Diabetic retinopathy is a microangiopathy of the retina that leads to capillary occlusion and leakage. 9 Histologic examination of the choroid of diabetic eyes showed an increase in tortuosity, focal narrowing or dilation of ves- sels, presence of sinus-like structures between the choroi- dal lobules, capillary dropout, and focal scarring. 10 Diabetic choroidopathy was also documented using indo- cyanine green angiography. 11 Reliable choroidalthickness measurement can be performed using OCT utilizing dif- ferent techniques to compensate for decreased signal strength posterior to the retinal pigment epithelium to visualize of the sclero-choroidal interface. 1 – 6
Diabetic retinopathy is the most common microvascular complication of diabetes melli- tus and occurs secondary to metabolic aberrations and retinal ischemia characteristic of diabetes mellitus. 1 Proliferative diabetic retinopathy (PDR) and diabeticmacularedema (DME) are the primary pathologies responsible for vision loss in diabetic eye disease. Panretinal photocoagulation (PRP) is the standard of care for prevention of vision loss in PDR. 2 This treatment ablates neurons in the peripheral retina to decrease metabolic demand in the peripheral retina and facilitate oxygen and nutrient supply to the inner retina, alleviating the ischemia that drives neovascularization in PDR. However, PRP may induce macularedema (ME) due to retinal in ﬂ ammation and increased vascular permeability. 3 This PRP-induced ME may cause temporary or permanent vision loss. 2
Methods: Eighty-four (29 naïve and 55 previously treated) eyes were included in this retrospective study. For each patient, the BCVA [Early Treatment Diabetic Retinopathy Study (ETDRS) charts] and macularthickness on optical coherence tomography (OCT) at baseline visit and within the 2nd, 4th, and 6th months of follow-up were obtained. The main outcomes measurements were the mean change in BCVA and in CMT with respect to the baseline value. The percentage of patients gaining ≥ 5 letters and ≥ 10 letters in BCVA was also analyzed. Results: A total of 84 eyes, 29 (34.5%) naïve and 55 (65.5%) non-naïve, from 69 patients were included in the study. BCVA at baseline was 58.8 (16.4) and 61.8 (11.6) in naïve and refractory patients, respectively, p = 0.4513. At every visit, BCVA significantly improved from baseline in naïve and non-naïve eyes ( p < 0.0001 and p = 0.0003, respectively; Friedman rank sum test). At baseline, the mean CMT was 466.2 (189.7) μ m and 448.1 (110.7) μ m in the naïve and non-naïve patients, respectively ( p = 0.5830); and decreased to 339.3 (92.5) μ m and 357.5 (79.1) μ m, respectively ( p = 0.0004 and p < 0.0001, respectively, Wilcoxon signed-rank test). The proportion of patients gaining ≥ 10 letters was significantly greater in the naïve group, p = 0.0199. Conclusion: The intravitreal dexamethasone implant (Ozurdex) is effective for the treatment of diabeticmacularedema, even in refractory cases that have failed to respond to previous therapies.
Diabeticmacularedema (DME) is a major cause of visual impairment in diabetic patients with diabetic retinopathy (DR) in economically developed societies. 1,2 Vascular endothelial growth factor (VEGF) is an important angiogenic factor and plays an important role in the pathogenesis of DME; therefore, anti-VEGF treatments for DME have been developed. 3,4 Currently, there are many anti-VEGF drugs, such as bevacizumab, ranibizumab, and a ﬂ ibercept, that show some slight differences in terms of their ability to block VEGF isoforms; the ef ﬁ cacy of these drugs is similar in DME patients, causing relative vision improvements. 5,6 Conbercept is a fusion protein comprising extracellular domain-2 of vascular endothelial growth factor receptor (VEGFR)-1 and extracellular domain-3 and 4 of VEGFR-2. 7 Conbercept
Purpose: Estimate effects of ranibizumab on diabetic retinopathy (DR) severity in US Hispanic and non-Hispanic white persons with center-involved diabeticmacularedema (DME) causing vision impairment for whom ranibizumab treatment would be considered. Patients and Methods: This model simulated DR severity outcomes over 2 years in the better-seeing eye using US census, National Health and Nutrition Examination Survey, Wisconsin Epidemiologic Study of Diabetic Retinopathy, and Los Angeles Latino Eye Study data. Baseline DR severity estimated from Diabetic Retinopathy Clinical Research Network trial data. Changes in DR severity after 2 years, with/without monthly ranibizumab (0.3 or 0.5 mg), were estimated from Phase III clinical trial data (RIDE/RISE) using a 2-dimensional Monte Carlo simulation model. Number of patients over a 2-year period for whom 1) DR severity worsening was avoided, 2) DR severity improved, and 3) selected clinical events related to proliferative DR (PDR) occurred, was estimated.
Abstract: The aim of this article is to provide an overview of characteristics and principles of use of dexamethasone implant in patients with diabeticmacularedema (DME). The condensed information about patient selection, dosing, and postinjection management is provided to make the clinician ’ s decisions easier in real-life practice. DME is a common complication of diabetes and the leading cause of visual loss in the working-age population. In ﬂ ammation plays an important role in the pathogenesis of DME. The breakdown of the blood – retinal barrier involves the expression of in ﬂ ammatory cytokines and growth factors, including vascular endothelial growth factor (VEGF). Steroids have proved to be effective in the treatment of DME by blocking the production of VEGF and other in ﬂ ammatory cytokines, by inhibiting leukostasis, and by enhancing the barrier function of vascular endothelial cell tight junctions. Dexamethasone intravitreal implant has demonstrated ef ﬁ cacy in the treatment of DME resistant to anti-VEGF therapy and in vitrectomized eyes. Data from clinical trials suggest that dexamethasone implant can be considered as ﬁ rst-line treatment in pseudophakic eyes. Dexamethasone implant is also the ﬁ rst-line therapy in patients not suited for anti-VEGF therapy, pregnant women, and patients unable to return for frequent monitoring. It has been shown that the maximum effect of dexamethasone implant on visual gain and retinal thickness occurs approximately 2 months after injection. Various treatment regimens are used in real-life situations, and reported reinjec- tion intervals were usually <6 months. The number of retreatments needed decreased over time. Treatment algorithms should be personalized. Postinjection management and follow-up should consider potential adverse events such as intraocular pressure elevation and cataract.
Abstract: Here we reported a rare case of the implantation of a dexamethasone intravitreal implant (DEX) in which decreased retinal vessel density (VD) was found by optical coherence tomography angiography (OCTA). A 74-year-old male with diabetes mellitus presented with bilateral macularedema. The best-corrected visual acuity (BCVA) was 0.6 in the right eye. Diabeticmacularedema (DME) was diagnosed. A DEX for the right eye was planned, and the preoperative evaluation showed a super ﬁ cial VD of 48.74 percent, a deep VD of 53.12 percent, and a foveal avascular zone (FAZ) 0.165 mm 2 in size by OCTA. The BCVA in the right eye recovered to 0.8, and a notably lower super ﬁ cial VD of 45.97 percent and a deep VD of 45.40 percent were observed with an enlarged FAZ of 0.294 mm 2 one month postoperatively. Moreover, BCVA in the right eye was maintained at 0.8, while further reductions in both super ﬁ cial (40.07 percent) and deep (40.91 percent) VD were noted with a FAZ measured at 0.305 mm 2 two months postoperatively. In conclusion, retinal super ﬁ cial and deep VD decreased, while the FAZ increased, after the implantation of the DEX in a patient with DME.
MA formation in the posterior pole may be an initial and visible sign of increasing diabetic stress in the macula area of patients with DME. In fact, the results of recent studies indicated that a high MA turnover rate, ie, sum of MA formation and disappearance, is a high risk factor for the development of clinically significant macularedema. In addition, MA formation rates may be a predictive marker for the progression of macularedema. 13,14
The injection of the drug ziv-aflibercept and regular OCT scans were made free of charge. In both groups, patients were treated at monthly intervals until maximal resolution of intraretinal edema by OCT. If, on follow-up recurrent intraretinal fluid was noted, monthly ziv-aflibercept treatment was resumed until stable OCT parameters were reached. The injection regimen (in the injection-only group) followed the protocol for DME which was 5 initial monthly injec- tions then treat and extend by 2 weeks based on OCT. The injection regimen in the PPRP group was initial injection concomitant with the laser and then monthly recall for OCT or else whenever the patient can return at the earliest possible appointment (within 2 months period).
The average level of BCVA letter score improvement over all monthly post-baseline assessments from month 1 to month 12 was shown in Fig. 1. One month after treat- ment, statistically significant (p < 0.001) improvements in the BCVA letter score were observed for both the IVC group (6.5 ± 3.3) and the IVR group (6.6 ± 2.8). These im- provements were continued up to month 3 and were sus- tained until the last assessment time point at month 12 (Fig. 1). At month 12, the improvement in the BCVA let- ter score was 9.3 ± 5.2 in the IVC group (P < 0.001) and 8.9 ± 4.4 in the IVR group (P < 0.001). There was no sta- tistically significant difference of improvement in BCVA between two groups (P = 0.756, Table 2). At the time of month 12 visit, 30 eyes (83.3%) gained ≥5 ETDRS letters, 15 eyes (41.7%) gained ≥10 ETDRS letters, 7 eyes (19.4%) gained ≥15 ETDRS letters in the IVC group, and 26 eyes
This cross-sectional study was conducted in the depart- ments of ophthalmology and endocrinology at the Dokuz Eylul University School of Medicine in Izmir. A total of 413 eyes of 413 diabetic patients who were followed up in the clinics between January 2011 and July 2012 were enrolled. The demographic data, diabetes type, diabetic age, treatment modality, smoking and al- cohol consumption habits, as well as the systemic blood pressure, renal functional test results, hemoglobulin A1c (HbA1c) level, serum lipid profile, 24-h urine albumin level, and the existence of neuropathy were noted and statistically analyzed. The ophthalmological evaluation of each participant included the best corrected visual acuity (BCVA), slit-lamp biomicroscopy, intraocular pressure (IOP) measurement, and dilated fundoscopy. Fluorescein angiography and a central macularthickness (CMT) analysis with OCT were also performed. The relation- ships between the systemic findings and the prevalence of DME were studied.
Results: Average duration of diabetes and DME at baseline was 19 and 5 years, respectively, and average glycated hemoglobin was 7.21%. Severity of diabetic retinopathy before the implant had a slight bimodal distribution: moderate nonproliferative diabetic retinopathy (35%) and proliferative diabetic retinopathy (40%). Improvements in central foveal thickness from baseline were evident at 3 months (mean change – 74.2 µm, P<0.001) and sustained through 12 months ( – 55.3 µm; P=0.005) for most eyes. Mean visual acuity remained stable (66.2 letters at baseline versus 67.2 letters at 12 months, roughly equivalent to 20/50 vision; P=0.855). On average, eyes required one anti-VEGF injection every 1.9 months before and one every 6.6 months after the implant, while 60% of eyes did not require additional anti- VEGF injections. Small but signi ﬁ cant increases in IOP at months 3, 6, and 9 were not sustained to month 12, and mean IOP was normal throughout follow-up.
It has previously been acknowledged that DME diag- nosis and management remains suboptimal in many patients with diabetes, particularly in Asia. 3 Reasons for this include limited screening, and many patients present late into the course of the condition with poor visual acuity. 5 In China and Russia, more than 50% of patients with diabetes remain undiagnosed and untreated, 1 which may ultimately result in irreversible vision loss. It has been highlighted in the literature that lack of access to eye specialists, lack of adequate clinical guidance and low awareness of diabetes, diabetic retinopathy, and DME limit the optimal management of these conditions in many Asian countries. 5 As a consequence, healthcare cen- ters and resources are affected by the increase in diabetes seen in Asia in recent decades. In addition, treatment choices are in ﬂ uenced by cultural factors and sometimes
In this study, a retrospective chart review was performed on all diabetic patients (both type 1 and 2) with DME who undertook OCT evaluation at Al-Kahhal Medical Complex, Dammam, Saudi Arabia within a year from the period of January 2015 and January 2016. The study was approved by the Dhahran Eye Specialist Hospital-Institutional Review Board (DESH- IRB) and adhered to the tenets of the Declaration of Helsinki. Informed verbal consent was obtained from the all subjects in this study as approved by DESH-IRB. The inclusion criteria included diabetic patients with evidence of DME on clinical biomicroscopic, funduscopic examinations, who had an OCT evaluation with CMT more than 250 µm within 500 µm from the center of the fovea and/or more than 300-µm macularthickness within 1,500 µm from the center of the fovea. Furthermore, a comprehensive review of all patient records and collection of data included gender, type of diabetes, diabetes duration, refraction, best-corrected Snellen visual acuity, and stage of diabetic retinopathy was made. Snellen visual acuities were converted to the LogMAR scale. The sampled number met the threshold number required in med- ical research to give a reproducible result as de ﬁ ned by Schimel et al. 12 The exclusion criteria included; any diabetic patient, who received intravitreal injections, and/or who had tractional retinal detachment or vitreomacular traction. In addition, eyes with poor quality OCT scan or any other pro- cess that prohibited proper grading of OCT scan were excluded. In addition, patients having eyes with glaucoma, uveitis, retinitis pigmentosa and choroidal neovascular mem- brane were also excluded.
The RETAIN study 57 reported on the outcomes of intra- vitreal ranibizumab injections for RVO, and the results showed that one-half of the patients had a resolution of edema, and the other half still needed repeated injections even in the fourth year. The mean number of injections for macularedema due to CRVO was 10.9 in the a ﬂ ibercept group and 14.4 in the ranibizumab group with a follow-up period of 18 months. 60 In addition, serial anti-VEGF therapy did not prevent the developments of neovascular abnormalities ,61,62 and an increase in the size of the nonper- fused area. 63 These ﬁ ndings suggest that serial anti-VEGF therapy still requires repeat injections and treatments for neovascular events during long-term follow-ups. Smiddy 64 concluded that the relative cost and bene ﬁ ts of anti-VEGF therapy should also be considered when considering the treatment strategies. Vitrectomy was reported to be a useful method in terms of the relative costs and bene ﬁ ts for diabeticmacularedema 64 and proliferative diabetic retinopathy. 65 We believe that vitrectomy is a useful therapy for macularedema due to RVO in terms of the relative costs and bene ﬁ ts.
The choroid is the only source of oxygen and nutrients to the outer retina and the retinal pigment epithelium. Although diabetic retinopathy (DR) is described as a dis- ease primarily affecting the retinal microvasculature, the concept of diabetic choroidopathy came into light when it was first reported that there is a significantly higher loss of choriocapillaris in diabetic subjects than in aged control subjects . The loss of outer retinal oxygenation may be the reason for the loss of cones in diabetic retina even when there is no retinopathy present [2, 3]. Doppler flowmetry has also shown decreased choroidal perfusion in early DR .
Although the primary regulatory role of the choroid is well known, the in vivo clinical association of CT with MOPP has yet to be determined in HM pregnancy. Pre- vious studies have reported that ocular blood flow in- creases throughout gestation . In our study, we found that MOPP increased during the third trimester compared with postpartum groups (p < 0.05) (Fig. 2). However, no significant associations between CT and MOPP during pregnancy (p > 0.05) (Table 2) were found. These findings are in accordance with those of Kim et al., who found no significant correlation between subfo- veal CT and MOPP (p > 0.05) in healthy subjects . In contrast, Sayin et al. found subfoveal CT to be positively correlated with MOPP in pregnant women with no pre- eclampsia, while no correlation existed in pregnant women with pre-eclampsia . The reasons for there
In the retrospective case series, we collected and evalu- ated the data of 36 patients with unilateral ME second- ary to RVO. Nineteen patients had CRVO, and 17 patients had BRVO. The diagnosis was determined ac- cording to the fundus examination and fluorescein angi- ography. Inclusion criteria were as the follows: (1) the age ranged from 50 to 70 years; (2) recent-onset (less than 1.5 months) and treatment-naïve when presented to the hospital; (3) was ischemic subtype and had received at least one intravitreal ranibizumab injection after newly diagnosed; (4) had follow-up of at least 2 weeks; (5) had comprehensive ophthalmic examinations before and after treatment. Patients were excluded if their fel- low eyes had any macular disorder such as age-related degeneration (AMD), polypoidal choroidal vasculopathy (PCV) or central serous chorioretinopathy (CSC). Pa- tients were also excluded if the affected eyes or fellow eyes had any of the following criteria: (1) axial length > 26.00 mm or < 22.00 mm; (2) a history of pars plana vi- trectomy or other intraocular surgeries within half year. The present study followed the tenets of the declaration of Helsinki and was approved by the ethics committee in hospital. The subjects had been informed written con- sent on the study.
Materials and methods: A total of 151 eyes from 80 patients from the retina department of Istanbul Training and Research Hospital who had type 2 diabetes mellitus with diabetic retinopathy were studied retrospectively in this cross-sectional research. Patients were divided into three groups: mild–moderate nonproliferative diabetic retinopathy without macularedema (NPDR), mild–moderate nonproliferative diabetic retinopathy with macularedema (DME), and proliferative diabetic retinopathy (PDR). In addition, 40 eyes of 20 healthy individuals comprised a control group. Choroidalthickness was measured from the posterior edge of the retinal pig- ment epithelium to the choroid/sclera junction at 500-µm intervals up to 1,500 µm temporal and nasal to the fovea. The CMT measurement was obtained for each eye. Serum hemoglobin A 1c (HbA 1c ) levels were measured.
Spectral-Domain Optical Coherence Tomography images were acquired using the automated eye alignment eye-tracking software (TruTrack; Heidelberg Engineer- ing) to obtain 25 high-speed horizontal line scans of the macula of both eyes within the central 20° centered in the fovea. The central foveal thickness derived from the Early Treatment Diabetic Retinopathy Study (ETDRS) grid was selected as the outcome measure for evaluating the central macularedema (CME). SD-OCT with an EDI (enhanced depth imaging) protocol (horizontal and verti- cal scans, 20 × 20, 49 sections, high resolution mode, 30 frames) was also performed to obtain the central choroi- dal thickness (CCT). CCT was measured at the subfoveal position. The CCT measures were performed manually using the caliper of the Eye Explorer Software (v. 18.104.22.168; Heidelberg Engineering), with 80% zoom. The measure was obtained perpendicularly, from the outer edge of the hyperreflective retinal pigmented epithelium (RPE) to the hyperreflective inner sclera. All SD-OCT images were routinely obtained at the same time, avoiding diurnal var- iations of the choroidal and retinal thicknesses.