 |
 |

Triamcinolone as Adjunctive Treatment to Laser Panretinal Photocoagulation for Proliferative Diabetic Retinopathy
Francesco Bandello, MD;
Antonio Polito, MD;
Derri Roman Pognuz, MD;
Pietro Monaco, MD;
Andrea Dimastrogiovanni, MD;
Joannis Paissios, MD
Arch Ophthalmol. 2006;124:643-650.
ABSTRACT
 |  |
Objective To evaluate intravitreal injection of triamcinolone acetonide before laser panretinal photocoagulation (PRP) in the treatment of proliferative diabetic retinopathy.
Methods This interventional case series included 9 patients with bilateral proliferative diabetic retinopathy. One eye received intravitreal triamcinolone before PRP (injected eye) and the other, PRP alone (control eye). The main outcome measures were the change in planimetric area of fluorescein leakage from retinal neovascularization and in central macular thickness on optical coherence tomography at 3, 6, 9, and 12 months. Secondary end points were change in vision, intraocular pressure, and cataract progression.
Results All patients completed 9 months and 5 patients, 12 months of follow-up. Initial mean (SD) planimetric area of fluorescein leakage and central macular thickness were 7.22 (5.70) mm2 and 372.11 (91.88) µm in injected eyes and 9.08 (6.17) mm2 and 355.33 (115.23) µm in control eyes, respectively. At the 9- and 12-month intervals, the planimetric area of fluorescein leakage decreased by 86% and 88% in injected eyes and 33% and 50% in controls, respectively. Central macular thickness significantly decreased in injected eyes and increased in control eyes. Vision slightly improved in injected eyes and worsened in control eyes.
Conclusion Intravitreal injection of triamcinolone before PRP may be useful in improving the effects of PRP in eyes with proliferative diabetic retinopathy by reducing neovascularization and macular thickening.
INTRODUCTION
Proliferative diabetic retinopathy (PDR) is a leading cause of blindness. The Diabetic Retinopathy Study demonstrated that scatter laser panretinal photocoagulation (PRP) reduces the risk of severe visual loss by 50% or more in patients with high-risk PDR compared with no treatment.1 However, in patients with actively growing new vessels, long intervals between PRP sessions and the variable amount of time required for a favorable response may increase the incidence of complications due to the progression of PDR.2-3 In fact, neovascularization on and around the optic disc (NVD) and vitreous hemorrhage were found to be more frequently associated with severe visual loss despite PRP in the Diabetic Retinopathy Study and Early Treatment Diabetic Retinopathy Study (ETDRS), respectively.2, 4 On the other hand, a single episode of PRP or shorter intervals between PRP episodes, although desirable in severe PDR and when the patient must travel long distances for treatment, are often associated with acute visual disturbances due to exudative choroidal, retinal detachment, and macular edema.5-8 Although the risks of visual acuity loss may be less if focal or grid laser of the edema precedes PRP, the delay of PRP is not always feasible owing to risks of vitreous hemorrhage or neovascular glaucoma.
The exact pathogenic mechanism for macular edema following PRP has not been determined. Recently, a series of studies suggested postlaser release of inflammatory factors, accumulation of leukocytes in the nonphotocoagulated posterior pole, and up-regulation of angiogenic growth factors, such as vascular endothelial growth factor, play a role in the pathogenesis of the edema.9-14
Recent studies have demonstrated the usefulness of intravitreal injection of triamcinolone acetonide in the reduction of inflammation,15-17 vascular permeability,18-20 fibrovascular proliferation,14, 21-22 and macular thickening due to diffuse diabetic macular edema, at least in the short-term.23-26 The purpose of this prospective, controlled study was to evaluate the effectiveness of intravitreal triamcinolone injection plus PRP vs PRP alone on retinal neovascularization and macular thickening in patients with PDR.
METHODS
PATIENT ELIGIBILITY
Patients were included if they had bilateral PDR varying from mild proliferative PDR to high-risk PDR. To determine PDR severity, the same examiner (D.R.P.) graded the levels of retinopathy on the basis of slitlamp biomicroscopy and fluorescein angiography (FA). The patients could have clinically significant macular edema (CSME) on slitlamp contact lens biomicroscopy, as defined by the ETDRS.27 Glycated hemoglobin (HbA1c) levels had to be less than 9.5% and systolic and diastolic blood pressure, lower than 150 and 90 mm Hg, respectively. Patients with previous panretinal or focal or grid photocoagulation, signs of vitreomacular traction either on optical coherence tomography (OCT) or biomicroscopy, cataract extraction or lens implantation within the past 12 months, significant media opacities, and a history of glaucoma or ocular hypertension were excluded from the study. The tenets of the World Medical Association Declaration of Helsinki were followed. Each eligible patient was thoroughly informed about the study, both orally and in written form, and whoever agreed to participate signed a consent form.
PREOPERATIVE EXAMINATION
Baseline data included age, sex, type and duration of diabetes mellitus, blood pressure measurements, and HbA1c levels. Patients also underwent a clinical examination including objective refraction, nonmasked Snellen best-corrected visual acuity (BCVA) testing, classification of lenticular status using the Lens Opacities Classification System III,28 applanation tonometry, fundus examination and photography, FA, and OCT.
EXPERIMENTAL DESIGN
To assess whether intravitreal injection of triamcinolone prior to PRP affected the outcome, one eye of each patient was selected at random and underwent intravitreal triamcinolone injection 10 to 15 days prior to initial PRP (injected eye), and the other eye was treated with PRP alone (control eye). If CSME was present at baseline, focal or grid laser therapy was performed only in control eyes at the first episode of PRP. Focal or grid laser treatment was also considered during follow-up in control eyes with treatable lesions on FA and either increased foveal thickening or persistent foveal thickening and decreased vision. The randomization sequence was generated from a number table.
TRIAMCINOLONE INJECTION
Four milligrams of triamcinolone acetonide (Kenacort; Bristol-Myers Squibb, Sermoneta, Italy) in 0.1 mL were injected into the vitreous cavity (by the same surgeon, F.B.) with full asepsis under topical anesthesia. An eyelid speculum was used to stabilize the eyelids. The injection was performed 4 mm posterior to the limbus, through the inferior pars plana, with a 30-gauge needle. At the end of the injection, the surgeon verified central retina artery perfusion and the patient's light perception.
SCATTER PRP
Scatter PRP was performed using a diode-pumped, solid-state, 561-nm, yellow laser (Lumenis Ltd, Yokneam, Israel) in 3 sessions approximately 1 week apart, in both injected and control eyes. In the first session, several rows of burns were positioned far from the posterior pole and extended for 360° with the quadraspheric fundus lens. In the second session, laser burns were applied closer to the posterior pole, leaving the remainder of the periphery for the third session, in which the Goldmann 3-mirror lens was used. The size of the spots on the retina was between 250 to 1000 µm, and the power and duration of the applications were adjusted so that a gray-white lesion was performed. The number of spots in each session was around 400 to 600, and the mean (SD) total number of burns after completion of the treatment was 1293 (257) in injected eyes and 1465 (587) in control eyes. The mean (SD) power of the spots in injected eyes was 319 (57) mW and slightly but significantly less than that measured in control eyes, which was 390 (67) mW (P = .008, bilateral Wilcoxon test for paired samples). Topical anesthesia was used in all cases, and all patients were treated by the same specialist (F.B.).
OUTCOME MEASURES
The main outcome measures were the change in retinal neovascularization defined as the change in the area of vitreous leakage from NVD and new vessels elsewhere in the late phase of FA and the change in central macular thickness (CMT) on OCT at 3, 6, 9, and 12 months from baseline. The leakage and CMT were also assessed 10 to 15 days after intravitreal triamcinolone administration in the injected eyes prior to initial PRP to evaluate the response to intravitreal triamcinolone administration alone.
The planimetric area of fluorescein leakage was measured on digital angiograms captured with the Topcon retinal camera (model 50IX; Topcon, Tokyo, Japan) with IMAGEnet 2.11 software. These angiograms consisted of 10 50° fields, fields 1 and 2 being centered on the macula and disc, respectively, and fields 3 to 10 imaging the superonasal, nasal, inferonasal, inferior, inferotemporal, temporal, superotemporal, and superior quadrants. All angiograms were taken following the same photographic plan. An injection of a 20% fluorescein solution (4-6 seconds) in a 5-mL syringe and a 20-gauge needle was performed at all visits by the same nurse. The digital images were imported into an Image Tools program (Topcon) and the planimetric area of fluorescein leakage was measured by tracing around the borders of the hyperfluorescence from NVD and new vessels elsewhere with the appropriate tool by the same masked examiner (P.M.).
Central macular thickness was defined as the average thickness of the central macular region 1000 µm in diameter, centered on the patient's foveola, and automatically measured by the Retinal Map analysis protocol (Humphrey Instruments Inc, Dublin, Calif). Optical coherence tomography was performed using the Fast Macular Thickness Mapping Protocol of the commercially available Stratus OCT (Carl Zeiss Meditec, Dublin) with version 2.0 software. Good reproducibility of this protocol has been recently demonstrated by our group.29 The normal mean (SD) value for CMT is 209 (22) µm. Increased CMT at baseline was established if CMT was greater than 250 µm.
Secondary end points were change in BCVA, intraocular pressure, and progression of cataract. Follow-up visits were performed 10 to 15 days after intravitreal injection of triamcinolone and at 3, 6, 9, and 12 months from baseline. Lens status evaluation was performed only at the 6- and 12-month follow-up visits.
STATISTICAL ANALYSIS
For statistical analysis, paired series were compared, each treated eye being paired with the untreated eye of the same patient. Statistical analyses were performed using the bilateral Wilcoxon signed rank test for paired data. The null hypothesis was rejected for P values <.05. Analyses of visual acuity were performed by converting Snellen visual acuity measurements to log minimum angle of resolution (logMAR) equivalents. Results are presented in both logMAR units, which were used for analysis, and equivalent Snellen visual acuity notation.
RESULTS
Between January and September 2004, 9 patients (18 eyes) with mild to high-risk PDR were included in the study (8 men and 1 woman). In this preliminary report, we give the results for the 9 patients who had a follow-up of at least 9 months. Five of them were followed up for 12 months. The mean (SD) age of patients was 47.5 (2.3) years (range, 27-60 years). Three patients had type 1 diabetes and 6, type 2. The mean (SD) duration of diabetes was 15.8 (5.6) years (range, 8-24 years). All eyes were phakic. The clinical characteristics of the 18 enrolled eyes are presented in Table 1. Before intravitreal injection of triamcinolone, the mean (SD) HbA1c level was 8.2% (0.6%) (range, 7.2%-9%), and mean (SD) systolic and diastolic blood pressure were, respectively, 131.11 (8.2) mm Hg (range, 140-120 mm Hg) and 79.44 mm Hg (6.8) (range, 70-90 mm Hg). Fifteen eyes had CSME at the contact lens slitlamp examination.
|
|
|
|
Table 1. Baseline Clinical Characteristics of Injected and Control Eyes
|
|
|
PLANIMETRIC AREA OF FLUORESCEIN LEAKAGE FROM NEW VESSELS AND CMT
Table 2 summarizes the results for injected and control eyes. Mean (SD) planimetric areas of fluorescein leakage and CMTs of injected and control eyes at baseline and at 3, 6, 9, and 12 months after injection are given in Table 3. Ten to 15 days after injection, the mean (SD) planimetric area of fluorescein leakage and CMT of injected eyes were reduced by 52% to 3.09 (2.20) mm2 and by 31% to 244.56 (24.92) µm, respectively. In addition, FA showed a substantial regression of perivascular staining from large retinal vessels traversing areas of capillary nonperfusion in these eyes.
|
|
|
|
Table 2. Details of the Injected and Control Eyes
|
|
|
|
|
|
|
Table 3. Comparison of Planimetric Area of Fluorescence Leakage (PAFL), Central Macular Thickness (CMT), Visual Acuity, and Intraocular Pressure (IOP) for Injected and Control Eyes*
|
|
|
Relative decreases in planimetric area of fluorescein leakage at 3, 6, 9, and 12 months were 74%, 84%, 86%, and 88% in injected eyes and 19%, 22%, 33%, and 50% in control eyes, respectively (P = .01, .01, .02, and .04). One of the 9 injected eyes (patient 2) showed a complete regression of the leakage from new vessels at 3 months; 3 additional eyes (patients 1, 8, and 9), at 6 months; and 1 other eye, at 12 months (patient 3). Patient 1 is shown in the Figure. In the control group, only 1 eye showed a complete regression of leakage at 9 months (patient 9).
|
|
|
|
Figure. Patient 1. At baseline, fluorescein angiography (FA) reveals leakage from new vessels elsewhere (NVE) and neovascularization on and around the optic disc (NVD) in the control eye (A) and from NVD in the injected eye (B). The red outlined areas show the planimetric area of fluorescein leakage, which is 5.55 mm2 (4.23 + 0.66 + 0.42 + 0.24) in the control eye and 5.70 mm2 in the injected eye. At baseline, optical coherence tomography shows no remarkable foveal thickening in the control eye (C) and increased foveal and perifoveal thickness in the injected eye (D). At 12 months, FA reveals the regression of leakage from NVD and the increase of leakage from NVE due to the occurrence of new NVE along the inferotemporal vascular arcade (E). On the other hand, FA shows complete regression of leakage from NVD in the injected eye (F). The planimetric area of fluorescein leakage is 4.78 mm2 (3.87 + 0.91) and 0, respectively. Optical coherence tomography at 12 months indicates a greater increase of foveal thickness in the control eye (G) compared with the injected eye in which a localized increase in extrafoveal thickness is present inferotemporally to the fovea (H).
|
|
|
The CMT decreased by 31%, 28%, 24%, and 5% in injected eyes and increased by 12%, 17%, 7%, and 10% in control eyes at 3, 6, 9, and 12 months, respectively (P = .01, .01, .01, and .20).
SECONDARY END POINTS
For both injected and control eyes, mean (SD) LogMAR units and the equivalent Snellen BCVA at baseline and at 3, 6, 9, and 12 months are presented in Table 3. Injected eyes gained 1.2, 0.9, 0.7, and 0.2 Snellen lines and control eyes lost 1.7, 1.2, 1.7, and 2.8 Snellen lines during the same intervals, respectively (P = .01, .01, .03, .02, and .68).
The mean (SD) values for intraocular pressure in both groups are given in Table 3. In 4 of the 9 injected eyes, intraocular pressure exceeded 21 mm Hg at 3 months and in 1 case, at 6 and 9 months. However, in all cases it was controlled by topical medications. The maximal intraocular pressure was 34 mm Hg. No cataract progression or other injection-related complications were observed.
COMMENT
The preliminary results of this prospective study show efficacy of intravitreal injection of triamcinolone as adjunctive treatment to PRP on the regression of retinal new vessels and resolution of macular edema in patients with PDR. Both leakage due to retinal new vessels and macular thickening were significantly reduced in the combined treatment group, compared with control eyes. In addition, BCVA improved in injected eyes while it was slightly reduced in control eyes at 9 months.
Panretinal photocoagulation is the mainstay for the treatment of PDR, and its suppressive effect on retinal neovascularization has been well documented.1, 3, 5, 30 However, substantial regression of new vessels may take weeks after completion of PRP, and in up to one third of cases, new vessels continue to grow despite initial PRP.5, 30-32 In these cases, vitreous hemorrhage may induce visual loss and prevent complete laser. Moreover, macular edema may increase after PRP and cause transient or persistent visual loss.9-11
A growing number of studies are supporting the evidence of a corticosteroid action on reducing blood-retinal barrier breakdown and angiogenesis in diabetic retinopathy.33-35 Our group demonstrated that intravitreal injection of triamcinolone allowed PRP to be applied without worsening of macular edema and progression of retinopathy in a young patient with florid PDR.36 A similar beneficial response on leakage and macular thickening in eyes with PDR has been described by Brooks et al14 in a prospective study aimed to investigate the role of growth factors and chemokines before and after intravitreal injection of triamcinolone in the progression of diabetic retinopathy. Recently, Zacks and Johnson37 described the effectiveness of combined intravitreal injection of triamcinolone and PRP in preventing exacerbation of macular edema in patients with concomitant CSME and PDR.
To test the advantages of intravitreal injection of triamcinolone prior to PRP in patients with PDR, we used the paired eyes of patients with bilateral PDR to avoid possible bias due to systemic factors. The dose of the injected drug (4 mg) and the interval between injection and initial PRP were empirically chosen on the basis of the results of previous studies describing pharmacokinetics and pharmacodynamics of intravitreal triamcinolone.38-39 To determine the effect of intravitreal injection of triamcinolone on actively growing new vessels, we chose the change in vitreous leakage from retinal neovascularization as our primary outcome. The detection of NVD and new vessels elsewhere on FA allowed the use of a systematic morphometric approach to quantify and monitor the area of leaking new vessels over time. To determine the effect of intravitreal injection of triamcinolone on macular edema, we measured the change of retinal thickening with OCT.40-41
Both the regression of neovascularization and decrease of retinal thickening occurred in all injected eyes as soon as 10 to 15 days after intravitreal injection of triamcinolone prior to initial PRP. In particular, the regression of neovascularization continued up to 3, 6, and 9 months persisting through 12 months in the 5 eyes that reached the 12-month follow-up visit. In addition, in 4 of these eyes, all leakage completely disappeared at 6 months. A decrease in leakage from new vessels also occurred in control eyes throughout the entire follow-up period, but at a much slower rate. Mean CMT markedly decreased during the first 3 months and then stabilized in all injected eyes at 6 and 9 months, while it remained at higher than normal values at all visits in the control group. In 2 of the 5 injected eyes completing the 12-month follow-up visit, macular edema recurred. We also observed a significant difference between injected and control eyes with regard to the changes in visual acuity. After a marked increase for the first 3 months, visual acuity tended to stabilize at the end of the follow-up in injected eyes. In control eyes, visual acuity decreased during the first 3 months and remained lower than at the start of the study at 9 and 12 months.
Although the reduction in foveal thickness might have partly improved visual acuity in injected eyes, the entity of the improvement was not correlated with the amount of reduction in CMT, similar to the findings by Larsson et al.42 This suggests that other variables, such as the duration of the edema, may influence the functional response to intravitreal triamcinolone independently from its effect on the edema. Other explanations are additional actions of steroids, such as improving macular perfusion by reducing inflammation and leukostasis or by acting on retinal glial cells or photoreceptors.43
Similarly, in the control eyes, the progressive decrease in vision over time can be only partly explained by the increase in macular thickness. This may be owing to the relatively good initial visual acuity in eyes that "already" have a significant macular thickening prior to PRP, probably owing to a presumed short duration of the edema. In particular, 2 patients with severe thickening at baseline (528 and 463 µm) and relatively good vision were 27 and 30 years of age. The progressive decrease in vision might have occurred because of the persistence, rather than worsening, of the edema during the 9- to 12-month follow-up period. The presence of CSME at baseline in most of the eyes may have contributed to the decrease of visual acuity after PRP, similar to the outcome observed in a study by Shimura et al,8 where the decrease in visual acuity following PRP occurred only in the eyes with thicker macula at baseline.
No injection-related complication occurred. Intraocular pressure rose higher than 21 mm Hg in 4 of 9 injected eyes and was controlled by topical medication, and no cataract progression was observed.
The current study has several limitations, including a relatively small sample size, a relatively short duration of follow-up, and visual acuity measured on a Snellen as opposed to an ETDRS chart by a nonmasked examiner. However, the large difference in the quantitative morphologic outcomes between groups and the trend toward improvement in BCVA in injected eyes found at 9 months confirms our hypothesis that at least some eyes with PDR, such as those with preexisting macular edema or rapidly growing new vessels, may truly benefit from intravitreal injection of triamcinolone. Moreover, by increasing the chance of preserving a good initial visual acuity, intravitreal injection of triamcinolone prior to PRP may also improve the patient's compliance to treatment and follow-up visits.
In conclusion, intravitreal injection of triamcinolone seems a promising adjuvant treatment to PRP in that it may allow the achievement of a full, extensive PRP while minimizing the risk for exudative complications, progression of PDR, vitreous hemorrhage, and decreased vision, thus improving tolerance to PRP by patients. Although no serious complications of intravitreal injection of triamcinolone occurred in our series, further studies are needed to assess the efficacy and safety of intravitreal triamcinolone injection as adjunctive treatment to PRP in the treatment of PDR.
AUTHOR INFORMATION
Correspondence: Francesco Bandello, MD, Department of Ophthalmology, University of Udine, Piazzale Santa Maria della Misericordia, 33100 Udine, Italy (francesco.bandello{at}uniud.it).
Submitted for Publication: May 23, 2005; final revision received July 28, 2005; accepted August 10, 2005.
Financial Disclosure: None.
Author Affiliations: Department of Ophthalmology, University of Udine, Piazzale Santa Maria della Misericordia, Udine, Italy.
REFERENCES
 |  |
1. Diabetic Retinopathy Study Research Group. Photocoagulation treatment of proliferative diabetic retinopathy: clinical application of Diabetic Retinopathy Study (DRS): DRS report 8. Ophthalmology. 1981;88:583-600.
ISI
| PUBMED
2. Kaufman SC, Ferris FL III, Seigel DG, Davis MD, DeMets DL. Factors associated with visual outcome after photocoagulation for diabetic retinopathy: Diabetic Retinopathy Study Report 13. Invest Ophthalmol Vis Sci. 1989;30:23-28.
FREE FULL TEXT
3. Aylward GW, Pearson RV, Jagger JD, Hamilton AM. Extensive argon laser photocoagulation in the treatment of proliferative diabetic retinopathy. Br J Ophthalmol. 1989;73:197-201.
FREE FULL TEXT
4. Fong DS, Ferris FL III, Davis MD, Chew EY, Early Treatment Diabetic Retinopathy Study Research Group. Causes of severe visual loss in the early treatment diabetic retinopathy study: ETDRS report No. 24. Am J Ophthalmol. 1999;127:137-141.
FULL TEXT
|
ISI
| PUBMED
5. Doft BH, Blankenship GW. Single versus multiple treatment sessions of argon laser panretinal photocoagulation for proliferative diabetic retinopathy. Ophthalmology. 1982;89:772-779.
6. Ferris FL III, Podgor MJ, Davis MD. Macular edema in Diabetic Retinopathy Study (DRS): DRS report number 12. Ophthalmology. 1987;94:754-760.
ISI
| PUBMED
7. McDonald HR, Schatz H. Visual loss following panretinal photocoagulation for proliferative diabetic retinopathy. Ophthalmology. 1985;92:388-393.
ISI
| PUBMED
8. Shimura M, Yasuda K, Nakazawa T, Kano T, Ohta S, Tamai M. Quantifying alterations of macular thickness before and after panretinal photocoagulation in patients with severe diabetic retinopathy and good vision. Ophthalmology. 2003;110:2386-2394.
FULL TEXT
|
ISI
| PUBMED
9. Nonaka A, Kiryu J, Tsujikawa A, et al. Inflammatory response after scatter laser photocoagulation in nonphotocoagulated retina. Invest Ophthalmol Vis Sci. 2002;43:1204-1209.
FREE FULL TEXT
10. Tsujikawa A, Kiryu J, Dong J, et al. Quantitative analysis of diabetic macular edema after scatter laser photocoagulation with the scanning retinal thickness analyzer. Retina. 1999;19:59-64.
ISI
| PUBMED
11. McDonald HR, Schatz H. Macular edema following panretinal photocoagulation. Retina. 1985;5:5-10.
FULL TEXT
|
ISI
| PUBMED
12. Funatsu H, Yamashita H, Ikeda T, Mimura T, Shimizu E, Hori S. Relation of diabetic macular edema to cytokines and posterior vitreous detachment. Am J Ophthalmol. 2003;135:321-327.
FULL TEXT
|
ISI
| PUBMED
13. Del Maschio A, Zanetti A, Corada M, et al. Polymorphonuclear leukocyte adhesion triggers the disorganization of endothelial cell-to-cell adherens junctions. J Cell Biol. 1996;135:497-510.
FREE FULL TEXT
14. Brooks HL Jr, Caballero S Jr, Newell CK, et al. Vitreous levels of vascular endothelial growth factor and stromal-derived factor 1 in patients with diabetic retinopathy and cystoid macular edema before and after intraocular injection of triamcinolone. Arch Ophthalmol. 2004;122:1801-1807.
FREE FULL TEXT
15. Martidis A, Duker JS, Puliafito CA. Intravitreal triamcinolone for refractory cystoid macular edema secondary to birdshot retinochoroidopathy. Arch Ophthalmol. 2001;119:1380-1383.
FREE FULL TEXT
16. Antcliff RJ, Spalton DJ, Stanford MR, Graham EM, ffytche TJ, Marshall J. Intravitreal triamcinolone for uveitic cystoid macular edema: an optical coherence tomography study. Ophthalmology. 2001;108:765-772.
FULL TEXT
|
ISI
| PUBMED
17. Degenring RF, Jonas JB. Intravitreal injection of triamcinolone acetonide as treatment for chronic uveitis. Br J Ophthalmol. 2003;87:361.
FREE FULL TEXT
18. Degenring RF, Kamppeter B, Kreissig I, Jonas JB. Morphological and functional changes after intravitreal triamcinolone acetonide for retinal vein occlusion. Acta Ophthalmol Scand. 2003;81:548-550.
FULL TEXT
|
ISI
| PUBMED
19. Jonas JB, Kreissig I, Degenring RF. Intravitreal triamcinolone acetonide as treatment of macular edema in central retinal vein occlusion. Graefes Arch Clin Exp Ophthalmol. 2002;240:782-783.
ISI
| PUBMED
20. Greenberg PB, Martidis A, Rogers AH, Duker JS, Reichel E. Intravitreal triamcinolone acetonide for macular oedema due to central retinal vein occlusion. Br J Ophthalmol. 2002;86:247-248.
FREE FULL TEXT
21. Jonas JB, Sofker A, Degenring R. Intravitreal triamcinolone acetonide as an additional tool in pars plana vitrectomy for proliferative diabetic retinopathy. Eur J Ophthalmol. 2003;13:468-473.
ISI
| PUBMED
22. Jonas JB, Hayler JK, Panda-Jonas S. Intravitreal injection of crystalline cortisone as adjunctive treatment of proliferative vitreoretinopathy. Br J Ophthalmol. 2000;84:1064-1067.
FREE FULL TEXT
23. Martidis A, Duker JS, Greenberg PB, et al. Intravitreal triamcinolone for refractory diabetic macular edema. Ophthalmology. 2002;109:920-927.
FULL TEXT
|
ISI
| PUBMED
24. Jonas JB, Sofker A. Intraocular injection of crystalline cortisone as adjunctive treatment of diabetic macular edema. Am J Ophthalmol. 2001;132:425-427.
FULL TEXT
|
ISI
| PUBMED
25. Massin P, Audren F, Haouchine B, et al. Intravitreal triamcinolone acetonide for diabetic diffuse macular edema. Ophthalmology. 2004;111:218-225.
FULL TEXT
|
ISI
| PUBMED
26. Jonas JB, Kreissig I, Sofker A, Degenring RF. Intravitreal injection of triamcinolone for diffuse diabetic macular edema. Arch Ophthalmol. 2003;121:57-61.
FREE FULL TEXT
27. Early Treatment Diabetic Retinopathy Study Research Group. Photocoagulation for diabetic macular edema: Early Treatment Diabetic Retinopathy Study report number 1. Arch Ophthalmol. 1985;103:1796-1806.
ABSTRACT
28. Chylack LT Jr, Wolfe JK, Singer DM, et al. The Lens Opacities Classification System, III: the Longitudinal Study of Cataract Study Group. Arch Ophthalmol. 1993;111:831-836.
ABSTRACT
29. Polito A, Del Borrello M, Isola M, Zemella N, Bandello F. Repeatability and reproducibility of fast macular thickness mapping with the stratus optical coherence tomography. Arch Ophthalmol. 2005;123:1330-1337.
FREE FULL TEXT
30. KARNS. Randomized comparison of krypton versus argon scatter photocoagulation for diabetic disc neovascularization: the Krypton Argon Regression Neovascularization Study report number 1. Ophthalmology. 1993;100:1655-1664.
ISI
| PUBMED
31. Vander JF, Duker JS, Benson WE, Brown GC, McNamara JA, Rosenstein RB. Long-term stability and visual outcome after favorable initial response of proliferative diabetic retinopathy to panretinal photocoagulation. Ophthalmology. 1991;98:1575-1579.
ISI
| PUBMED
32. Reddy VM, Zamora RL, Olk RJ. Quantitation of retinal ablation in proliferative diabetic retinopathy. Am J Ophthalmol. 1995;119:760-766.
PUBMED
33. Wilson CA, Berkowitz BA, Sato Y, Ando N, Handa JT, de Juan E Jr. Treatment with intravitreal steroid reduces blood-retinal barrier breakdown due to retinal photocoagulation. Arch Ophthalmol. 1992;110:1155-1159.
ABSTRACT
34. Danis RP, Bingaman DP, Yang Y, Ladd B. Inhibition of preretinal and optic nerve head neovascularization in pigs by intravitreal triamcinolone acetonide. Ophthalmology. 1996;103:2099-2104.
ISI
| PUBMED
35. Jonas JB, Sofker A. Intravitreal triamcinolone acetonide for cataract surgery with iris neovascularization. J Cataract Refract Surg. 2002;28:2040-2041.
FULL TEXT
|
ISI
| PUBMED
36. Bandello F, Roman PD, Pirracchio A, Polito A. Intravitreal triamcinolone acetonide for florid proliferative diabetic retinopathy. Graefes Arch Clin Exp Ophthalmol. 2004;242:1024-1027.
PUBMED
37. Zacks DN, Johnson MW. Combined intravitreal injection of triamcinolone acetonide and panretinal photocoagulation for concomitant diabetic macular edema and proliferative diabetic retinopathy. Retina. 2005;25:135-140.
PUBMED
38. Audren F, Tod M, Massin P, et al. Pharmacokinetic-pharmacodynamic modeling of the effect of triamcinolone acetonide on central macular thickness in patients with diabetic macular edema. Invest Ophthalmol Vis Sci. 2004;45:3435-3441.
FREE FULL TEXT
39. Beer PM, Bakri SJ, Singh RJ, Liu W, Peters GB III, Miller M. Intraocular concentration and pharmacokinetics of triamcinolone acetonide after a single intravitreal injection. Ophthalmology. 2003;110:681-686.
FULL TEXT
|
ISI
40. Browning DJ, McOwen MD, Bowen RM Jr, O'Marah TL. Comparison of the clinical diagnosis of diabetic macular edema with diagnosis by optical coherence tomography. Ophthalmology. 2004;111:712-715.
FULL TEXT
|
ISI
| PUBMED
41. Massin P, Vicaut E, Haouchine B, Erginay A, Paques M, Gaudric A. Reproducibility of retinal mapping using optical coherence tomography. Arch Ophthalmol. 2001;119:1135-1142.
FREE FULL TEXT
42. Larsson J, Zhu M, Sutter F, Gilles MC. Relation between reduction of foveal thickness and visual acuity in diabetic macular edema treated with intravitreal triamcinolone. Am J Ophthalmol. 2005;139:802-806.
FULL TEXT
| PUBMED
43. Tamura H, Miyamoto K, Kiryu J, et al. Intravitreal injection of corticosteroid attenuates leukostasis and vascular leakage in experimental diabetic retina. Invest Ophthalmol Vis Sci. 2005;46:1440-1444.
FREE FULL TEXT
THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES
Cytotoxicity of Triamcinolone Acetonide on Human Retinal Pigment Epithelial Cells
Chang et al.
IOVS 2007;48:2792-2798.
ABSTRACT
| FULL TEXT
|