ABSTRACT
PURPOSE: To evaluate the effects of intravitreal bevacizumab (IVB) injections for secondary macular edema of branch retinal vein occlusion (BRVO). SUBJECTS AND METHODS: We treated 91 patients (91 eyes) with IVB injections (1.25 mg/0.05 ml), including 27 eyes which received two injections. Visual acuity and central retinal thickness (CRT) were measured at 1, 4, 8 and 12 weeks after injection. RESULTS: The mean visual acuity and CRT improved from 0.25 (610.8 microm) at baseline to 0.47 (238.4 microm) 4 weeks after injection and 0.45 (368.7 microm) after 12 weeks. Twenty seven eyes among the total of 91 eyes had a second injection due to recurrence or worsened metamorphopsia. In these cases, mean visual acuity and CRT improved from 0.33 (483.7 microm) at baseline to 0.44 (234.3 microm) 4 weeks after injection and 0.42 (296.8 microm) after 12 weeks. Comparing the efficacy by the number of treatments, visual acuity and CRT improved more significantly in a first time treatment group. CONCLUSIONS: IVB injection is generally effective, but recurrence occurred in 26/47 eyes based on CRT. The second injection is effective, however, its effect is weak when compared with the first injection.
Subject(s)
Angiogenesis Inhibitors/administration & dosage , Antibodies, Monoclonal/administration & dosage , Macular Edema/drug therapy , Macular Edema/etiology , Retinal Vein Occlusion/complications , Adult , Aged , Aged, 80 and over , Antibodies, Monoclonal, Humanized , Bevacizumab , Female , Humans , Injections, Intraocular , Macular Edema/pathology , Macular Edema/physiopathology , Male , Middle Aged , Recurrence , Retina/pathology , Retinal Vein Occlusion/pathology , Retinal Vein Occlusion/physiopathology , Treatment Outcome , Visual AcuitySubject(s)
Arginine/genetics , Choroid Diseases/genetics , Intermediate Filament Proteins/genetics , Leucine/genetics , Membrane Glycoproteins , Nerve Tissue Proteins/genetics , Point Mutation , Aged , Amino Acid Substitution , Choroid Diseases/diagnosis , Codon , Electroretinography , Fluorescein Angiography , Genes, Dominant , Humans , Male , Middle Aged , Pedigree , PeripherinsABSTRACT
The purpose of this study was to investigate the effects of glutamate accumulation in vitreous on retinal structure and function, due to a diet high in sodium glutamate. Three different diet groups were created, consisting of rats fed on a regular diet (diet A), a moderate excess of sodium glutamate diet (diet B) and a large excess of sodium glutamate diet (diet C). After 1, 3 and 6 months of the administration of these diets, amino acids concentrations in vitreous were analyzed. In addition, retinal morphology and function by electroretinogram (ERG) of three different diet groups were studied. Significant accumulation of glutamate in vitreous was observed in rats following addition of sodium glutamate to the diet as compared to levels with a regular diet. In the retinal morphology, thickness of retinal neuronal layers was remarkably thinner in rats fed on sodium glutamate diets than in those on a regular diet. TdT-dUTP terminal nick-end labelling (TUNEL) staining revealed significant accumulation of the positive staining cells within the retinal ganglion cell layers in retinas from diets B and C as compared with that from diet A. Similar to this, immunohistochemistry demonstrated increased expression of glial fibrillary acidic protein (GFAP) within the retinal inner layers from diets B and C as compared with diet A. Functionally, ERG responses were reduced in rats fed on a sodium glutamate diets as compared with those on a regular diet. The present study suggests that a diet with excess sodium glutamate over a period of several years may increase glutamate concentrations in vitreous and may cause retinal cell destruction.
Subject(s)
Diet , Food Additives/pharmacology , Retina/drug effects , Sodium Glutamate/pharmacology , Amino Acids/analysis , Animals , Apoptosis/drug effects , Body Weight/drug effects , Electroretinography , Female , Food Additives/administration & dosage , Glial Fibrillary Acidic Protein/metabolism , In Situ Nick-End Labeling , Microscopy, Fluorescence , Rats , Rats, Inbred Lew , Retina/pathology , Retina/physiopathology , Sodium Glutamate/administration & dosage , Vitreous Body/chemistryABSTRACT
BACKGROUND: Retinitis pigmentosa (RP) is primary, chronic, and hereditary chorioretinal degeneration characterized by photopsia, progressive visual loss with ring scotoma, and impairment of dark adaptation. Although modern molecular biology and molecular genetics have identified many causative genes, the molecular pathophysiology of RP is not fully understood, and no effective treatments have been found yet. In recent studies using animal models of RP, new treatments have been devised and their clinical use is being considered. METHOD: In terms of the molecular pathophysiology of RP, we summarized previous studies of genetic impairment of proteins involved in the phototransduction pathway and introduced new possible therapies for RP. RESULTS: We found that most abnormalities of the genes related with the photoxcitation and its inhibition process in the photoreceptor cells caused a variety of clinical manifestations of RP. CONCLUSION: So far, a variety of abnormalities of the genes causing RP have been identified. However, further studies of the relationship between the abnormalities and clinical expression are needed for better understanding of the pathophysiology of RP.