Efecto del bevacizumab intravítreo en la presión intraocular de pacientes tratados en el Instituto Regional de Oftalmología
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Date
2023-12-19
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Universidad Nacional de Trujillo
Abstract
Desde la aparición de los fármacos intravítreos con propiedades anti-factor de crecimiento endotelial vascular (VEGF), el tratamiento de muchas patologías caracterizadas por la ruptura de la barrera hematorretiniana, la liberación de mediadores inflamatorios y la aparición de neovasos han tenido un buen resultado clínico, logrando incluso mejorar la agudeza visual final y evitando el deterioro de la visión. Sin embargo, el globo ocular es una estructura hermética que contiene un volumen casi constante de líquidos, los cuales se mantienen en un equilibrio homeostático debido a sus sistemas de producción y drenaje del humor acuoso. (1, 3)
Durante la aplicación intravítrea de fármacos se crea un aumento cuantificable del volumen vítreo, pudiendo ocasionar aumentos de presión intraocular (PIO) transitorios o incluso permanentes que podrían afectar su control, sobre todo en individuos anatómica o funcionalmente predispuestos a estos sucesos. (2)
Los agentes con propiedades anti – VEGF más utilizados en nuestro medio son bevacizumab (Avastin, Genentech, Inc.), ranibizumab (Lucentis, Genentech, Inc.) y aflibercept (Eylea, Regeneron, Tarrytown, Nueva York);, estos medicamentos son indicados para el tratamiento de diferentes enfermedades del segmento posterior como el edema macular diabético, la degeneración macular húmeda, la neovascularización coroidea y retiniana, muchos de ellos con esquemas multidosis con un periodo interterapia de 4 – 6 semanas y que pueden ser necesarios de forma crónica. (4,5)
Se han descrito diferentes mecanismos causantes de la elevación de la presión en estos pacientes. Incluyendo respuesta inflamatoria, un efecto tóxico directo de los agentes anti – VEGF sobre la malla trabecular, inyección de un alto volumen de fármaco o un bloqueo mecánico de la malla trabecular por agregados contaminantes o proteínas
Abstract Since the appearance of intravitreal drugs with anti-vascular endothelial growth factor (VEGF) properties, the treatment of many pathologies characterized by the breakdown of the blood-retinal barrier, the release of inflammatory mediators and the appearance of neovessels have had a good clinical result, even achieving an improvement in final visual acuity and avoiding deterioration of vision. However, the eyeball is a hermetic structure that contains an almost constant volume of liquids, which are maintained in a homeostatic balance due to its production and drainage systems of aqueous humor. (1, 3) During the intravitreal application of drugs, a quantifiable increase in vitreous volume is created, which may cause transient or even permanent increases in intraocular pressure (IOP) that could affect its control, especially in individuals anatomically or functionally predisposed to these events. (2) The most commonly used agents with anti-VEGF properties in our setting are bevacizumab (Avastin, Genentech, Inc.), ranibizumab (Lucentis, Genentech, Inc.) and aflibercept (Eylea, Regeneron, Tarrytown, New York); these drugs are indicated for the treatment of different diseases of the posterior segment such as diabetic macular edema, wet macular degeneration, choroidal and retinal neovascularization, many of them with multidose regimens with an intertherapy period of 4-6 weeks and which may be necessary on a chronic basis. (4,5) Different mechanisms causing the increase in pressure in these patients have been described. These include inflammatory response, a direct toxic effect of anti-VEGF agents on the trabecular meshwork, injection of a high volume of drug, or mechanical blockage of the trabecular meshwork by contaminating aggregates or proteins
Abstract Since the appearance of intravitreal drugs with anti-vascular endothelial growth factor (VEGF) properties, the treatment of many pathologies characterized by the breakdown of the blood-retinal barrier, the release of inflammatory mediators and the appearance of neovessels have had a good clinical result, even achieving an improvement in final visual acuity and avoiding deterioration of vision. However, the eyeball is a hermetic structure that contains an almost constant volume of liquids, which are maintained in a homeostatic balance due to its production and drainage systems of aqueous humor. (1, 3) During the intravitreal application of drugs, a quantifiable increase in vitreous volume is created, which may cause transient or even permanent increases in intraocular pressure (IOP) that could affect its control, especially in individuals anatomically or functionally predisposed to these events. (2) The most commonly used agents with anti-VEGF properties in our setting are bevacizumab (Avastin, Genentech, Inc.), ranibizumab (Lucentis, Genentech, Inc.) and aflibercept (Eylea, Regeneron, Tarrytown, New York); these drugs are indicated for the treatment of different diseases of the posterior segment such as diabetic macular edema, wet macular degeneration, choroidal and retinal neovascularization, many of them with multidose regimens with an intertherapy period of 4-6 weeks and which may be necessary on a chronic basis. (4,5) Different mechanisms causing the increase in pressure in these patients have been described. These include inflammatory response, a direct toxic effect of anti-VEGF agents on the trabecular meshwork, injection of a high volume of drug, or mechanical blockage of the trabecular meshwork by contaminating aggregates or proteins
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Keywords
Bevacizumab Intravítreo, Presión Intraocular, Hipertensión Ocular, Glaucoma