RESUMO
La atrofia geográfica se caracteriza por un déficit visual severo cuya etiología y fisiopatología aún están por dilucidar. Como hipótesis de trabajo, el daño oxidativo desencadenaría una inflamación crónica en el complejo membrana de Bruch-EPR-coriocapilar, cobrando protagonismo la activación del complemento. Algunos sujetos con mutaciones en el sistema del complemento y otros factores tienen menor capacidad en la modulación de la respuesta inflamatoria, lo que se traduce en daño celular y acumulación de desechos. Esta acumulación de desechos intracelulares y extracelulares se manifiesta como drusas y alteraciones pigmentarias que preceden a la atrofia de fotorreceptores, EPR y coriocapilar, existiendo un proceso isquémico de base con disminución del flujo coroideo. Todos estos procesos se objetivan como hallazgos tomográficos y signos de la autofluorescencia que son útiles en la evaluación de los pacientes con DMAE atrófica, pudiendo establecer un pronóstico individualizado. Terapias antiinflamatorias, antioxidantes y reductora de la acumulación de toxinas para la preservación de células del EPR y fotorreceptores están siendo investigadas para disminuir el avance de esta enfermedad
Geographic atrophy is characterized by severe visual deficit whose etiology and pathophysiology are yet to be elucidated. As a working hypothesis, oxidative damage could trigger a chronic inflammation in Bruch's membrane-RPE-choriocapillaris complex, mostly due to complement pathway overactivation. Some individuals with mutations in the complement system and other factors have diminished capacity in the modulation of the inflammatory response, which results in cell damage and waste accumulation. This accumulation of intracellular and extracellular waste products manifests as drusen and pigmentary changes that precede the atrophy of photoreceptors, RPE, choriocapillaris with an ischemic process with decreased choroid flow. All these processes can be detected as tomographic findings and autofluorescence signals that are useful in the evaluation of patients with atrophic AMD, which helps to establish an individualized prognosis. Anti-inflammatory, antioxidant and therapies that decrease the accumulation of toxins for the preservation of the RPE cells and photoreceptors are being investigated in order to slow down the progression of this disease
Assuntos
Humanos , Atrofia Geográfica/etiologia , Degeneração Macular/etiologia , Drusas Retinianas/complicações , Atrofia Geográfica/terapia , Fatores de Risco , Inflamação/complicações , Proteínas do Sistema Complemento/análise , Estresse Oxidativo , Lipofuscina/análiseRESUMO
Geographic atrophy is characterized by severe visual deficit whose etiology and pathophysiology are yet to be elucidated. As a working hypothesis, oxidative damage could trigger a chronic inflammation in Bruch's membrane-RPE-choriocapillaris complex, mostly due to complement pathway overactivation. Some individuals with mutations in the complement system and other factors have diminished capacity in the modulation of the inflammatory response, which results in cell damage and waste accumulation. This accumulation of intracellular and extracellular waste products manifests as drusen and pigmentary changes that precede the atrophy of photoreceptors, RPE, choriocapillaris with an ischemic process with decreased choroid flow. All these processes can be detected as tomographic findings and autofluorescence signals that are useful in the evaluation of patients with atrophic AMD, which helps to establish an individualized prognosis. Anti-inflammatory, antioxidant and therapies that decrease the accumulation of toxins for the preservation of the RPE cells and photoreceptors are being investigated in order to slow down the progression of this disease.
