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1.
PLoS One ; 15(8): e0236819, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32817645

RESUMO

AIMS: To examine the relationship between baseline structural characteristics of the optic nerve head (ONH) and retinal nerve fiber layer (RNFL) and functional disease progression in patients with open-angle glaucoma (OAG) over 5 years. METHODS: 112 OAG patients were prospectively examined at baseline and every 6 months over a period of five years. Structural glaucomatous changes were examined with optical coherence tomography (OCT) and Heidelberg retinal tomography-III (HRT-III), and functional disease progression with automated perimetry (Humphrey visual fields). Cox proportional hazard models were used to assess the relationship between baseline structural measurements and functional disease progression. RESULTS: From baseline over a 5-year period, statistically significant increases were found in OCT disc (D) area (p<0.001), cup (C) area (p<0.001), C/D area ratio (p<0.001), C/D horizontal ratio (p<0.001), C/D vertical ratio (p = 0.018), and a decrease in superior RNFL thickness (p = 0.008). Statistically significant increases were found in HRT-III C volume (p = 0.021), C/D area ratio (p = 0.046), mean C depth (p = 0.036), C shape (p = 0.008), and height variation contour (p = 0.020). Functional disease progression was detected in 37 of the 112 patients (26 of European descent and 11 of African descent; 33%). A statistically significant shorter time to functional progression was seen in patients with larger baseline OCT D area (p = 0.008), C area (p = 0.003), thicker temporal RNFL (p = 0.003), and in patients with a larger HRT-III C area (p = 0.004), C/D area ratio (p = 0.004), linear C/D ratio (p = 0.007), C shape (p = 0.032), or smaller rim area (p = 0.039), rim volume (p = 0.005), height variation contour (p = 0.041), mean RNFL thickness (p<0.001), or RNFL cross-sectional area (p = 0.002). CONCLUSION: Baseline ONH and RNFL structural characteristics were associated with a significantly shorter time to functional glaucomatous progression and visual field loss through the five-year period in OAG patients.


Assuntos
Cegueira/diagnóstico , Glaucoma de Ângulo Aberto/patologia , Fibras Nervosas/fisiologia , Disco Óptico/fisiopatologia , Idoso , Cegueira/etiologia , Complicações do Diabetes/patologia , Progressão da Doença , Feminino , Glaucoma de Ângulo Aberto/complicações , Humanos , Pressão Intraocular , Masculino , Pessoa de Meia-Idade , Fibras Nervosas/patologia , Disco Óptico/diagnóstico por imagem , Modelos de Riscos Proporcionais , Estudos Prospectivos , Retina/diagnóstico por imagem , Retina/fisiopatologia , Tomografia de Coerência Óptica , Testes de Campo Visual
2.
Expert Opin Pharmacother ; 20(14): 1703-1709, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31343372

RESUMO

Introduction: Bromfenac is a topical ophthalmic non-steroidal anti-inflammatory drug (NSAID) used to reduce pain and treat post-operative inflammation after cataract surgery. Bromfenac 0.075% in the DuraSite™ vehicle is a newly-approved formulation which has been shown to be efficacious and safe for use in cataract surgery to reduce pain and treat inflammation. It has been shown to have a slightly better posterior segment ocular bioavailability compared to similar topical ophthalmic NSAIDs. However, there is a paucity of studies investigating its role in the prevention and treatment of post-operative pseudophakic cystoid macular edema. Areas covered: In this review, the authors provide an overview of similar products available, describe the novelty of bromfenac 0.075% in the DuraSite vehicle, and discuss the relevant clinical studies to determine if the formulation is safe and efficacious. Expert opinion: Bromfenac 0.075% in the DuraSite vehicle is a new topical ophthalmic medication which has been approved by the FDA for the prevention of pain and treatment of post-operative inflammation. It provides cataract surgeons with an additional medication for cataract surgery. However, no robust studies have been performed showing the effect that it has on the reduction or prevention of post-operative pseudophakic cystoid macular edema.


Assuntos
Anti-Inflamatórios não Esteroides/uso terapêutico , Benzofenonas/uso terapêutico , Bromobenzenos/uso terapêutico , Catarata/patologia , Inflamação/tratamento farmacológico , Dor Pós-Operatória/tratamento farmacológico , Anti-Inflamatórios não Esteroides/efeitos adversos , Anti-Inflamatórios não Esteroides/química , Benzofenonas/efeitos adversos , Benzofenonas/química , Bromobenzenos/efeitos adversos , Bromobenzenos/química , Extração de Catarata/efeitos adversos , Ensaios Clínicos como Assunto , Composição de Medicamentos , Humanos , Dor Pós-Operatória/etiologia , Resultado do Tratamento
3.
J Glaucoma ; 26(4): 390-395, 2017 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-28169917

RESUMO

Transforming growth factor-ß (TGF-ß) may play a role in the pathogenesis of primary open-angle glaucoma (POAG). Elevated levels of TGF-ß are found in the aqueous humor and in reactive optic nerve astrocytes in patients with glaucoma. In POAG, aqueous humor outflow resistance at the trabecular meshwork (TM) leads to increased intraocular pressure and retinal ganglion cell death. It is hypothesized that TGF-ß increases outflow resistance by altering extracellular matrix homeostasis and cell contractility in the TM through interactions with other proteins and signaling molecules. TGF-ß may also be involved in damage to the optic nerve head. Current available therapies for POAG focus exclusively on lowering intraocular pressure without addressing extracellular matrix homeostasis processes in the TM. The purpose of this review is to discuss possible therapeutic strategies targeting TGF-ß in the treatment of POAG. Herein, we describe the current understanding of the role of TGF-ß in POAG pathophysiology, and examine ways TGF-ß may be targeted at the levels of production, activation, downstream signaling, and homeostatic regulation.


Assuntos
Anti-Hipertensivos/uso terapêutico , Glaucoma de Ângulo Aberto/tratamento farmacológico , Terapia de Alvo Molecular/métodos , Fator de Crescimento Transformador beta/antagonistas & inibidores , Anti-Hipertensivos/farmacologia , Humor Aquoso/metabolismo , Astrócitos/metabolismo , Ensaios Clínicos como Assunto , Matriz Extracelular/metabolismo , Glaucoma de Ângulo Aberto/fisiopatologia , Humanos , Pressão Intraocular/efeitos dos fármacos , Pressão Intraocular/fisiologia , Disco Óptico/metabolismo , Transdução de Sinais/fisiologia , Malha Trabecular/fisiologia , Fator de Crescimento Transformador beta/fisiologia
4.
F1000Prime Rep ; 6: 102, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-25580256

RESUMO

Open-angle glaucoma is a multifactorial optic neuropathy characterized by progressive loss of retinal ganglion cells and their axons. It is an irreversible disease with no established cure. The only currently approved treatment is aimed at lowering intraocular pressure, the most significant risk factor known to date. However, it is now clear that there are other risk factors involved in glaucoma's pathophysiology. To achieve future improvements in glaucoma management, new approaches to therapies and novel targets must be developed. Such therapies may include new tissue targets for lowering intraocular pressure, molecules influencing ocular hemodynamics, and treatments providing neuroprotection of retinal ganglion cells. Furthermore, novel drug delivery systems are in development that may improve patient compliance, increase bioavailability, and decrease adverse side effects.

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