Uso de dexametasona subconjuntival en el post-operatorio de la cirugía de cataratas

Objetivo: Determinar la efectividad antinflamatoriade dexametasona subconjuntival en el post-operatoriode la cirugía de catarata.Método: 140 operados de cataratas (78 EECC;62 FACO) fueron evaluados. En forma randomizadase formaron 2 grupos: el grupo A (75 pacientes) recibió0.5 ml de dexametasona subconjuntival, el grupoB (65 pacientes) fue el grupo control. Se evaluó lareacción inflamatoria de la cámara anterior el día 1 y8 del postoperatorio.Resultado: En el día 1, la reacción de cámara anteriorfue 2.08 + en pacientes del grupo A y 2.35 +en el grupo B (p = 0.096). En el día 8 la reacción delgrupo A fue de 0.96 + y del grupo B 1.06 (p=0.936).Conclusion: El uso de dexametasona subconjuntivaltiende a disminuir la reacción de cámara anterior,pero no existe una diferencia estadísticamente significativaentre ambos grupos; sin embargo, al tomar encuenta el tipo de cirugía, en la EECC, el grupo A enel día 1 muestra una disminución de la reacción inflamatoriacon diferencia estadísticamente significativa(p = 0.001)

Síndrome uveo meníngeo de Vogt-Koyanagi- Harada. A propósito de un caso

Objetivo: Reportar un caso de Síndrome de Vogt-Koyanagi-Harada y describir las características clínicasdel cuadro.Diseño: Reporte de caso único, intervencionistaMétodos: Presentación de las características clínicasdel caso.Resultados: Se presenta un caso de Sx. de Vogt-Koyanagi-Harada en una paciente de 25 años deedad, tratada con corticoides a altas dosis, sin mejoríade la AV a pesar del tratamiento.Conclusión: El Sx. de Vogt-Koyanagi-Harada esuna panuveítis granulomatosa bilateral con comprometimientoauditivo, de las meninges y de la piel, lapérdida de la agudeza visual asociada es moderadaa severa

Primer Screening de Hipertensión Ocular en Asunción, Paraguay

Objetivo: Crear conciencia e informar a la poblaciónsobre el glaucoma. Realizar un screening de hipertensiónocular (HTO). Determinar la prevalenciade HTO en Asunción, Paraguay.Método: En la calle principal de la ciudad enforma gratuita se realizó toma de presión intraocular(PIO) a los interesados con neumotonómetro. Se proporcionóinformación oral y escrita sobre glaucoma.Resultado: 170 personas fueron evaluadas, 79mujeres y 91 varones, con edad promedio de 55.2años. 20 individuos presentaron PIO ≥ 21 mmHg(11.76%), que fueron derivados a un especialista.Conclusión. 20 individuos presentaron PIO ≥ 21mmHg siendo sospechosos de glaucoma. La prevalenciade HTO es 11.76% en Asunción, Paraguay

An association between polymorphism of the heme oxygenase-1 and -2 genes and age-related macular degeneration

Iron may be implicated in the generation of oxidative stress by the catalyzing the Haber–Weiss or Fenton reaction. On the other hand, oxidative stress has been implicated in the pathogenesis of age-related macular degeneration (AMD) and heme oxygenase-1 (HO-1), encoded by the HMOX1 gene and heme oxygenase-2 (HO-2), encoded by the HMOX2 gene are important markers of iron-related oxidative stress and its consequences. Therefore, variability of the HMOX1 and HMOX2 genes might be implicated in the pathogenesis of AMD through the modulation of the cellular reaction to oxidative stress. In the present work, we investigated the association between AMD and a G → C transversion at the 19 position in the HMOX1 gene (the 19G>C-HMOX1 polymorphism, rs2071747) and a A → G transition at the −42 + 1444 position in the HMOX2 gene (the −42 + 1444A>G-HMOX2 polymorphism, rs2270363) and its modulation by some environmental factors. 279 patients with AMD and 105 controls were recruited in this study and the polymorphisms were typed by restriction fragment length polymorphism and allele-specific polymerase chain reaction (PCR). We observed an association between the occurrence of dry AMD and the G/A genotype of the −42 + 1444A>G-HMOX2 polymorphism (odds ratio (OR) 2.72), whereas the G/G genotype reduced the risk of dry AMD (OR 0.41). The G/C genotype and the C allele of the 19 G>C-HMOX1 polymorphism and the G/G genotype and the G allele of the −42 + 1444A>G-HMOX2 polymorphism were associated with progression of AMD from dry to wet form (OR 4.83, 5.20, 2.55, 1.69, respectively). On the other hand, the G/G genotype and the G allele of the 19 G>C-HMOX1 polymorphism and the A/G genotype and the A allele of the −42 + 1444A>G-HMOX2 polymorphism protected against AMD progression (OR 0.19, 0.19, 0.34, 0.59, respectively). Therefore, the 19G>C-HMOX1 and the −42 + 1444A>G-HMOX2 polymorphisms may be associated with the occurrence and progression of AMD

Genetic polymorphism of the iron-regulatory protein-1 and -2 genes in age-related macular degeneration

Iron can be involved in the pathogenesis of AMD through the oxidative stress because it may catalyze the Haber–Weiss and Fenton reactions converting hydrogen peroxide to free radicals, which can induce cellular damage. We hypothesized that genetic polymorphism in genes related to iron metabolism may predispose individuals to the development of AMD and therefore we checked for an association between the g.32373708 G>A polymorphism (rs867469) of the IRP1 gene and the g.49520870 G>A (rs17483548) polymorphism of the IRP2 gene and AMD risk as well as the modulation of this association by some environmental and life-style factors. Genotypes were determined in DNA from blood of 269 AMD patients and 116 controls by the allele-specific oligonucleotide-restriction fragment length polymorphism and the polymerase chain reaction-restriction fragment length polymorphism. An association between AMD, dry and wet forms of AMD and the G/G genotype of the g.32373708 G>A-IRP1 polymorphism was found (OR 3.40, 4.15, and 2.75). On the other hand, the G/A genotype reduced the risk of AMD as well as its dry or wet form (OR 0.23, 0.21, 0.26). Moreover, the G allele of the g.49520870 G>A-IRP2 polymorphism increased the risk of the dry form of the disease (OR 1.51) and the A/A genotype and the A allele decreased such risk (OR 0.43 and 0.66). Our data suggest that the g.32373708 G>A-IRP1 and g.49520870 G>A-IRP2 polymorphisms may be associated with increased risk for AMD

Genetic insights into age-related macular degeneration: Controversies addressing risk, causality, and therapeutics

Age-related macular degeneration (AMD) is a common condition among the elderly population that leads to the progressive central vision loss and serious compromise of quality of life for its sufferers. It is also one of the few disorders for whom the investigation of its genetics has yielded rich insights into its diversity and causality and holds the promise of enabling clinicians to provide better risk assessments for individuals as well as to develop and selectively deploy new therapeutics to either prevent or slow the development of disease and lessen the threat of vision loss. The genetics of AMD began initially with the appreciation of familial aggregation and increase risk and expanded with the initial association of APOE variants with the disease. The first major breakthroughs came with family-based linkage studies of affected (and discordant) sibs, which identified a number of genetic loci and led to the targeted search of the 1q31 and 10q26 loci for associated variants. Three of the initial four reports for the CFH variant, Y402H, were based on regional candidate searches, as were the two initial reports of the ARMS2/HTRA1 locus variants. Case-control association studies initially also played a role in discovering the major genetic variants for AMD, and the success of those early studies have been used to fuel enthusiasm for the methodology for a number of diseases. Until 2010, all of the subsequent genetic variants associated with AMD came from candidate gene testing based on the complement factor pathway. In 2010, several large-scale genome-wide association studies (GWAS) identified genes that had not been previously identified. Much of this historical information is available in a number of recent reviews.(Chen et al., 2010b; Deangelis et al., 2011; Fafowora and Gorin, 2012b; Francis and Klein, 2011; Kokotas et al., 2011) Large meta analysis of AMD GWAS has added new loci and variants to this collection.(Chen et al., 2010a; Kopplin et al., 2010; Yu et al., 2011) This paper will focus on the ongoing controversies that are confronting AMD genetics at this time, rather than attempting to summarize this field, which has exploded in the past 5 years

The Injury Response Factor JUN is Expressed in Multiple Retinal Cell Types After Excitotoxic Insult

Excitotoxicity has been suggested to contribute to retinal ganglion cell (RGC) death in many diseases. The transcription JUN plays a major role in regulating RGC death after a variety of insults and has been shown to control excitotoxic neuronal death in other systems. Also, a recent study suggested that TNF released from Muller glial cells mediates excitotoxicity induced RGC death. Interestingly, JUN can control injury induced TNF expression. Therefore, JUN may play a central role in excitotoxicity induced RGC death

Desprendimiento Regmatogeno de la Retina y su Retinopexia Quirurgica

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