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AIMS: To evaluate the rate of complications after intravitreal injection of bevacizumab and triamcinolone. METHODS: The clinical interventional case-series study included 5403 intravitreal injections of about 20 mg triamcinolone acetonide (n=1588) or 1.5 mg bevacizumab (n=3818) consecutively performed in the period from 2000 to 2007 by three surgeons for treatment of various intraocular edematous or neovascular diseases. Follow-up after each injection was at least 4 weeks. RESULTS: An infectious endophthalmitis which necessitated pars plana vitrectomy was detected in two eyes (2/5403 or 0.04+/-0.03%) from the bevacizumab group. Two eyes (2/5403 or 0.04+/-0.03%) from the bevacizumab group showed a painless vitreous clouding which subsided after intensified topical antibiotic therapy; one eye (1/5403 or 0.02+/-0.02%) developed a retinal detachment; and three eyes (3/5403 or 0.06+/-0.03%) (two eyes from the bevacizumab group) showed a rapidly progressive cataract. The total rate of these complications was 8/5403 (0.15+/-0.05%). It was statistically independent of the surgeon (P=0.18), the drug injected (P=0.45), and the age of the patients (P=0.87). CONCLUSIONS: Injection-related complications such as infectious endophthalmitis, retinal detachment, and traumatic cataract may occur with a frequency of about 0.15+/-0.05% after intravitreal injections of bevacizumab or triamcinolone, independently of the drug injected.

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PURPOSE: To report on the follow-up of patients who received an intravitreal triamcinolone acetonide injection (IVTA) as treatment of exudative age-related macular degeneration. METHODS: The clinical interventional case-series study included 205 patients (222 eyes) with progressive exudative age-related macular degeneration with subfoveal neovascularization who consecutively received an IVTA of about 20 mg as only therapeutic procedure and for whom follow-up was at least 3 months. Mean follow-up was 10.4+/-7.1 months (range, 3-35.7 months). RESULTS: Visual acuity improved significantly (P<0.001) from baseline (0.90+/-0.45 logarithm of the minimum angle of resolution (LogMar)) to a mean minimum of 0.79+/-0.42 LogMar during follow-up. In 86 (38.7%) eyes and in 55 (24.8%) eyes, best visual acuity increased by at least two and three Snellen lines, respectively. Comparing the measurements at specific postinjection examination dates showed that visual acuity measurements taken at 1, 2, and 3 months after injection were not significantly different from the baseline value. Measurements taken at 6, 9, and 12 months after the injection were significantly (P<0.001) lower than the measurements at baseline. Mean loss at 6 months was 1.4+/-3.8 Snellen lines, at 9 months, 2.5+/-4.6 lines, and at 12 months after the injection, 2.6+/-4.0 lines. Intraocular pressure increased significantly (P<0.001) during the first 6 months, and returned to baseline at 9 months after injection. CONCLUSIONS: Single injection high-dosage IVTA did not show an apparent benefit at 12 months after injection in patients with neovascular age-related macular degeneration.

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PURPOSE: To report on the treatment of exudative age-related macular degeneration by intravitreal bevacizumab (Avastin). METHODS: A 78-year-old patient experienced a progressive loss of visual acuity in her right eye due to an occult subfoveal neovascular membrane in age-related macular degeneration. She received an intravitreal injection of 1.5 mg bevacizumab. RESULTS: Within 4 weeks after the injection, visual acuity improved from 0.40 to 0.60 with complete resolution of subretinal and intraretinal leakage and edema as shown on optical coherence tomography. Pre-existing metamorphopsias disappeared. Intraocular pressure remained in the normal range. During the follow-up, there were no sings of intraocular inflammation or any other intraocular pathology induced by the intravitreal injection. CONCLUSIONS: Intravitreal bevacizumab may potentially be helpful in the treatment of exudative age-related macular degeneration and may deserve further evaluation.

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PURPOSE: To report on the follow-up of patients who received an intravitreal high-dosage injection of triamcinolone acetonide (IVTA) as treatment of diffuse diabetic macular edema. METHODS: The clinical interventional case-series study included 109 eyes (90 patients) with diffuse diabetic macular edema who consecutively received an IVTA of about 20 mg. Mean follow-up was 11.2 +/- 6.2 months. RESULTS: Visual acuity improved significantly (p<0.001) from 0.89 +/- 0.33 logMAR to a best minimum of 0.65 +/- 0.35 logMAR. An increase in best visual acuity by at least 1 Snellen line, 2 lines, and 3 lines was found in 91 (83%) eyes, 68 (62%) eyes, and 45 (41%) eyes, respectively. Differences in visual acuity between baseline and follow-up examinations were significant for measurements performed at 1 month (p<0.001), 2 months (p<0.001), 3 months (p<0.001), and at 6 months (p=0.001) after the injection. At 9 months after the injection, mean visual acuity regressed significantly so that visual acuity at 9 months (p=0.83) and at 12 months after the injection (p=0.58) compared with baseline values did not differ significantly. Forty-seven (43%) eyes developed a rise in intraocular pressure (pressure >21 mmHg) for 6 to 8 months after the injection. No other severe complications were detected. CONCLUSIONS: The duration of a visual acuity increase and intraocular pressure rise after high-dosage IVTA in diffuse diabetic macular edema is about 6 to 8 months. Compared with data in the literature, the high-dosage IVTA may not have a markedly higher profile of side effects than low-dosage IVTA.

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PURPOSE: To report on the occurrence of histology-proven sympathetic ophthalmia in a patient with VATER association and persisting hyperplastic primary vitreous (PHPV) after a cyclodestructive procedure was performed to treat secondary angle-closure glaucoma. METHODS: The left eye of a 13-year-old boy with VATER association was microphthalmic from birth and had been diagnosed with PHPV at age 1 year. It developed iris neovascularization and secondary angle-closure glaucoma, which was treated by combined cyclocryocoagulation and cyclophotocoagulation. Six weeks later, a bilateral fibrinous iritis developed. Despite intensive topical and systemic steroid treatment, the iritis persisted so that the left blind eye was enucleated. RESULTS: Histology of the enucleated eye showed a marked intraocular inflammation with lymphocytes, epithelioid cells, and multinuclear giant cells grouped around remnants of melanin-bearing cells. CONCLUSIONS: Sympathetic ophthalmia may occur in patients with VATER association and PHPV after a secondary angle-closure glaucoma is treated by a combined cyclocryocoagulation and cyclophotocoagulation.

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Neovascularization in the retinopathy of prematurity (ROP) mouse eye is a self-limiting phenomenon. Free endostatin is known to be anti-angiogenic. In this study, we identified the localization of endostatin-like protein (ELP) sequences and investigated their possible role in this process. ROP was induced in C57Bl/6 mice and the eyes observed 1-11 days after termination of high oxygen supply (P13-P21). Sagittal sections and retinal flatmounts were double-stained with antibodies against a protein-sequence of endostatin, vascular endothelial growth factor (VEGF), lectin, and smooth-muscle alpha actin. The fluorescence was visualized by traditional and confocal microscopy. Intense staining for VEGF in the inner retina was limited to the early stages of neovascularization and diminished at P19-P21. In contrast, staining for ELPs appeared at P15 around the newly formed vessels and remained even after degeneration of their endothelial cells. Staining of the inner retinal vasculature for ELPs was restricted to P17-P19, the known maximum of the neovascular response. Outer retinal vessels did not show presence of ELPs at any time. Our study demonstrates that ELPs, absent at the beginning of neovascular sprouting, increases with the amount of neovascularization and thus, varies reciprocally to VEGF in the time period investigated. ELPs remain during the regression of the vessels and might therefore play an important role in the self-limiting process of ROP neovascularization.

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PURPOSE: To report on the occurrence of histology-proven sympathetic ophthalmia in a patient with VATER association and persisting hyperplastic primary vitreous (PHPV) after a cyclodestructive procedure was performed to treat secondary angle-closure glaucoma. METHODS: The left eye of a 13-year-old boy with VATER association was microphthalmic from birth and had been diagnosed with PHPV at age 1 year. It developed iris neovascularization and secondary angle-closure glaucoma, which was treated by combined cyclocryocoagulation and cyclophotocoagulation. Six weeks later, a bilateral fibrinous iritis developed. Despite intensive topical and systemic steroid treatment, the iritis persisted so that the left blind eye was enucleated. RESULTS: Histology of the enucleated eye showed a marked intraocular inflammation with lymphocytes, epithelioid cells, and multinuclear giant cells grouped around remnants of melanin-bearing cells. CONCLUSIONS: Sympathetic ophthalmia may occur in patients with VATER association and PHPV after a secondary angle-closure glaucoma is treated by a combined cyclocryocoagulation and cyclophotocoagulation. (Eur J Ophthalmol 2006; 16: 171-172).

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AIM: To evaluate the effect of different doses of intravitreal triamcinolone acetonide on diffuse diabetic macular oedema. METHODS: The prospective, randomised, double masked, clinical interventional study included 27 eyes (27 patients) with diffuse diabetic macular oedema. They were randomly divided into three study groups receiving an intravitreal injection of filtered triamcinolone acetonide of about 2 mg (n = 8 eyes), 5 mg (n = 10), or 13 mg (n = 9), respectively. Dosage measurement was performed before filtration. Mean follow up was 6.6 (SD 2.4) months (3-12 months). Main outcome measures were visual acuity and intraocular pressure. RESULTS: Maximal increase in visual acuity was significantly (p = 0.046; 95% CI: 0.032 to 2.99; r = 0.38) correlated with the dosage of intravitreal triamcinolone acetonide. Additionally, the duration of the effect of intravitreal triamcinolone acetonide increased significantly with the dosage of intravitreal triamcinolone acetonide (r = 0.45; p = 0.014). Increase in intraocular pressure during follow up was statistically not significantly associated with the dosage used (p = 0.77). CONCLUSIONS: In patients with diffuse diabetic macular oedema receiving intravitreal triamcinolone acetonide, treatment response may last longer and be more pronounced with a dosage of 13 mg than in lower doses of 5 mg or 2 mg. Triamcinolone acetonide induced increase in intraocular pressure may not be markedly associated with the dosage used.

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AIM: To assess the effect of crystalline triamcinolone acetonide on retinal endothelial cell proliferation in vivo and in vitro. METHODS: For in vitro analysis, a sprouting assay was employed. Bovine retinal endothelial cells were stimulated with basic fibroblast growth factor (bFGF) and incubated with different concentrations of triamcinolone acetonide (0.05 mg/ml to 8 mg/ml). For in vivo analysis, a retinopathy of prematurity (ROP) model was used. 16 C57BL/J6 mice were exposed to 75% oxygen from postnatal day 7 to day 12. On day 12, triamcinolone acetonide was intravitreally injected into one eye ("study eye") and isotonic saline into the contralateral eye ("control eye"). On day 17, the mice were sacrificed and the eyes removed for quantitative analysis of preretinal neovascularisation. Four non-exposed mice served as negative control. RESULTS: The sprouting assay demonstrated a dose dependent inhibition of bovine retinal endothelial cell proliferation from 0.05 mg triamcinolone acetonide/ml (no inhibition) to 3 mg triamcinolone acetonide/ml (complete inhibition). Dosages of more than 2 mg/ml resulted in cytotoxic changes of endothelial cells. The ROP model demonstrated a significantly lower neovascular cell count of 58% in the study group compared to the control group (6.35 (SD 2.1) cells per histological section versus 14.9 (SD 5.3) cells; p<0.005). CONCLUSIONS: Triamcinolone acetonide inhibits bFGF induced proliferation of retinal endothelial cells in vivo and in vitro. These findings contribute to understanding the mode of action and effects of triamcinolone acetonide on retinal neovascularisation.

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