ABSTRACT
OBJECTIVE: To investigate the lipid peroxidation (PEROX) processes in primary open-angle glaucoma (POAG) patients, and whether this mechanism may be related to disease progression. MATERIAL AND METHODS: A prospective, observational, cross-sectional, non-experimental, and analytical study was conducted on a case and a comparison group, consisting of 175 surgical patients divided into: 1) POAG group (GG; n=88) and 2) comparison group of patients with cataracts (CG; n=87). Demographic data, patient characteristics, lifestyle data, as well as ophthalmological examination were registered in an Excel spreadsheet. Biochemical data were obtained by processing the aqueous humor collected at the beginning of surgery. Determination of malondialdehyde/thiobarbituric acid reactive substances (MDA/TBARS) and total antioxidant activity (AAO) was assayed using enzymatic-colorimetric methods in the aqueous humor samples. Statistical analysis was performed using SPSS 15.0 software. RESULTS: Aqueous humor MDA/TBARS levels were significantly higher (P<.001) and the AAO significantly lower (P<.001) in the GG than in the GC. The MDA/TBARS directly correlated with intraocular pressure (IOP) values and the cup-to-disc ratio (CDR). Decreased AAO activity correlated inversely with IOP and CDR. Differences between groups were noticeably higher in the GG as regards obesity, alcohol consumption, anxiety, depression, and sedentary lifestyle. In the multivariate analysis, the variables that showed a better predictive ability were: MDA/TBARS, PIO, AAO, CDR, and depression. CONCLUSIONS: The POAG patients have a PEROX background that is reflected in the aqueous humor by variations in MDA/TBARS and AAO. Moreover, both the MDA/TBARS and AAO correlated with IOP values and the CDR. We propose that determination of MDA/TBARS and AAO in the aqueous humor of POAG patients can be used as biomarkers for monitoring the disease, as well the changes in lifestyle and other related risk factors.
Subject(s)
Antioxidants/analysis , Aqueous Humor/chemistry , Glaucoma, Open-Angle/metabolism , Lipid Peroxidation , Thiobarbituric Acid Reactive Substances/analysis , Adult , Aged , Aged, 80 and over , Cataract/metabolism , Colorimetry , Cross-Sectional Studies , Female , Humans , Male , Malondialdehyde/analysis , Middle Aged , Prospective StudiesABSTRACT
CASE REPORT: We report the follow-up of a case of choroideremia who underwent three white-on-white automated visual field and three scanning laser polarimetry (SLP) examinations by means of a GDx VCC in the course of one year. A bilateral perimetric deterioration in indices and scotomas was found. As a result, retinal nerve fiber layer retardation parameters and maps changed on GDx VCC advanced serial analyses in both eyes. DISCUSSION: Serial analyses with GDx VCC may be used as objective and quantitative tests to assess the progression of chorioretinal dystrophies like choroideremia
Subject(s)
Choroideremia/diagnosis , Diagnostic Techniques, Ophthalmological , Disease Progression , Follow-Up Studies , Humans , Lasers , Male , Middle Aged , Scotoma/diagnosis , Time Factors , Visual Field Tests , Visual FieldsABSTRACT
PURPOSE: Previous work from our group demonstrated that regular high consumption of ethanol during pregnancy induces a delay in growth and structural changes in the developing eye and vision (Pinazo-Duran et al., Teratology '93; Eur J Ophthalmol '97; Stromland and Pinazo-Duran, Teratology '94; Alcohol Alcoholism '02). Our main goal is to study at a cellular and molecular level, whether or not the prenatal alcohol exposure may change the development of the glial cells and inducing the optic nerve dysmorphogenesis. We have used key protein markers to analyse the expression in the rat optic nerve throughout the pre- and postnatal periods. METHODS: To better understanding the actions of ethanol on optic nerve development in alcohol-induced and control dams, these were fed a liquid diet during gestation and lactation, containing either ethanol (5% w/, 35% of the daily food intake) or isocaloric carobydrates (35% of the daily food intake). Eyes were enucleated and processed to immunocytochemical and morphological tecnhiques and western blot approaches, using antibodies against the glial fibrillary acidid protein (GFAP), neurofilament protein (NFP) and myelin basic protein (MBP). RESULTS: Three main observations were made in the ethanol-exposed and control groups: 1) the optic nerve size was significantly lower in the ethanol group than in the control group, 2) there were statistically significant changes in optic nerve astrocytes and oligodendrocytes, optic axons and myelin sheaths and 3) a delay and altered expression of developmental proteins. CONCLUSIONS: All data support our earlier studies confirming the deleterious effects of ethanol on the developing visual system. We suggest that ethanol may alter the expression of precise genes involved in eye development and posterior remodelling. These results can be extrapolated to clinical advances in fetal alcohol syndrome and toxic optic neuropathies.
