71 research outputs found

    Pseudophakic cystoid macular edema: update 2016

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    Andrzej Grzybowski,1,2 Bartosz L Sikorski,3 Francisco J Ascaso,4,5 Valentín Huerva6,7 1Department of Ophthalmology, University of Warmia and Mazury, Olsztyn, Poland; 2Department of Ophthalmology, Poznan City Hospital, Poznan, Poland; 3Department of Ophthalmology, Nicolaus Copernicus University, Bydgoszcz, Poland; 4Department of Ophthalmology, Hospital Clínico Universitario “Lozano Blesa”, Zaragoza, Spain; 5Instituto de Investigación Sanitaria Aragón (IIS Aragón), Zaragoza, Spain; 6Department of Ophthalmology, Universitary Hospital Arnau de Vilanova, Lleida, Spain; 7IRB Lleida, Lleida, Spain Abstract: Pseudophakic cystoid macular edema (PCME) is the most common complication of cataract surgery, leading in some cases to a decrease in vision. Although the pathogenesis of PCME is not completely understood, the contribution of postsurgical inflammation is generally accepted. Consequently, anti-inflammatory medicines, including steroids and nonsteroidal anti-inflammatory drugs, have been postulated as having a role in both the prophylaxis and treatment of PCME. However, the lack of a uniformly accepted PCME definition, conflicting data on some risk factors, and the scarcity of studies comparing the role of nonsteroidal anti-inflammatory drugs to steroids in PCME prevention make the problem of PCME one of the puzzles of ophthalmology. This paper presents an updated review on the pathogenesis, risk factors, and use of anti-inflammatory drugs in PCME that reflect current research and practice. Keywords: Pseudophakic cystoid macular edema, cataract surgery, cataract surgery complications, retina, post-operative complication

    Pigmentary retinopathy

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    Valoración de la efectividad del tratamiento del síndrome de apnea-hipopnea del sueño (SAHS) a través del estudio de la retina mediante tomografía de coherencia óptica (OCT)

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    El síndrome de apnea-hipopnea del sueño (SAHS) es uno de los trastornos respiratorios del sueño más frecuentes en la población general, a pesar de estar infradiagnosticado. Sus graves secuelas y el elevado gasto sanitario que conlleva, hacen que sean necesarios buenos métodos de diagnóstico para un tratamiento precoz. La tomografía de coherencia óptica (OCT), prueba sencilla, incruenta, barata y accesible, es una de las técnicas que se han propuesto para el diagnóstico del SAHS. Múltiples publicaciones coinciden en que la OCT es capaz de demostrar afectación de la retina en estos pacientes. Nuestro estudio da un paso más y plantea la OCT como técnica de seguimiento tras el tratamiento del SAHS. En una muestra de 96 ojos de 52 pacientes, divididos según nivel de gravedad de SAHS y en función del tipo de tratamiento recibido (CPAP, cirugía o un tratamiento combinado), se ha hecho un seguimiento a 6 meses, comparando los parámetros maculares, de la capa de fibras nerviosas de la retina (CFNR) a nivel peripapilar y datos morfométricos de la cabeza del nervio óptico, medidos con OCT antes y después del tratamiento. Los SAHS leve-moderados, que presentaban a priori mayores espesores maculares y de la CFNR, presentaron una disminución estadísticamente significativa de estos parámetros tras el tratamiento, mientras que los SAHS graves, cuyos espesores estaban reducidos, presentaron un aumento estadísticamente significativo del grosor foveal y del espesor medio de la CFNR peripapilar. Dichos resultados son compatibles con la teoría de una posible inflamación retiniana en los SAHS leve-moderados y de un proceso de adelgazamiento o atrofia en los SAHS graves, que parece revertir tras el tratamiento, a pesar de que futuros estudios con muestras más amplias son necesarios para contrastar dichos resultados. Bibliografía: 1. Durán-cantolla J, Puertas-Cuesta FJ, Pin-Arboledas G, Santa María-Cano J y el Grupo Español de Sueño (GES). Documento de consenso nacional sobre el síndrome de apneas-hipopneas del sueño. Arch Bronconeumol 2005;41:1-110. 2. Montserrat JM, Hernández L, Nacher M, Barbé F. Nuevos aspectos patogénicos en el síndrome de apneas e hipopneas durante el sueño (SAHS). Arch Bronconeumol 2004;40:27-34. 3. Vicente E, Marin JM, Vicente P, Guallar M, Forner M. Consecuencias médicas del síndrome de apnea-hipopnea durante el sueño (SAHS). En: Plaza G, Baptista PM, O´Connor C. Trastornos respiratorios del sueño: actualización en diagnóstico y tratamiento quirúrgico. Barcelona:Indica;2015.p.103-22. 4. Sher EA, Schechtman KB, Piccirillo JF. The efficacy of surgical modifications of the upper airway in adults with obstructive sleep apnea syndrome. Sleep 1996;19:156-77. 5. Vicente E, Marín JM, Carrizo S, Naya MJ. Tongue-base suspension in conjunction with uvulopalatopharyngoplasty for treatment of severe obstructive sleep apnea: long-term follow-up results. Laryngoscope 2006;116:1223-7. 6. Marin JM, Carrizo SJ, Vicente E, Agusti AG. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet 2005;365:1046–53. 7. Lin PW, Friedman M, Lin HC, Chang HW, Pulver TM, Chin CH. Decreased retinal nerve fiber layer thickness in patients with obstructive sleep apnea/hypopnea syndrome. Graefes Arch Clin Exp Ophthalmol 2011;249:585-93. 8. Casas P, Ascaso FJ, Vicente E, Tejero-Garcés G, Adiego MI, Cristóbal JA. Retinal and optic nerve evaluation by optical coherence tomography in adults with obstructive sleep apnea-hypopnea syndrome (OSAHS). Graefes Arch Clin Exp Ophthalmol 2013;251:1625-1634. 9. Sagiv O, Fishelson-Arev T, Buckman G, Mathalone N, Wolfson J, Segev E, Peled R, Lavi I, Geyer O. Retinal nerve fiber layer thickness measurements by optical coherence tomography in patients with sleep apnea syndrome. Clin Experiment Ophthalmol 2014;42:132-8. 10. Zengin MO, Tuncer I, Karahan E. Retinal nerve fiber layer thickness changes in obstructive sleep apnea syndrome: one year follow-up results. Int J Ophthalmol 2014;7:704-8. 11. Kiekens S, De Groot V, Coeckelbergh T, Tassignon MJ, Van de Heyning P, De Backer W, Verbraecken J. Continuous positive airway pressure therapy is associated with an increase in intraocular pressure in obstructive sleep apnea. Invest Ophthalmol Vis Sci 2008;49:934-40. 12. Ascaso FJ, Rodriguez-Jiménez R, Cabezón L, López-Antón R, Santabárbara J, De la Cámara C, Modrego PJ, Quintanilla MA, Bagney A, Guitierrez L, Cruz N, Cristóbal JA, Lobo A. Retinal nerve fiber layer and macular thickness in patients with schizophrenia: influence of recent illness episodes. Psychiatry Res 2015;229:230-6

    Corrigendum: Suitability of potyviral recombinant virus-like particles bearing a complete food allergen for immunotherapy vaccines

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    In the published article, there was an error in the author list, and author Marina Amores-Borge was erroneously excluded. The corrected author list appears below. “Diego Pazos-Castro, Clémence Margain, Zulema Gonzalez-Klein, Marina Amores- Borge, Carmen Yuste-Calvo, Maria Garrido-Arandia, Lucia Zurita, Vanesa Esteban, Jaime Tome-Amat, Araceli Diaz-Perales, Fernando Ponz”In the published article, there was an error. The missing author was not included in the Author Contributions section. A correction has been made to Author contributions. This sentence previously stated: “DP-C: Conceptualization, investigation, writing original draft. CM: Investigation. ZG-K: Conceptualization, investigation, writing review. CY-C: Investigation. MG-A: Investigation, writing review. LZ: Investigation. VE: Writing review, resources, funding acquisition. JT-A: Conceptualization, investigation, writing original draft. AD-P: Conceptualization, writing original draft, resources, funding acquisition. FP: Conceptualization, writing review,resources, funding acquisition. All authors contributed to the article and approved the submitted version.” The corrected sentence appears below: “DP-C: Conceptualization, investigation, writing original draft. CM: Investigation. ZG-K: Conceptualization, investigation, writing review. MA-B: Investigation. CY-C: Investigation. MG-A: Investigation, writing review. LZ: Investigation. VE: Writing review, resources, funding acquisition. JT-A: Conceptualization, investigation, writing original draft. AD-P: Conceptualization, writing original draft, resources, funding acquisition. FP: Conceptualization, writing review, resources, funding acquisition. All authors contributed to the article and approved the submitted version.” The authors apologize for these errors and state that they do not change the scientific conclusions of the article in any way. The original article has been updated.Peer reviewe

    A dose-response strategy reveals differences between normal-weight and obese men in their metabolic and inflammatory responses to a high-fat meal

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    A dose-response strategy may not only allow investigation of the impact of foods and nutrients on human health but may also reveal differences in the response of individuals to food ingestion based on their metabolic health status. In a randomized crossover study, we challenged 19 normal-weight (BMI: 20-25 kg/m(2)) and 18 obese (BMI: >30 kg/m(2)) men with 500, 1000, and 1500 kcal of a high-fat (HF) meal (60.5% energy from fat). Blood was taken at baseline and up to 6 h postprandially and analyzed for a range of metabolic, inflammatory, and hormonal variables, including plasma glucose, lipids, and C-reactive protein and serum insulin, glucagon-like peptide-1, interleukin-6 (IL-6), and endotoxin. Insulin was the only variable that could differentiate the postprandial response of normal-weight and obese participants at each of the 3 caloric doses. A significant response of the inflammatory marker IL-6 was only observed in the obese group after ingestion of the HF meal containing 1500 kcal [net incremental AUC (iAUC) = 22.9 ± 6.8 pg/mL × 6 h, P = 0.002]. Furthermore, the net iAUC for triglycerides significantly increased from the 1000 to the 1500 kcal meal in the obese group (5.0 ± 0.5 mmol/L × 6 h vs. 6.0 ± 0.5 mmol/L × 6 h; P = 0.015) but not in the normal-weight group (4.3 ± 0.5 mmol/L × 6 h vs. 4.8 ± 0.5 mmol/L × 6 h; P = 0.31). We propose that caloric dose-response studies may contribute to a better understanding of the metabolic impact of food on the human organism. This study was registered at clinicaltrials.gov as NCT01446068
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