Choroidal thickness measurements in children with isolated growth hormone deficiency.

PurposeThe aim of this study was to determine the choroidal thickness measurement values in cases with isolated growth hormone deficiency (IGHD), to compare them with the healthy control group by using enhanced depth imaging optical coherence tomography (EDI-OCT), and to evaluate the effect of growth hormone (GH) treatment on choroid.Patients and methodsIn this study, 23 cases who were diagnosed with IGHD as a study group and 46 healthy subjects as a control group were included. All patients and controls underwent a complete ophthalmologic examination, including an examination with EDI-OCT. Choroidal thickness (CT) was measured at the fovea and at 1000 µm intervals from the foveal center in both temporal and nasal directions.ResultsThe mean subfoveal choroidal thickness (SFCT) was 329.04±88.49 µm in the cases with IGHD and 365.35±50.48 µm in the control group (P=0.033). The mean CT at temporal 1 and 2 mm were thinner in the IGHD group than that of control group (P=0.033 and P=0.043, respectively). Nasal quadrant measurements were also found to be thinner in the IGHD cases than that of control group, but the difference was not statistically significant. We found a significant positive correlation between pubertal staging and SFCT (rs=0.607, P=0.006). There was no statistically significant difference in CT values of the study group between before and 12 months after GH treatment (P>0.05).ConclusionThis study shows patients with IGHD has a thinner CT when compared with healthy pediatric cases. GH treatment seems to be not associated with the choroidal development.

Multiple sclerosis and optic nerve: an analysis of retinal nerve fiber layer thickness and color Doppler imaging parameters.

PURPOSE: To compare both retinal nerve fiber layer thickness and orbital color Doppler ultrasonography parameters in patients with multiple sclerosis (MS) versus healthy controls. METHODS: This is an observational case-control study. Forty eyes from MS patients and twenty eyes from healthy volunteers were examined. Eyes were classified into three groups as group 1, eyes from MS patients with previous optic neuritis (n=20); group 2, eyes from MS patients without previous optic neuritis (n=20); and group 3, eyes from healthy controls (n=20). Following complete ophthalmologic examination and retinal nerve fiber layer thickness measurement for each group, blood flow velocities of posterior ciliary arteries, central retinal artery, ophthalmic artery, and superior ophthalmic vein were measured. Pourcelot index (resistive index), an indicator of peripheral vascular resistance, was also calculated. The statistical assessment was performed with the assistance of Pearson's Chi-square test, Mann-Whitney U-test, Kruskal-Wallis test, and Spearman's correlation test. RESULTS: The studied eyes exposed similar values in terms of intraocular pressure and central corneal thickness, implying no evidence in favor of glaucoma. All nerve fiber layer thickness values, except superior nasal quadrants, in group 1 were found to be significantly thinner than groups 2 and 3. Blood flow velocity and mean resistivity index parameters were similar in all the groups. CONCLUSIONS: In MS patients, especially with previous optic neuritis, diminished retinal nerve fiber layer thickness was observed. Contrary to several studies in the current literature, no evidence supporting potential vascular origin of ocular involvement in MS was found.

Chorioretinectomy for perforating eye injuries.

PURPOSE: To report the outcomes of chorioretinectomy in severe ocular injuries where a foreign body penetrated the choroid or perforated the globe. METHODS: The study sample consisted of a retrospective, non-comparative, consecutive interventional case series of 13 perforating or severe intraocular foreign body ocular injuries that were treated at a single institution from March 2008 to March 2010. All the patients were operated with 20-gauge three-port pars plana vitrectomy (PPV) by removing the choroid and/or retina with scar tissue at the perforation site of the foreign body. The reports of patients were examined for best-corrected visual acuity, globe survival, retinal detachment status, and proliferative vitreoretinopathy. RESULTS: A total of 13 eyes of 13 patients with a mean age of 25.8 ± 9.0 years (range, 11-38 years) were followed for a median of 13.8 ± 5.4 months (range, 8-29 months). The mean time period between injury and the vitreoretinal surgery was 13.6 ± 9.3 days. All had an exit/impact site wound, eight of which were located in the posterior pole, which caused choroidal and retinal incarceration in the macular area. PPV together with chorioretinectomy, endolaser applications, silicone oil tamponade, with/without encircling band, and lensectomy surgery was applied to all of them. Final best-corrected visual acuity (BCVA) ≥20/200 occurred in 4 of 13 (30.76%) patients. Globe survival rates were 100% (13 of 13), and final retinal attachment rate was 84.6% (11 of 13). The proliferative vitreoretinopathy rate was 2 of 13 (15.3%). CONCLUSION: Chorioretinectomy is a surgical option that may decrease post-traumatic proliferative vitreoretinopathy and tractional retinal detachment rates, thus improving final BCVA and increasing globe survival rates when a foreign body penetrates the choroid and perforates the globe.

Proinflammatory cytokines in a mouse model of central retinal artery occlusion.

PURPOSE: To analyze cytokines in the retina and serum in an experimental model of central retinal artery occlusion (CRAO) in mice. METHODS: CRAO was induced by laser activation of intravenously injected rose bengal, a photosensitive dye, in 60 C57Bl/6 mice. mRNA and protein levels of macrophage inhibitory protein-2 (MIP-2), interleukin-6 (IL-6), and tumor necrosis factor- alpha (TNF-alpha) were analyzed using real-time polymerase chain reaction, and western blot, respectively. Cytokine levels in serum were measured by ELISA. Analysis was performed at various time intervals from CRAO induction. RESULTS: In the retina, MIP-2 and IL-6 mRNA expression decreased 3 h after induction of CRAO and increased thereafter, peaking at 12-24 h. By 7 days, levels were again mostly undetectable. TNF-alpha mRNA expression increased at 3 h and decreased to control levels at 7 days. At the protein level, all cytokines were present at 3 h, following similar patterns to their respective gene expression thereafter. In serum, MIP-2 and TNF-alpha levels peaked early, and decreased to control levels at 12 h, with a second late rise of TNF-alpha. IL-6 levels increased between 3 and 12 h and decreased at 24 h. CONCLUSIONS: Temporal variations in cytokines were observed following the induction of CRAO, both at the retinal mRNA expression and protein levels. These temporal changes, and the variable effects of the cytokines at the different time intervals, should be taken into account during the formulation of therapeutic strategies.

Progressive damage along the optic nerve following induction of crush injury or rodent anterior ischemic optic neuropathy in transgenic mice.

PURPOSE: To characterize the histological changes that occur in response to induction of ischemic or mechanical optic nerve damage in transgenic mice. METHODS: Either optic nerve crush injury or rodent anterior ischemic optic neuropathy (rAION) were induced in the right eye of mice transgenic for the Thy1 gene promoter expressing cyan fluorescent protein (CFP; n=40) and mice transgenic for the cyclic nucleotide phosphodiesterase (CNPase) gene promoter expressing green fluorescent protein (GFP; n=40). The left eye served as a control. The mice were euthanized at different times after injury. Eyes were enucleated, and the brain together with the optic nerves was completely dissected. Cryopreserved sections of both optic nerves were analyzed by fluorescence microscopy. In addition, flat-mounted retinas from the Thy1-CFP mice were analyzed for retinal ganglion cell (RGC) loss. RESULTS: Axonal loss was detected in the right eye of the Thy1-CFP mice, and demyelination was detected in the CNPase-GFP mice. Both processes occurred simultaneously in the two models of injury. The damage proceeded retrogradely and, in the crush-injury group, crossed the chiasm within 4 days. At 21 days after injury, RGC loss measured 70% in the crush-injury group and 25% in the rAION group. CONCLUSIONS: Axonal injury and demyelination along the optic nerves occur simultaneously in transgenic mice exposed to ischemic or crush injury. The degree of RGC loss reflects the severity of the injury. Loss of oligodendrocytes and myelin apparently leads to axonal loss. Transgenic mice offer a promising model for exploring the damage caused by optic nerve injury. Use of fluorescence labeling makes it possible to better understand the underlying pathophysiology, which can help researchers formulate neuroprotective agents.