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Retinopathy of prematurity, formerly known as a retrolental fibroplasia, is a leading cause of infantile blindness worldwide. Retinopathy of prematurity is caused by the failure of central retinal vessels to reach the retinal periphery, creating a nonperfused peripheral retina, resulting in retinal hypoxia, neovascularization, vitreous hemorrhage, vitreoretinal fibrosis, and loss of vision. We established a potential retinopathy of prematurity model by using a green fluorescent vascular endothelium zebrafish transgenic line treated with cobalt chloride (a hypoxia-inducing agent), followed by GS4012 (a vascular endothelial growth factor inducer) at 24 hours postfertilization, and observed that the number of vascular branches and sprouts significantly increased in the central retinal vascular trunks 2–4 days after treatment. We created an angiography method by using tetramethylrhodamine dextran, which exhibited severe vascular leakage through the vessel wall into the surrounding retinal tissues. The quantification of mRNA extracted from the heads of the larvae by using real-time quantitative polymerase chain reaction revealed a twofold increase in vegfaa and vegfr2 expression compared with the control group, indicating increased vascular endothelial growth factor signaling in the hypoxic condition. In addition, we demonstrated that the hypoxic insult could be effectively rescued by several antivascular endothelial growth factor agents such as SU5416, bevacizumab, and ranibizumab. In conclusion, we provide a simple, highly reproducible, and clinically relevant retinopathy of prematurity model based on zebrafish embryos; this model may serve as a useful platform for clarifying the mechanisms of human retinopathy of prematurity and its progression.

The aim of the study was to explore the correlation between central corneal thickness (CCT) and the degree of myopia in Taiwanese adults. A total of 528 individuals were enrolled to undergo myopic laser refractive surgery from January 2004 to December 2006. Preoperative CCT was measured using the Orbscan corneal topography system and refractive status was determined by cycloplegic spherical equivalent. The relationship between CCT and refractive error was investigated by interindividual and intraindividual analyses. Participants had a mean age of 34.8 ± 7.3 years, and 79.9% were female. The mean refractive error was -7.27 ± 2.96 diopters and the mean CCT measurement was 560 ± 35 μm. CCT revealed that there was no association with age. However, CCT was significantly (p = 0.012) less in females than in males. The CCT also showed no significant association with refractive error (p = 0.49). Among the 67 participants with myopic anisometropia, the mean difference between both eyes was 3.09 ± 1.06 diopters. There was no association between the intereye CCT difference and refractive error (p = 0.57). The results remained the same after adjusting for age and sex. In conclusion, there was no correlation between CCT and the degree of myopia among adults in Taiwan. These data might contribute to the ongoing discussion about the role of CCT in the higher incidence of development and progression of glaucoma in myopic individuals.

Hypotony maculopathy is a sight-threatening complication after trabeculectomy. We report on a 34-year-old man with juvenile open-angle glaucoma and high myopia, who developed hypotony maculopathy 14 years after trabeculectomy without bleb leak. This represents the longest known period from trabeculectomy to the development of hypotony maculopathy without bleb leak. The possible mechanisms for the development of late-onset hypotony maculopathy in the highly myopic patient are progressive scleral thinning, reduced scleral rigidity, and scleral morphologic change with aging. These changes might weaken the biomechanical properties of sclera and then contribute to the collapse of the scleral wall during hypotony. This case serves as a reminder that hypotony maculopathy can happen up to 14 years after tabeculectomy even without bleb leak and hypotony should be avoided after trabeculectomy in highly myopic patients with juvenile open-angle glaucoma.

ABSTRACT.Purpose: To assess the relationship between diabetic polyneuropathy (DPN) and the risk of diabetic retinopathy (DR). Methods: From 1997 to 2010, we identified 5031 newly diagnosed DPN patients and 20 124 controls matched for sex, age, and index year. Cox proportional hazards regression analyses were used to estimate the adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) of DR between the DPN patients and the non-DPN group. The adjusted hazard ratio was calculated and adjusted for age, sex, duration of diabetes and comorbidities of hypertension, cardiovascular disease and diabetic nephropathy. Results: The incidence rate of DR was 5.87-fold higher in the DPN patients than in the non-DPN group (44.0 vs. 7.22 per 1000 person-years), with an adjusted HR of 5.41(95% CI = 4.92-5.94). The DPN-to-non-DPN DR incidence rate ratio decreased with age (adjusted HR = 6.63 for subgroup younger than 65 years and adjusted HR = 3.91 for subgroup aged 65 years or older). Compared with the non-DPN group, the DPN patients had a 5.63-fold risk of non-proliferative DR (adjusted HR = 5.63, 95% CI = 5.11-6.21) and a 3.67-fold risk of proliferative DR (adjusted HR = 3.67, 95% CI = 2.57-5.23). Conclusion: The patients with DPN had an increased risk of developing DR and advanced DR compared with the non-DPN group, particularly among the subgroup aged younger than 65 years.

Chronic inflammatory demyelinating polyneuropathy (CIDP) is a condition that mainly affects the peripheral nervous system; however, the central nervous system has also been involved in rare cases. Herein, we describe the case of a 33-year-old man with CIDP who presented with progressively blurred vision and pain with eye movement in both eyes for 1 month. Ocular examination revealed reduced visual acuities of 0.15 (oculus unitas or OU) and unremarkable fundi (OU). Furthermore, bitemporal visual field defects and prolonged visually evoked potentials were evident. Brain magnetic resonance imaging revealed nothing remarkable along the optic nerve and chiasm. These findings were compatible with the diagnosis of bilateral optic neuritis. The patient's symptoms and visual acuity improved after 5 days of intravenous (IV) corticosteroid pulse therapy, which was subsequently replaced by oral prednisolone therapy with a tapering schedule. The patient's visual acuity returned to 1.0 (OU) 6 months after treatment. However, bilateral optic neuritis recurred in 7 months while the patient was on oral prednisolone and azathioprine. IV corticosteroid pulse therapy was subsequently reinitiated and the patient's visual acuity returned gradually to 1.0 (OU). Bilateral optic neuritis is a rare manifestation of CIDP. It responded well to IV corticosteroid therapy in our case.