RESUMO
Glaucoma is an optic neuropathy in which the primary risk factor is increased intraocular pressure (IOP), attributed to increased resistance to trabecular outflow of aqueous humor (AH). This resistance is believed to result from trabecular degeneration secondary to chronic oxidative stress and cellular senescence but may also involve inflammatory mechanisms whose roles are little known. In fact, inflammatory processes play a major role in the pathophysiology of glaucoma to varying degrees, affecting all structures of the eye, including the ocular surface, the anterior and posterior segments, and even the visual pathways of the brain. These processes are thought to result from dysfunction of a regulatory, protective para-inflammation, becoming chronic and harmful in glaucoma. While the mechanisms of the retinal inflammation which accelerates the degeneration of retinal ganglion cells (RGC) as well as the inflammation of the ocular surface aggravated by long-term use of preserved glaucoma eye drops have been described for several years, very little is known about the pathophysiology of trabecular inflammation in glaucoma. The objective of this literature review is to provide a synthesis of knowledge on the roles and mechanisms of inflammation in both the healthy and glaucomatous trabecular meshwork, as well as its role in the pathophysiology of glaucoma. Therefore, after a review of the mechanisms of cellular senescence and oxidative stress - sources of trabecular inflammation, we will approach the study of the expression and roles of the main inflammatory mediators within the trabecular meshwork. Finally, we will discuss current knowledge on the toxicity of glaucoma eye drops and their preservatives on the ocular surface and trabecular meshwork as well as their role in trabecular inflammation.
Assuntos
Glaucoma , Glaucoma/etiologia , Humanos , Inflamação/complicações , Pressão Intraocular , Soluções Oftálmicas , Malha Trabecular/químicaRESUMO
Glaucoma is a blinding optic neuropathy, the main risk factor for which is increased intraocular pressure (IOP). The trabecular meshwork, located within the iridocorneal angle, is the main pathway for drainage of aqueous humor (AH) out of the eye, and its dysfunction is responsible for the IOP elevation. The trabecular meshwork is a complex, fenestrated, three-dimensional structure composed of trabecular meshwork cells (TMC) interdigitated into a multilayered organization within the extracellular matrix (ECM). The purpose of this literature review is to provide an overview of current understanding of the trabecular meshwork and its pathophysiology in glaucoma. Thus, we will present the main anatomical and cellular bases for the regulation of aqueous humor outflow resistance, the pathophysiological mechanisms involved in trabecular dysfunction in the various types of glaucoma, as well as current and future therapeutic strategies targeting the trabecular meshwork.
Assuntos
Glaucoma/etiologia , Malha Trabecular/química , Malha Trabecular/fisiologia , Glaucoma/patologia , Glaucoma/fisiopatologia , Humanos , Pressão Intraocular/fisiologia , Doenças do Nervo Óptico/patologia , Doenças do Nervo Óptico/fisiopatologia , Malha Trabecular/citologia , Malha Trabecular/patologiaRESUMO
The authors conducted a literature review about bilateral acute iris transillumination (BAIT) syndrome, a new and relatively unknown syndrome that should be described and made known to the greatest number to avoid potential diagnostic and therapeutic errors. The first cases date back only to 2004 and a total of 79 cases have been published to date, mainly in Europe and especially in Turkey and Belgium. It mainly affects young women between the ages of 30 and 50, and symptoms are often preceded by an upper airway infection. There is also a majority of cases where the onset of the syndrome follows oral intake of moxyfloxacin. The clinical signs are dominated by strong photophobia, secondary to a spectacular transillumination of the iris. Other classical symptoms are conjunctival infection, eye pain, blurred vision, temporary ocular hypertonia, fixed mid-dilated pupils, and pigment dispersion in the anterior chamber with pigmentary deposits in the trabecular meshwork in gonioscopy, symptoms that may be mistaken for uveitis. After a few weeks or months of evolution, persistent sequelae were pupillary atony and chronic and bilateral transillumination of the iris, leading to significant photophobia and sometimes persistent ocular hypertension. The BAIT syndrome is close to the bilateral acute depigmentation of the iris (BADI) syndrome, which is similar to BAIT but lacks associated transillumination. A few cases of patients with BAIT syndrome on one eye and BADI syndrome on the contralateral eye have been described, which confirms some form of link between the two clinical entities.
RESUMO
Academic and industrial research has brought new insights into the pathogenesis of glaucoma, aiming at identifying and targeting specific mechanisms to improve our current therapeutic strategy. Retinal neurodegeneration is still the main focus, whether in terms of extrinsic factors such as neurotrophin deprivation, glutamate toxicity, vascular deficiency and neuro-inflammation from glial cells, or in terms of retinal ganglion cell intrinsic sensibility to proapoptotic signals. However, glaucoma is not solely a retinal disease but also involves retinal and trabecular meshwork degeneration, extending into and/or even originating from the brain. The present review summarizes our current knowledge of key mechanisms involved in glaucoma degeneration, focusing on the direction of current research towards the future of glaucoma therapy.
Assuntos
Glaucoma/complicações , Degeneração Retiniana/etiologia , Degeneração Retiniana/terapia , Malha Trabecular , Humanos , RetinaRESUMO
PURPOSE: To determine long-term efficacy of selective Laser Trabeculoplasty (SLT) over 12 years in chronic open-angle glaucoma (OAG) patients. METHODS: In this retrospective study, all patients treated by SLT between 1997 and 1999 for OAG were included and followed up every 6 months. The procedure was performed with a Coherent Selecta 7000 Nd:YAG with 100 ± 10 non overlapping 400 µm spots over 360 degrees centered on the trabecular meshwork. Patients were excluded in the case of prior filtration surgery or Argon laser trabeculoplasty. Our primary study parameter was the number of patients requiring filtration surgery within the follow-up period. Our secondary parameters were intraocular pressure (IOP) and SLT-related complications. RESULTS: We included 46 eyes of 28 patients. The 12-year success rate was 26.1%. Thirty-nine percent of all eyes underwent filtration surgery (failure) during the follow-up period, and 34.8% were lost to follow-up. In the pigmentary glaucoma (PG) subgroup, the 12-year success rate was 16%, while it was 37.5% in the Primary OAG subgroup. The overall mean IOP was 22.8 mm Hg (D.S. 3.78) prior to laser, 16.08 mm Hg (D.S. 2.7) at 1 year and 15 mm Hg (D.S. 1.8) at 12 years. The mean number of medications was 1.6 (D.S. 0.8) prior to SLT, 1.36 (D.S. 0.8) at 1 year, and 1.3 (D.S. 1.2), 12 years after SLT respectively. No patients had a second SLT treatment. No significant complications occurred during follow-up. CONCLUSION: Selective laser trabeculoplasty may at times be a useful resource to lower IOP in patients with OAG. Nonetheless, the failure rate is significant especially in PG, which requires confirmation by larger prospective studies.