alongside more widely used treatments available to the practitioner such as anti-VEGF agents like aflibercept (Eylea) and ranibizumab (Lucentis) which at present are the mainstay of pharmacological treatment of DME.

• Diabetic macular edema
• Diabetic macular oedema
• Triamcinolone
• Anti-vascular endothelial growth factor agents
• Steroids
• Non-steroidal anti-inflammatory drugs
• Biologicals
• Protein kinase C inhibitors

• Diabetes related complications
• amputations
• end stage renal disease
• myocardial infarction
• nephropathy
• neuropathy
• retinopathy
• stroke