1,720,982 research outputs found
Pathophysiology and treatment of diabetic retinopathy
In the past years, the management of diabetic retinopathy (DR) relied primarily on a good systemic control of diabetes mellitus, and as soon as the severity of the vascular lesions required further treatment, laser photocoagulation or vitreoretinal surgery was done to the patient. Currently, even if the intensive metabolic control is still mandatory, a variety of different clinical strategies could be offered to the patient. The recent advances in understanding the complex pathophysiology of DR allowed the physician to identify many cell types involved in the pathogenesis of DR and thus to develop new treatment approaches. Vasoactive and proinflammatory molecules, such as vascular endothelial growth factor (VEGF), play a key role in this multifactorial disease. Current properly designed trials, evaluating agents targeting VEGF or other mediators, showed benefits in the management of DR, especially when metabolic control is lacking. Other agents, directing to the processes of vasopermeability and angiogenesis, are under investigations, giving more hope in the future management of this still sight-threatening disease
Near-Infrared Fundus Autofluorescence in Subclinical Best Vitelliform Macular Dystrophy
PURPOSE: To describe fundus autofluorescence (FAF) on short-wavelength FAF and near-infrared FAF in the subclinical form of Best vitelliform macular dystrophy. DESIGN: Cross-sectional prospective study. METHODS: Patients affected by the subclinical form of Best vitelliform macular dystrophy (positive testing for BEST1 gene mutation, fully preserved best-corrected visual acuity, normal fundus appearance) were recruited. Each patient underwent a complete ophthalmologic examination, including electro-oculogram (EOG), short-wavelength FAF, near-infrared FAF, spectral-domain OCT (SD OCT), and microperimetry. Main outcome measure was the identification of abnormal FAF patterns. RESULTS: Forty-six patients showing mutations in the BEST1 gene were examined. Forty patients presented a bilateral Best vitelliform macular dystrophy, 2 patients showed a unilateral Best vitelliform macular dystrophy, and 4 patients had a bilateral subclinical form. Patients with the unilateral form (2 eyes) and patients with the subclinical form (8 eyes) were analyzed. Three BEST1 sequence variants were identified: c.73C > T (p.Arg25Trp), c.28G > A (p.Ala10Thr), and c.652C > G (p.Arg218Gly). Short-wavelength FAF was normal in all eyes. Near-infrared FAF detected a pattern consisting of a central hypo-autofluorescence surrounded by a round area of hyper-autofluorescence. A bilateral reduced EOG response was detected in 1 patient. SD OCT revealed a thicker, well-defined, and more reflective interdigitation zone in 2 patients (4 eyes, 40%). Microperimetry of the central 10 degrees revealed a slight, diffuse reduction of retinal sensitivity. Mean retinal sensitivity within the central 2 and 4 degrees was lower and matched the hypo-autofluorescent area detected on near-infrared FAF. Additional relative scotomata were detected within the 10-degree area. No change in clinical, functional, or FAF pattern was found over the follow-up. CONCLUSIONS: Subclinical Best vitelliform macular dystrophy is characterized by the absence of biomicroscopic fundus abnormality and fully preserved visual acuity, but shows an abnormal near-infrared FAF pattern, with central hypo-autofluorescence. (C) 2014 by Elsevier Inc. All rights reserved
Il d.l. 73/2022 sul rilascio del nulla osta al lavoro: un’opportunità non priva di rischi
Intravitreal Dexamethasone Implant in Patients with Persistent Diabetic Macular Edema
Purpose: To evaluate the effects of a single injection of Ozurdex over 6 months in eyes with persistent diabetic macular edema (DME). Methods: In this retrospective interventional study, 9 patients with decreased visual acuity, as a result of persistent DME, received Ozurdex (intravitreal dexamethasone implant 0.7 mg). Main outcome measures included changes in best-corrected visual acuity (BCVA) and central retinal thickness (CRT). Results: Nine eyes of 9 patients (5 males, 4 females; mean age 58 years) were included in the analysis. The mean duration of DME was 49.9 months (range 24-85). All patients had undergone previous treatments for DME (intravitreal injection of anti-vascular endothelial growth factor, steroids or laser photocoagulation) before entering the study. At baseline, the mean BCVA was 0.74 +/- 0.33 logMAR, and the mean CRT was 502 +/- 222.16 mu m. The mean BCVA was unchanged on the third day (0.74 +/- 0.38 logMAR, p = 0.5), improved to 0.62 +/- 0.32 logMAR (p = 0.02), 0.59 +/- 0.26 logMAR (p = 0.02) and 0.63 8 0.38 logMAR (p = 0.6) after the first, third and fourth months, respectively, and decreased again to 0.73 +/- 0.35 logMAR (p = 0.4) at 6 months. The mean CRT improved to 397 +/- 115.31 mu m (p = 0.17), 271 +/- 99.97 mu m (p = 0.007), 325 +/- 133.05 mu m (p = 0.03) and 462 +/- 176.48 mu m (p = 0.36) on the third day and after 1, 3 and 4 months of follow-up and then increased again to 537 +/- 265.42 mu m (p = 0.33) at 6 months. Eight patients needed retreatments in the sixth month. One eye developed a transient intraocular pressure (IOP) increase 1 month after injection, which was successfully managed with topical IOP-lowering medication. Conclusion: In eyes with persistent DME, Ozurdex produces improvement in BCVA and CRT as soon as the first days after the injection. Such improvement is maintained until the fourth month. Copyright (C) 2012 S. Karger AG, BaselPurpose: To evaluate the effects of a single injection of Ozurdex over 6 months in eyes with persistent diabetic macular edema (DME). Methods: In this retrospective interventional study, 9 patients with decreased visual acuity, as a result of persistent DME, received Ozurdex (intravitreal dexamethasone implant 0.7 mg). Main outcome measures included changes in best-corrected visual acuity (BCVA) and central retinal thickness (CRT). Results: Nine eyes of 9 patients (5 males, 4 females; mean age 58 years) were included in the analysis. The mean duration of DME was 49.9 months (range 24-85). All patients had undergone previous treatments for DME (intravitreal injection of anti-vascular endothelial growth factor, steroids or laser photocoagulation) before entering the study. At baseline, the mean BCVA was 0.74 +/- 0.33 logMAR, and the mean CRT was 502 +/- 222.16 mu m. The mean BCVA was unchanged on the third day (0.74 +/- 0.38 logMAR, p = 0.5), improved to 0.62 +/- 0.32 logMAR (p = 0.02), 0.59 +/- 0.26 logMAR (p = 0.02) and 0.63 8 0.38 logMAR (p = 0.6) after the first, third and fourth months, respectively, and decreased again to 0.73 +/- 0.35 logMAR (p = 0.4) at 6 months. The mean CRT improved to 397 +/- 115.31 mu m (p = 0.17), 271 +/- 99.97 mu m (p = 0.007), 325 +/- 133.05 mu m (p = 0.03) and 462 +/- 176.48 mu m (p = 0.36) on the third day and after 1, 3 and 4 months of follow-up and then increased again to 537 +/- 265.42 mu m (p = 0.33) at 6 months. Eight patients needed retreatments in the sixth month. One eye developed a transient intraocular pressure (IOP) increase 1 month after injection, which was successfully managed with topical IOP-lowering medication. Conclusion: In eyes with persistent DME, Ozurdex produces improvement in BCVA and CRT as soon as the first days after the injection. Such improvement is maintained until the fourth month. Copyright (C) 2012 S. Karger AG, Base
The Role of Angiogenesis in the Development of Proliferative Diabetic Retinopathy: Impact of Intravitreal Anti-VEGF Treatment
Although cellular and molecular bases of proliferative diabetic retinopathy are only partially understood, it is evident that this complication of diabetes is characterized by the formation of new vessels inside the retina showing abnormal architecture and permeability. This process, if not controlled by selective laser photocoagulation, leads to irreversible retinal damages and loss of vision. Angiogenesis, that is, the condition characterized by the growth of new blood vessels originated from preexisting ones, was shown to have a major role in the pathogenesis of proliferative retinopathy and, as a consequence, intravitreal antiangiogenic injection was suggested as a feasible treatment for this disease. Here, we describe the different antiangiogenic approaches used to treat this disease along with the respective advantages and limitations when compared to laser treatment. Altogether, even though further and longer studies are still needed to clarify the best possible therapeutic protocol, the antiangiogenic treatment will reasonably have a future role in the therapy and prevention of proliferative diabetic retinopathy
Fundus Autofluorescence Patterns in Best Vitelliform Macular Dystrophy
PURPOSE: To provide a systematic classification of fundus autofluorescence (FAF) patterns in patients affected by Best vitelliform macular dystrophy. DESIGN: Cross-sectional prospective study. METHODS: Patients affected by Best vitelliform macular dystrophy at different stages of the disease were prospectively enrolled from January 2012 to July 2013. Eighty eyes of 40 patients were included in the study. All patients underwent a complete ophthalmologic examination, including genetic characterization, short-wavelength FAF, and near-infrared FAF. Main outcome measures were the recognition of the FAF patterns in the different stages and the identification of a relationship between FAF patterns and best-corrected visual acuity (BCVA). RESULTS: Six FAF patterns for both short-wavelength and near-infrared FAF were identified, including normal, hyper-autofluorescent, hypo-autofluorescent, patchy, multifocal, and spoke-like patterns. Applying Gass's classification for defining consecutive stages of Best vitelliform macular dystrophy (namely vitelliform, pseudohypopyon, vitelliruptive, atrophic, and cicatricial) identified no pattern as stage-specific. Patchy patterns had the highest prevalence. A statistically significant difference (Kruskat-Wallis ANOVA) was. found among hyperautofluorescent, patchy, and hypo-autofluorescent patterns, both in short-wavelength (P =. 001) and near-infrared FAF (P = .001). Hyper-autofluorescent and hypo-autofluorescent patterns were associated with better and worse BCVA, respectively. CONCLUSIONS: Six main patterns on both short-wavelength and near-infrared FAF were identified in Best vitelliform macular dystrophy. No FAF pattern can be considered stage-specific. Although a difference in the BCVA among the FAF patterns was registered, only a longitudinal study designed to evaluate the clinical and FAF modifications over the follow-up will help clarify the prognostic implications of each FAF pattern. (C) 2014 by Elsevier Inc. All rights reserved
Primitive Retinal Vascular Abnormalities: Tumors and Telangiectasias
Primitive retinal vascular abnormalities are benign conditions of the retinal circulation that comprise vascular tumors and telangiectasias. The principal vascular tumors of the retina include retinal capillary hemangioma, cavernous hemangioma of the retina, racemose hemangiomatosis of the retina and retinal vasoproliferative tumor, while primary retinal telangiectasias include Coats' disease, Leber's miliary aneurysms and idiopathic juxtafoveal telangiectasias. In most cases, these alterations result in significant visual impairment due to exudation determined by the structural abnormalities of the retinal vasculature. The aim of this review is to assess the different clinical and diagnostic features of the single pathological entities and to discuss the available treatment modalities including the onset of intravitreal antivascular endothelial growth factor therapy. Copyright (C) 2012 S. Karger AG, Basel OI Knutsson, Karl Anders/0000-0002-9615-2839Primitive retinal vascular abnormalities are benign conditions of the retinal circulation that comprise vascular tumors and telangiectasias. The principal vascular tumors of the retina include retinal capillary hemangioma, cavernous hemangioma of the retina, racemose hemangiomatosis of the retina and retinal vasoproliferative tumor, while primary retinal telangiectasias include Coats' disease, Leber's miliary aneurysms and idiopathic juxtafoveal telangiectasias. In most cases, these alterations result in significant visual impairment due to exudation determined by the structural abnormalities of the retinal vasculature. The aim of this review is to assess the different clinical and diagnostic features of the single pathological entities and to discuss the available treatment modalities including the onset of intravitreal antivascular endothelial growth factor therapy. Copyright (C) 2012 S. Karger AG, Base
CHOROIDAL THICKNESS IN BEST VITELLIFORM MACULAR DYSTROPHY
Purpose:To assess the changes in choroidal thickness in different stages of Best vitelliform macular dystrophy (VMD).Methods:Thirty-four patients affected by VMD were prospectively enrolled and underwent a complete ophthalmologic examination, including best-corrected visual acuity measurement, biomicroscopic examination, and spectral domain optical coherence tomography. The Gass classification was used in defining the stages of VMD. Twenty healthy subjects served as the control group. Main outcome measures were the identification of choroidal changes in different stages of VMD and detection of a correlation between choroidal thickness and best-corrected visual acuity.Results:No significant difference was found in the subfoveal choroidal thickness (SFCT) between eyes displaying Stage 1 and the control group (P = 0.181). Stages 2 and 3 showed an increased SFCT (320.4 and 319.1 m, respectively) compared with that of control patients (P < 0.001 and P = 0.004, respectively). Stage 4 had a significantly inferior SFCT compared with Stages 2 and 3 (P = 0.007 and P = 0.025, respectively) but no significant difference was found between Stage 4 and control patients (P = 0.733). The Stage 5 group displayed a significant decrease in SFCT compared with that of the control group (181.3 m and 238.4 m, respectively, P = 0.002). Analyzing the association between SFCT and best-corrected visual acuity in patients affected by clinical VMD (Stages 2-5), the authors found that the best-corrected visual acuity decreased as the choroid thinned (P = 0.004).Conclusion:Choroidal thickness varies according to the stage of VMD, being higher in the vitelliform stage and thinner in the atrophic/cicatricial stage. Long-term studies are warranted to provide a more precise evaluation of the morphofunctional alterations in the different stages of VMD
Posterior polymorphous corneal dystrophy concomitant to large colloid drusen
Purpose: To describe the previously unreported concomitance of 2 uncommon ocular conditions: posterior polymorphous corneal dystrophy (PPCD) and large colloid drusen (LCD). Methods: A 45-year-old woman underwent a complete ophthalmologic examination with slit-lamp biomicroscopy and blue fundus autofluorescence with spectral-domain optical coherence tomography, as well as complete systemic examination and renal function investigation. Results: On slit-lamp biomicroscopy, a corneal lesion located at Descemet membrane was observed in the right eye. The clinical features of deep posterior stromal-endothelial linear bands with vesicles and irregular opacities of posterior corneal surface were consistent with the diagnosis of PPCD. Fundus biomicroscopy and blue fundus autofluorescence showed LCD. Discussions: We report the unusual coexistence of PPCD and LCD in a young, healthy subject. Posterior polymorphous corneal dystrophy and LCD share morphologic similarities and dysfunctions of collagen architecture in the basement membrane layer, which suggests a possible common pathogenic pathway. OI Corvi, Federico/0000-0002-2661-5500Purpose: To describe the previously unreported concomitance of 2 uncommon ocular conditions: posterior polymorphous corneal dystrophy (PPCD) and large colloid drusen (LCD). Methods: A 45-year-old woman underwent a complete ophthalmologic examination with slit-lamp biomicroscopy and blue fundus autofluorescence with spectral-domain optical coherence tomography, as well as complete systemic examination and renal function investigation. Results: On slit-lamp biomicroscopy, a corneal lesion located at Descemet membrane was observed in the right eye. The clinical features of deep posterior stromal-endothelial linear bands with vesicles and irregular opacities of posterior corneal surface were consistent with the diagnosis of PPCD. Fundus biomicroscopy and blue fundus autofluorescence showed LCD. Discussions: We report the unusual coexistence of PPCD and LCD in a young, healthy subject. Posterior polymorphous corneal dystrophy and LCD share morphologic similarities and dysfunctions of collagen architecture in the basement membrane layer, which suggests a possible common pathogenic pathway
Enhanced depth imaging optical coherence tomography in type 2 diabetes
Purpose:To investigate the changes in choroidal thickness within the macula of eyes with various stages of diabetic retinopathy, using enhanced depth imaging optical coherence tomography (EDI OCT).Methods:Sixty-three consecutive diabetic patients without (NDR) or with diabetic retinopathy (non-proliferative diabetic retinopathy [NPDR] and no clinically significant macular edema [CSME-]; NDPR and clinically significant macular edema [CSME+]) underwent EDI OCT. Twenty-one age and sex matched healthy subjects (21 eyes) also underwent EDI OCT.Results:A total of 63 eyes of 63 consecutive diabetic patients (26 female (41.2%); mean age 65.4 ± 8.9 years, range 48-83 years) were included in the analysis. Mean BCVA was 0.13±0.25 LogMAR (range 0-1). Mean CMT was 272.47±16.24 μm in 21 NDR eyes, 294.52±23.51 μm in 21 NPDR/CSME- eyes, and 385.61±75.07 μm in 21 NPDR/CSME+ eyes. There was no difference in mean subfoveal choroidal thickness among each diabetic group (238.42±47.95 μm [NDR], 207.0±55.95 μm [NPDR/CSME-], 190.85±48.43 μm NPDR/CSME+; p=0.18). The mean subfoveal choroidal thickness was significantly reduced in each diabetic group compared with the control group (309.76±58.52 μm, p<0.001).Conclusions:In diabetic eyes there is an overall thinning of the choroid on EDI OCT. A decreased choroidal thickness may lead to tissue hypoxia and consequently increase the level of VEGF, resulting in the breakdown of the blood-retinal barrier and the development of macular edema
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