Neuroretinitis with branch retinal artery occlusion in a 15-year-old female.

We report a case of Bartonella henselae neuroretinitis with significant disc and peripapillary edema, branch retinal artery occlusion without macula involvement and well preserved central vision. A 15-year-old female presented with loss of vision over 4 weeks in the left eye. She had a history of cat exposure, but a cat scratch, insect bite or conjunctivitis was not reported. An inferotemporal arcuate scotoma developed during the acute phase and persisted over the course of the follow-up.

The impact of cataract on the quantitative, non-invasive assessment of retinal blood Flow.

PURPOSE: The aim of the study was to determine the impact of cataract on the quantitative, non-invasive assessment of retinal blood flow assessed by bidirectional laser Doppler flowmetry and simultaneous vessel densitometry. METHODOLOGY: Ten patients scheduled for extracapsular cataract extraction using phacoemulsification and intraocular lens implantation between the ages of 61 and 84 (mean age 73 years, SD ± 8) were prospectively recruited. Two visits were required to complete the study; one visit prior to extracapsular cataract extraction and one at least 6 weeks after the surgery to allow for sufficient postoperative recovery. The severity of cataract was documented using the Lens Opacity Classification System (LOCS, III) at the first visit. Retinal arteriolar hemodynamics were measured at both visits using the high-intensity setting of the Canon Laser Blood Flowmeter. RESULTS: All eyes showed no clinical signs of postoperative intraocular inflammation. The quantitative assessment of retinal arteriolar diameter and blood flow were reduced following extracapsular cataract extraction (Wilcoxon signed-rank test, p = 0.022 and p=0.028, respectively); however, centreline blood velocity was not significantly changed (Wilcoxon signed-rank test, p=0.074). Intraocular pressure was unchanged pre- and postcataract extraction. CONCLUSIONS: Retinal vessel densitometry assessment in the presence of cataract results in the erroneous elevation of the diameter measurement and thereby the calculation of blood flow. The bidirectional Doppler assessment of blood velocity appears to be more robust to light scatter induced by cataract. Care needs to be exercised in the interpretation of studies of retinal vessel diameter or blood flow that utilize similar densitometry techniques.

p53-regulated increase in oxidative-stress--induced apoptosis in Fuchs endothelial corneal dystrophy: a native tissue model.

PURPOSE: This study compared susceptibility of Fuchs endothelial corneal dystrophy (FECD) and normal corneal endothelial cells (CECs) to oxidative stress, and studied the mechanism of oxidative-stress-induced apoptosis in FECD-affected endothelium. METHODS: For in vitro studies, immortalized normal and FECD human corneal endothelial cell lines (HCECi and FECDi, respectively) were exposed to tert-butyl hydroperoxide (tBHP). Apoptotic cell populations were distinguished using flow cytometry. Reactive oxygen species production was measured by a horseradish peroxidase assay. For ex vivo studies, CECs were exposed to tBHP. Oxidative DNA damage and apoptosis were assessed by anti-8-hydroxydeoxyguanosine antibody and TUNEL assay, respectively. p53 and phospho-p53 levels were assessed by Western blot and immunohistochemistry. RESULTS: Flow cytometry revealed a higher rate of apoptosis in FECDi than that in HCECi after exposure to 0.5 mM (P=0.010) and 1.0 mM tBHP (P=0.041). Further analysis showed increased production of H2O2 by FECDi than that by HCECi. Oxidative DNA damage increased in both normal and FECD CECs after exposure to 0.5 mM tBHP (P=0.031 and 0.022, respectively), leading to a 21% increase in TUNEL-positive CECs in FECD (P=0.015) but no change in normal. Baseline p53 expression was twofold higher in FECD than that in normal endothelium (P=0.002). Immunofluorescence revealed an increase in p53 and phospho-p53 levels in FECD compared with that in normal endothelium. CONCLUSIONS: FECD CECs are more susceptible to oxidative DNA damage and oxidative-stress-induced apoptosis than normal. Increased activation of p53 in FECD suggests that it mediates cell death in susceptible CECs. The authors conclude that p53 plays a critical role in complex mechanisms regulating oxidative-stress-induced apoptosis in FECD.

Fuchs endothelial corneal dystrophy.

Fuchs endothelial corneal dystrophy (FECD) is characterized by progressive loss of corneal endothelial cells, thickening of Descement's membrane and deposition of extracellular matrix in the form of guttae. When the number of endothelial cells becomes critically low, the cornea swells and causes loss of vision. The clinical course of FECD usually spans 10-20 years. Corneal transplantation is currently the only modality used to restore vision. Over the last several decades genetic studies have detected several genes, as well as areas of chromosomal loci associated with the disease. Proteomic studies have given rise to several hypotheses regarding the pathogenesis of FECD. This review expands upon the recent findings from proteomic and genetic studies and builds upon recent advances in understanding the causes of this common corneal disorder.

Evidence of oxidative stress in the pathogenesis of fuchs endothelial corneal dystrophy.

Fuchs endothelial corneal dystrophy (FECD) is a progressive, blinding disease characterized by corneal endothelial (CE) cell apoptosis. Corneal transplantation is the only measure currently available to restore vision in these patients. Despite the identification of some genetic factors, the pathophysiology of FECD remains unclear. In this study, we observed a decrease in the antioxidant response element-driven antioxidants in FECD corneal endothelium. We further demonstrated that nuclear factor erythroid 2-related factor 2, a transcription factor known to bind the antioxidant response element and activate antioxidant defense, is down-regulated in FECD endothelium. Importantly, we detected significantly higher levels of oxidative DNA damage and apoptosis in FECD endothelium compared with normal controls and pseudophakic bullous keratopathy (iatrogenic CE cell loss) specimens. A marker of oxidative DNA damage, 8-hydroxy-2'-deoxyguanosine, colocalized to mitochondria, indicating that the mitochondrial genome is the specific target of oxidative stress in FECD. Oxidative DNA damage was not detected in pseudophakic bullous keratopathy corneas, whereas it colocalized with terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive cells in FECD samples. Ex vivo, oxidative stress caused characteristic morphological changes and apoptosis of CE, suggestive of findings that characterize FECD in vivo. Together, these data suggest that suboptimal nuclear factor erythroid 2-related factor 2-regulated defenses may account for oxidant-antioxidant imbalance in FECD, which in turn leads to oxidative DNA damage and apoptosis. This study provides evidence that oxidative stress plays a key role in FECD pathogenesis.

Renal tumors and the risk of malignancy based on size.

PURPOSE: To determine the incidence of malignancy in resected renal tumors in a subpopulation of Canadian patients and the significance of tumor size, patient's demographics, and whether the tumor was an incidental finding. METHODS: Medical records of 168 consecutive nephrectomies performed between March 2003 and June 2008 at our institution were reviewed retrospectively. RESULTS: Average age of the patients was 61 years old (SD 11, range 28-89) and male to female ratio was 1.3:1. Total of 180 masses were resected in 168 nephrectomies (128 radical, 40 partial) during the study period. Of the 180 masses, 20 (11%) were benign and 160 (89%) were malignant lesions. Fifty-five percent of the resected renal masses were incidentally found on preoperative imaging. Based on the pathology reports, the average size of the masses was 5.5 cm (SD 4.0, range 0.3-25.0). The larger masses were more likely to be malignant than the smaller masses (Pearson's chi-square test, p = 0.040). CONCLUSION: The present study assists us to adequately assess the risk of malignancy of a renal mass in a Canadian population based on size which allows us to properly advise the patients and suggest best possible treatment options. We recommend more aggressive therapies for masses larger than 4 cm and parenchymal sparing procedures for masses smaller than 4 cm as large proportion of these are benign.

Impact of simulated light scatter on the quantitative, noninvasive assessment of retinal arteriolar hemodynamics.

We determine the impact of artificial light scatter on quantitative, noninvasive assessment of retinal arteriolar hemodynamics. One eye from each of 10 healthy young subjects between the ages of 18 and 30 (23.6+/-3.4) is randomly selected. To simulate light scatter, cells comprising a plastic collar and two plano lenses are filled with solutions of differing concentration of polystyrene microspheres (Polysciences Inc., USA). We prepare 0.002, 0.004, 0.006, and 0.008% microsphere concentrations as well as distilled water only. The Canon laser blood flowmeter (CLBF) is used to noninvasively assess retinal arteriolar blood flow. After a preliminary screening to confirm subject eligibility, seven arteriolar blood flow measurements are taken by randomly placing the cells between the instrument objective lens and the subjects' cornea. To achieve a baseline, subjects are first imaged with no cell in place. Both low- and high-intensity CLBF laser settings are assessed. Our light scatter model results in an artifactual increase of retinal arteriolar diameter (p<0.0001) and thereby increased retinal blood flow (p<0.0001). The 0.006 and 0.008% microsphere concentrations produce significantly higher diameter and flow values than baseline. Centerline blood velocity, however, is not affected by light scatter. Retinal arteriolar diameter values are significantly less with the high-intensity laser than with the low-intensity laser (p=0.0007). Densitometry assessment of vessel diameter is increasingly impacted as the magnitude of artificial light scatter increases; this effect can be partially negated by increasing laser intensity. A cataract is an inevitable consequence of aging and, therefore, care must be exercised in the interpretation of studies of retinal vessel diameter that use similar densitometry techniques.