90 research outputs found
Management of diabetic macular edema patients in clinical practice in Spain
Purpose: Diabetic macular edema is the main cause of blindness in diabetic patients. Vascular endothelial growth factor is involved in diabetic macular edema pathogenesis. Vascular endothelial growth factor inhibitors are an important option in diabetic macular edema therapy. This survey investigates actual clinical practice in diabetic macular edema in Spain.
Methods: An expert advisory panel of 17 Spanish ophthalmologists developed a 30-item anonymous questionnaire about diagnosis, treatment, and follow-up in diabetic macular edema. A total of 137 ophthalmologists from 10 Spanish regions completed the questionnaire online.
Results: Almost all of the respondents (99.3%) record the measured visual acuity and perform biomicroscopic anterior (94.9%) and posterior (91.2%) segment examinations. Similarly, 100% of responding ophthalmologists always/almost always or frequently perform optical coherence tomography. Most respondents (65%) always/almost always or frequently perform a retinography. More than 50% rarely perform fluorescein angiography. Nearly, all (96.4%) of the specialists responded that, in center-involved diabetic macular edema, the first treatment is an anti–vascular endothelial growth factor drug. For corticosteroids, the first choice of most respondents (91.2%) was the dexamethasone implant. In the follow-up, almost all (96.4%) specialists record the measured visual acuity and most also perform biomicroscopic anterior (82.5%) and posterior (83.2%) segment examination.
Conclusion: This survey shows the actual clinical practice in diabetic macular edema in Spain, finding that anti–vascular endothelial growth factor therapy is frequently used, and that diagnosis, treatments, and follow-up examinations used by specialists are homogeneous and according to diabetic macular edema guidelines
Does posterior capsule opacification affect the results of diagnostic technologies to evaluate the retina and the optic disc?
The visual outcome obtained after cataract removal may progressively decline because of posterior capsular opacification (PCO). This condition can be treated by creating an opening in the posterior lens capsule by Nd:YAG laser capsulotomy. PCO optical imperfections cause several light reflection, refraction, and diffraction phenomena, which may interfere with the functional and structural tests performed in different ocular locations for the diagnosis and follow-up of ocular disease, like macular and optic nerve diseases. Some parameters measured by visual field examinations, scanning laser polarimetry, and optical coherence tomography (OCT) have changed after PCO removal. Imaging quality also changes following capsulotomy. Consequently, the results of ancillary tests in pseudophakic eyes for studying ocular diseases like glaucoma or maculopathies should be correlated with other clinical examinations, for example, slit-lamp biomicroscopy or funduscopy. If PCO is clinically significant, a new baseline should be set for future comparisons following capsulotomy when using automated perimetry and scanning laser polarimetry. To perform OCT in the presence of PCO, reliable examinations (considering signal strength) apparently guarantee that measurements are not influenced by PCO
Smoking and age-related macular degeneration: review and update
Age-related macular degeneration (AMD) is one of the main socioeconomical health issues worldwide. AMD has a multifactorial etiology with a variety of risk factors. Smoking is the most important modifiable risk factor for AMD development and progression. The present review summarizes the epidemiological studies evaluating the association between smoking and AMD, the mechanisms through which smoking induces damage to the chorioretinal tissues, and the relevance of advising patients to quit smoking for their visual health
Fingolimod: therapeutic mechanisms and ocular adverse effects.
Fingolimod is an oral immunomodulating drug used in the management of relapsing-remitting multiple sclerosis (RRMS). We aim to review the published literature on ocular manifestations of fingolimod therapy and their possible underlying mechanisms. The therapeutic effects of fingolimod are mediated via sphingosine receptors, which are found ubiquitously in various organs, including lymphoid cells, central nervous system, cardiac myocytes, and smooth muscle cells. Fingolimod-associated macular oedema (FAME) is the most common ocular side effect but retinal haemorrhages and retinal vein occlusion can occur. The visual consequences appear to be mild and, in cases of FAME, resolution is often attained with discontinuation of therapy. However, in cases of retinal vein occlusion, discontinuation of fingolimod alone may not be sufficient and intra-vitreal therapy may be required. We also propose a pragmatic service pathway for monitoring patients on fingolimod therapy, which includes stratifying them by risk and visual acuity
Intravitreal bevacizumab in diabetic retinopathy. Recommendations from the Pan-American Collaborative Retina Study Group (PACORES): The 2016 knobloch lecture
The advent of intravitreal anti-vascular endothelial growth factor (anti-VEGF) medications has revolutionized the treatment of diabetic eye diseases. Herein, we report the outcomes of clinical studies carried out by the Pan-American Collaborative Retina Study Group (PACORES), with a specific focus on the efficacy of intravitreal bevacizumab in the management of diabetic macular edema and proliferative diabetic retinopathy. We will also discuss the use of intravitreal bevaci-zumab as a preoperative, adjuvant therapy before vitrectomy for prolif-erative diabetic retinopathy. Copyright © 2017 by Asia Pacific Academy of Ophthalmology
Correlation of sectoral choroidal vascularity with angiographic leakage in central serous chorioretinopathy
Comparison of Morphological Features of Type 1 CNV in AMD and Pachychoroid Neovasculopathy: An OCTA Study
Caracterización bioquímica del nervio óptico en el ratón que sobreexpresa el gen p53. Análisis de estrés oxidativo
[EN]: [Purpose]: The tumour inhibitor p53 gene has the
ability of triggering proliferation arrest and cellular
death by apoptosis subsequent to several factors,
among them oxidative stress. The p53 protein is a
major regulator of gene expression. Using genetically
manipulated mice carrying an extra copy of
gene p53 (transgenic mice super p53) versus control
mice, we have investigated the generation of reactive
oxygen species and antioxidant activity in the
optic nerve of mice in relation to p53 availability.
[Methods]: We studied two groups of 12-month-old
mice of the strain C57BL/6: 1) super p53 group
(Sp53) and 2) wild-type control group (CG). Mice
were anesthetized in ether atmosphere and the eyeball
and retrobulbar optic nerves were excised, washed,
soaked in PBS, and stored in liquid nitrogen at
–85ºC until processing. Three-four optic nerves
from the same group were placed in an eppendorf
tube, homogenized and enzymatic-colorimetric
methods used to determine oxidative and antioxidant
activities and the nitric oxide synthesis. [Results]: A significant increase in free radical formation
(via lipid peroxidation; p<0.001), antioxidant
activity (p<0.001) and nitric oxide synthesis
(p<0.001) was found in the optic nerves from transgenic
super p53 mice compared to respective controls.
[Conclusion]: The presence of an extra copy of the
p53 gene correlated with redox status in the mouse
optic nerve. This transgenic mouse could be useful
as an experimental model to study cell resistance to
neurodegenerative processes in relation to oxidative
stress and to apoptosis induction, such as glaucomatous
optic neuropathy or age-related macular
degeneration.[ES]: [Objetivos]: El gen supresor tumoral p53 detiene la
proliferación y la muerte celular por apoptosis subsecuente
a la acción de diversos factores, entre ellos
el estrés oxidativo. La proteína p53 es fundamentalmente
un regulador de la expresión génica. Utilizando
ratones genéticamente manipulados para presentar
una copia extra del gen p53 (transgénicos
super p53) frente a ratones controles, hemos investigado
el estado oxidativo y antioxidante en los nervios
ópticos, en relación a p53.
[Método]: Se han utilizado ratones de la cepa
C57BL/6 de 12 meses de edad en dos grupos: 1)
grupo super p53 (Sp53) y 2) grupo de controles
wild-type (GC). Los ratones fueron anestesiados en
atmósfera de éter, extrayendo los globos oculares y
nervios ópticos que se lavaron en PBS, manteniendo
las muestras en nitrógeno líquido y en congelador
de –85ºC hasta su procesamiento. Se homogeneizaron
3-4 nervios ópticos por cada eppendorf,
clasificando por grupos y determinando mediante
métodos enzimático-colorimétricos la actividad peroxidativa y actividad antioxidante total y la concentración
de oxido nítrico.
[Resultados]: Existe aumento significativo en la formación
de radicales libres via peroxidación lipídica
(p<0,001), de la actividad antioxidante (p<0,001) y
síntesis de óxido nítrico (p<0,05) en los nervios
ópticos de los ratones transgénicos super p53, frente
a los ratones controles.
[Conclusiones]: La presencia de una copia extra del
gen p53 está ligada a modificaciones de la actividad
redox en el nervio óptico del ratón, sugiriendo que
p53 otorga una mayor resistencia a la agresión oxidativa.
Valoramos la utilización de este modelo de
ratón transgénico en procesos neurodegenerativos
relacionados con el estrés oxidativo y la inducción
de la apoptosis, como la neuropatía óptica glaucomatosa
o la degeneración macular asociada a la
edad.7 páginas, 4 figuras.Peer reviewe
- …