Potential environmental effect of reducing the variation of disposable materials used for cataract surgery.

PURPOSE: To analyze the cataract package variability in 1 country, Austria. SETTING: Austrian Departments of Ophthalmology. DESIGN: Cross-sectional study. METHODS: The cataract package components of 3 different Austrian hospitals were weighed and life cycle assessment on each product performed. This data was then extrapolated to the sales figures of the main Austrian cataract package suppliers to estimate the carbon footprint of all cataract packages used in Austria in 2021. RESULTS: There were 55 different cataract package compositions in use with an average weight of 0.7 kg. These compositions differ significantly in weight and composition considering that the smallest package was 57% lighter than the largest package. The size of the surgical drapes also showed considerable variation, with a difference of up to 71%. This is substantial, considering that drapes and covers account for about 53% of the package weight. CONCLUSIONS: There was a considerable variation in package composition and product size, which could provide opportunities to save carbon dioxide emissions in cataract surgery. If all Austrian eye departments were to reduce the material quantities and drape sizes to the lower third of the cataract packages used in the Austria in 2021, cataract package associated CO 2 emissions could be reduced by 34%.

Systemic counterregulatory response of angiopoietin-2 after aflibercept therapy for nAMD: a potential escape mechanism.

PURPOSE: To analyse the effect of intravitreal aflibercept injections on systemic angiopoietin-2 (Ang2) and vascular endothelial growth factor (VEGF)-A levels in patients with neovascular age-related macular degeneration (nAMD). METHODS: In a prospective, randomized study, aflibercept (2.0 mg/50 µl) or ranibizumab (0.5 mg/50 µl) was administered intravitreally to 38 treatment-naive patients. Blood samples were taken before, 7 days after, and 28 days after the first intravitreal therapy. Cytokine levels were measured by enzyme-linked immunosorbent assay. Twenty-two age- and sex-matched individuals served as controls. RESULTS: At baseline, there were no significant differences of systemic Ang2 and VEGF-A levels among the treatment and control groups. After intravitreal aflibercept administration, median (interquartile range: IQR) systemic Ang2 was significantly upregulated from 1819 pg/ml (1262-3099) to 2123 pg/ml (1441-3769; p = 0.011) 7 days after the drug injection and remained non-significantly elevated at 1944 pg/ml (1431-2546 pg/ml; p = 0.653) 28 days after the drug injection. Median (IQR) systemic VEGF-A levels were significantly reduced from 43 pg/ml (30-57) to 8 pg/ml (8-8; p < 0.0001) 7 days and 16 pg/ml (8-26; p = 0.001) 28 days after the injection in the aflibercept group. There were no significant effects on systemic VEGF-A and Ang2 levels in the ranibizumab group at any time point following the first injection. CONCLUSION: In this study, we report significant systemic upregulation of Ang2 after intravitreal aflibercept administration. This counterregulatory response may represent a potential escape mechanism from antiangiogenic therapy.

Triamcinolone in small-gauge vitrectomy for epiretinal membrane peeling.

OBJECTIVE: We compared visual and macular morphological outcomes after epiretinal membrane (ERM) peeling, with and without IVTA treatment. DESIGN: Interventional, retrospective, consecutive case-control study. PARTICIPANTS: Forty-one eyes of 41 participants (17 men, 24 women) were included. Twenty-one were treated by standard vitrectomy and peeling (controls) and 20 patients received intravitreal triamcinolone after vitrectomy and peeling. METHODS: Pre-and postoperative letter score and central foveal thickness (CFT) through the foveal centre were compared between both groups. Best-corrected visual acuity (BCVA) was measured using Snellen charts and converted to logMAR for statistical analyses. RESULTS: CFT and BCVA had improved by the 6-month follow-up from baseline. In the control group, the mean logMAR BCVA improved from 0.57 (SD: 0.22) to 0.21 (0.17) (p < 0.01), and the mean CFT reduced from 462.5 (98.6) µm to 329.8 (82.7) µm (p < 0.01). The mean logMAR BCVA of the IVTA group improved from 0.73 (0.17) to 0.36 (0.31) (p < 0.01), and the mean CFT reduced from 561.45 (131.0) µm to 339.25 (72.6) µm (p < 0.01). Visual improvement and CFT did not differ significantly at follow up (p = 0.583; p= 0.85). Significant reduction of CFT is seen in the IVTA group (p = 0.048). CONCLUSIONS: Visual acuity and macular morphology improved after ERM peeling, with or without IVTA. Although conjunctive IVTA did not significantly influence visual outcome at 6 months, a significant decrease in CFT was observed after IVTA administration.

Effects of Intravitreal Aflibercept on Galectin-1 and Vascular Endothelial Growth Factor-A Plasma Levels in Patients with Diabetic Retinopathy.

PURPOSE: To analyze the interaction between aflibercept and galectin-1 and evaluate the plasma levels of galectin-1 and vascular endothelial growth factor (VEGF)-A after intravitreal injection of aflibercept in patients with diabetic retinopathy (DR). METHODS: Interaction of galectin-1 with aflibercept was determined via immunoprecipitation. Seventeen patients with type 2 diabetes and diabetic macular edema (DME) were each treated with a single intravitreal injection of aflibercept (2.0 mg, 50 µL) monthly for three consecutive months. Plasma galectin-1 and VEGF-A levels were measured just before an injection was administered, 1 week after the first injection, and 2 months after the last injection. Nineteen age- and sex-matched healthy participants served as controls. RESULTS: Irrespective of the tested galectin-1 concentration, 24% of added galectin-1 was precipitated by aflibercept. Baseline plasma concentrations of galectin-1 were 22.0 and 23.0 ng/mL in the control and aflibercept-treated groups, respectively. Systemic galectin-1 levels increased to 27.0 and 24.0 ng/mL at 7 days and 4 weeks, respectively, after treatment. At week 8, plasma galectin-1 levels significantly increased to 36.0 ng/mL. This level persisted for 20 weeks. Systemic VEGF-A levels significantly reduced to below the minimum detectable dose in 16 DME patients at 7 days after treatment. This level persisted for 4 weeks. Plasma VEGF-A levels were reduced at weeks 8 (p = 0.099) and 20 (p = 0.023). Decreased plasma VEGF-A levels were observed in all patients after treatment. CONCLUSION: We confirmed that physiological aflibercept levels precipitate galectin-1 in in vitro assays. Additionally, systemic upregulation of galectin-1 might be induced by intravitreal aflibercept, which may be relevant in the clinical outcomes of DR treatment.

Systemic counterregulatory response of placental growth factor levels to intravitreal aflibercept therapy.

PURPOSE: Placental growth factor (PlGF) has been implicated as a contributor to resistance against anti-VEGF therapy. The purpose of the present study was to analyze the systemic levels of PlGF, VEGF-A, and VEGF-B in patients with neovascular age-related macular degeneration (AMD) after treatment with aflibercept, ranibizumab, or bevacizumab. METHODS: Totals of 19 patients were treated with intravitreal aflibercept, 19 with ranibizumab, and 18 with bevacizumab. The cytokine levels were measured by ELISA just before the injection, and 7 days and 1 month thereafter. Age- and sex-matched participants (n = 22) served as controls. RESULTS: The median PlGF plasma concentration at baseline was <12.0 pg/mL in the control group as well as in all three anti-VEGF treatment cohorts. After intravitreal aflibercept injection, a significant upregulation of systemic PlGF could be observed in all treated patients (38.0 [31.0-44.0] pg/mL after 1 week [P < 0.001] and 16.0 [0.0-19.0] pg/mL [P = 0.005] after 4 weeks). No significant effects on plasma PlGF concentrations could be detected in those treated with ranibizumab and bevacizumab. The systemic VEGF-A levels were significantly reduced 1 and 4 weeks after intravitreal aflibercept (P < 0.001, P < 0.001) and bevacizumab (P < 0.001, P < 0.01) injections. No significant effects on plasma cytokine concentrations could be observed in the ranibizumab cohort. No significant effects on systemic VEGF-B could be observed in any of the treatment groups. CONCLUSIONS: In this study, we report a significant systemic upregulation of the proangiogenic cytokine PlGF after intravitreal administration of aflibercept. This might represent a counter-regulatory response to antiangiogenic therapy.

Systemic levels of vascular endothelial growth factor before and after intravitreal injection of aflibercept or ranibizumab in patients with age-related macular degeneration: a randomised, prospective trial.

PURPOSE: To evaluate the changes of vascular endothelial growth factor (VEGF) plasma levels after intravitreal injections of aflibercept or ranibizumab in patients with exudative age-related macular degeneration (AMD). METHODS: Thirty-eight patients with exudative AMD were included in this randomised, prospective study. Nineteen patients were randomised to treatment with intravitreal aflibercept (2.0 mg) and 19 to intravitreal ranibizumab (0.5 mg). The concentration of VEGF was measured by ELISA just before the injection, after 7 days and 1 month. Twenty-two age- and sex-matched healthy patients without chorioretinal diseases served as control. RESULTS: The median baseline plasma VEGF concentration was 61.0 pg/ml in the control group, 43.0 pg/ml in the aflibercept group and 59.0 pg/ml in the ranibizumab group (p=0.127). Seven days after intravitreal injection of aflibercept plasma levels were significantly reduced to values below the minimum detectable dose (MDD) in 17 of 19 patients (89.5%) resulting in a median VEGF concentration of <9 pg/ml (p<0.001). The reduction persisted throughout 1 month with values below the MDD in 5 of 19 patients (26.3%) and a median measurement of 17.0 pg/ml (p<0.001). In patients treated with ranibizumab no significant effects could be observed with a baseline VEGF of 59.0 pg/ml, 54.0 pg/ml at 7 days (p=0.776) and 58.5 pg/ml at 4 weeks of follow-up (p=0.670). CONCLUSION: After intravitreal aflibercept injection, the systemic VEGF levels were significantly reduced throughout the observational period of 4 weeks. No significant systemic effects of intravitreal ranibizumab on plasma VEGF were observed.

Systemic upregulation of PDGF-B in patients with neovascular AMD.

PURPOSE: To determine the plasma levels of platelet-derived growth factor-B (PDGF-B), VEGF, and TNF-α in patients with neovascular AMD and in patients with diabetic macular edema (DME). METHODS: Thirty patients with neovascular AMD, 30 patients with DME, and 12 healthy controls were included in this prospective study. The concentrations of PDGF-B, VEGF, and TNF-α were measured by ELISA. RESULTS: The PDGF-B concentration in the plasma of controls was (median [25th-75th percentile]) 263.5 (162.0-513.3) pg/mL and in patients with DME 219.0 (122.8-604.8) pg/mL. In patients with neovascular AMD, PDGF-B levels were significantly higher with a median plasma concentration of 783.5 (289.3-1183.5) pg/mL (P = 0.003). The VEGF concentrations in patients with DME 33.0 (21.8-73.0) pg/mL and in patients with neovascular AMD 55.0 (37.0-116.3) pg/mL showed no significant differences (P = 0.159). A positive correlation of PDGF-B and VEGF plasma levels was found in patients with neovascular AMD and in patients with DME (r = 0.683, P < 0.001, and r = 0.612, P < 0.001, respectively). No significant differences of systemic TNF-α levels could be found between the three study groups. CONCLUSIONS: Patients with neovascular AMD have significantly higher plasma PDGF-B levels compared with patients with DME and healthy controls. Our study data indicate that PDGF-B may be involved in the pathogenesis of neovascular AMD. (https://eudract.ema.europa.eu number, EudraCT 2010-024654-11)

Reduced-fluence photodynamic therapy combined with ranibizumab for nonproliferative macular telangiectasia type 2.

PURPOSE: To report the efficacy of reduced-fluence photodynamic therapy (PDT) combined with intravitreal ranibizumab for the treatment of nonproliferative macular telangiectasia (MacTel) type 2. METHODS: Noncomparative, interventional, retrospective case series; 5 eyes of 4 patients were studied. Patients were treated with reduced-fluence PDT and intravitreal ranibizumab within 24 h. After initial treatment, follow-up was at least 12 months in all patients. RESULTS: At baseline median logMAR (logarithm of the minimal angle of resolution) best-corrected visual acuity (BCVA) was 1.0 (range, 1.0-0.3). At 3 months of follow-up vision increased in 3 out of 5 eyes and median BCVA was 0.4 (range, 1.0-0.2). The gain of BCVA ranged from 6 lines to 1 line. Visual acuity remained stable in the other 2 study eyes. No eyes lost vision at 3 months of follow-up. At 12 months of follow-up median logMAR BCVA was 0.7 (range, 1.3-0.3). Two eyes had maintained their gain in BCVA compared to baseline. Two eyes lost vision compared to baseline and 1 eye showed unchanged visual acuity at 12 months of follow-up. CONCLUSION: A combination therapy with reduced-fluence PDT and intravitreal ranibizumab might be a valuable treatment option for eyes with progressive vision loss due to nonproliferative MacTel type 2.

Correlation of vascular endothelial growth factor plasma levels and glycemic control in patients with diabetic retinopathy.

PURPOSE: To determine whether glycemic control of patients with diabetic retinopathy (DR) due to type 2 diabetes was related to VEGF plasma levels. METHODS: The prospective study included 30 patients with DR due to type 2 diabetes. Retinopathy was classified according to the international clinical DR disease severity scale. The concentrations of VEGF in the blood plasma were measured by ELISA. Glycosylated hemoglobin (HbA1c) was assessed all patients. Results were reported as DCCT/NGSP-HbA1c (%) values. RESULTS: The median plasma level of VEGF was 34.5 (range 15-217) pg/ml. Median HbA1c was 7.5 (range 5.3-10.6). The highest individual plasma VEGF measurements were found in patients with severe non-proliferative DR. HbA1c levels revealed a significant correlation with plasma VEGF concentrations (r = 0.573, p = 0.001). Age (r = 0.097, p = 0.611), gender (r = -0.315, p = 0.09) and severity of DR (r = 0.256, p = 0.172) were with no significant relationship to the VEGF measurements. CONCLUSION: Poor glycemic control is positively correlated with increased levels of plasma VEGF in patients with type 2 diabetes. As normalization of HbA1c is one of the most effective ways to prevent progression of DR and VEGF has been to shown to be clearly implicated in the development of DR, it affirms the importance of glycemic control in patients with DR.

Plasma levels of vascular endothelial growth factor before and after intravitreal injection of bevacizumab, ranibizumab and pegaptanib in patients with age-related macular degeneration, and in patients with diabetic macular oedema.

AIMS: To determine the level of vascular endothelial growth factor (VEGF) in the plasma of patients with diabetic macular edema (DME) and of patients with exudative age-related macular degeneration (ARMD) before and after intravitreal injection of bevacizumab, ranibizumab or pegaptanib. METHODS: 30 patients with DME and 30 patients with ARMD were included in this randomized controlled study. Patients were randomized to treatment with ranibizumab (0.5 mg), bevacizumab (1.25 mg) or pegaptanib (0.3 mg). 10 patients with DME received bevacizumab, 10 ranibizumab and 10 pegaptanib. The same randomized treatment allocation applied to the 30 patients with ARMD. The concentrations of VEGF were measured by ELISA just before the injection, after 7 days and 1 month. RESULTS: Plasma VEGF in patients with exudative ARMD before the injection of bevacizumab was 89.7 pg/ml. It was significantly reduced to 25.1 pg/ml after 7 days (p=0.01), and to 22.8 pg/ml after 1 month (p=0.008). In patients with DME the same systemic reduction by bevacizumab was observed with a significant decrease of baseline VEGF level from 72.2 pg/ml to 13.7 pg/ml after 7 days (p=0.008) and 17.1 pg/ml at 4 weeks with (p=0.012). No significant reductions of plasma VEGF levels were observed in patients receiving ranibizumab or pegaptanib during follow-up. CONCLUSIONS: Bevacizumab significantly reduces the level of VEGF in the blood plasma for up to one month in patients with DME as well as in those with ARMD. No significant systemic effects of intravitreal ranibizumab or pegaptanib on plasma VEGF could be observed.

[Diagnosis, therapy and follow up of diabetic eye disease]. / Diagnose, Therapie und Verlaufskontrolle der diabetischen Augenerkrankung.

Diabetes mellitus causes diabetic retinopathy, diabetic macular edema, optic neuropathy, cataract or dysfunction of the eye muscles. The incidence of these defects correlates with disease duration and quality of the metabolic control. The recommendations of the Austrian Diabetes Association for the diagnosis, the therapeutic procedures and requirements for adequate follow up depending on the stages of the different forms of diabetic eye disease are summarized.

VIP, PACAP-38, BDNF and ADNP in NMDA-induced excitotoxicity in the rat retina.

PURPOSE: To evaluate the effect of intravitreal injection of N-methyl-D-aspartate (NMDA) on brain-derived neurotrophic factor (BDNF), pituitary adenylate cyclase-activating peptide-38 (PACAP-38), vasoactive intestinal peptide (VIP) and the VIP-associated glial protein activity-dependent neuroprotective protein (ADNP) in the rat retina. These elements have well-documented neuroprotective properties and may thus be integrated in endogenous neuroprotective mechanisms in the retina which break down in NMDA excitotoxicity. METHODS: A volume of 2 µl of 100 nmol NMDA was intravitreally injected into one eye of rats, the untreated eye served as a control. Time-dependent effects of NMDA on VIP, PACAP-38 and BDNF were detected by radioimmunoassay and ELISA, and the effect on the expression of VIP, PACAP-38 and ADNP was evaluated by quantitative RT-PCR 20 days after NMDA injection. Topical flunarizine served to find out whether the effect of NMDA is counteracted. RESULTS: Compared to PACAP-38, VIP levels significantly decreased on days 1, 7, 14, 28 and 56 after NMDA injection indicating that VIPergic cells are more vulnerable than PACAP-38-expressing cells. The expression of VIP and ADNP but not of PACAP-38 was found to be reduced, and application of topical flunarizine counteracted the decrease of VIP. BDNF levels significantly increased after days 1 and 3. CONCLUSION: The early upregulation of BDNF seems to act neuroprotectively and leads to a delay of ganglion cell loss. Although there is no direct evidence, the decrease of VIP and ADNP - the consequence of the presence of NMDA receptors on these peptide-expressing cells - might contribute to the breakdown of endogenous neuroprotective mechanisms given that the decrease of the VIP-related ADNP runs in parallel with the decrease of VIP. Activating and maintaining these mechanisms must be the primary aim in the therapy of diseases with retinal neuronal degeneration.

Safety and feasibility of a novel intravitreal tamponade using a silicone oil/acetyl-salicylic acid suspension for proliferative vitreoretinopathy: first results of the Austrian Clinical Multicenter Study.

BACKGROUND: The safety and efficacy of a new surgical method of intravitreal tamponade using silicone oil suspended with aspirin (acetylsalicylic acid) was investigated for the treatment of proliferative vitreoretinopathy. METHODS: The study was designed as a prospective, randomized, controlled, double-blind multicenter study. A total of 29 patients were included; 15 patients were treated with the silicone oil suspended with aspirin, and 14 patients represented the control group receiving only silicone oil. A standard three-port pars plana vitrectomy was performed in 29 eyes of 29 patients. In cases in which the natural lens was present, simultaneous phacoemulsification was required. The control group received as standard therapy a vitreous tamponade with pure 5000 mPas silicone oil and the treatment group received silicone oil containing 0.2 mg/ml aspirin (AS SiO). At 6 months after surgery, the tamponade was removed from all eyes. The main outcome measure was the incidence of retinal redetachment requiring reoperation. Secondary outcome measures were visual acuity and ophthalmic examination results. RESULTS: The rate of redetachment, defined as the primary outcome parameter, was the same for both groups. The AS SiO was well tolerated and remained clear during the 6-month study period. Clinical examination revealed no signs of local or systemic adverse effects. The visual acuities were well matched before inclusion in the study and there were no significant differences during the follow-up period and in the final visual outcome between the two groups. CONCLUSIONS: Aspirin delivery by intravitreal silicone oil in the human eye is safe and also may provide a delivery vehicle for other antiproliferative agents to the posterior pole.

Secretoneurin and the tachykinins substance P and neurokinin-A/B in NMDA-induced excitotoxicity in the rat retina.

In a recent investigation using the NMDA-excitotoxicity model in the rat retina, we found that, whereas, following intravitreal injection of NMDA, a time-dependent decrease of the levels of a neuropeptide, namely vasoactive intestinal polypeptide (VIP), was fully counteracted by topical treatment with flunarizine eye drops, the levels of pituitary adenylate-cyclase activating peptide-38 (PACAP-38), another neuropeptide, remained unchanged. The aim of the present study was to find out if NMDA causes reduction in the levels of other neuropeptides such as secretoneurin (SN), neurokinin-A/B (NKA/NKB) and substance P (SP), and if so, whether flunarizine has the ability to counteract this effect or prevent such reduction. The reduction of the levels of SN and NKA/NKB 14 days after intravitreal injection of 2 µl of 100 nmol NMDA into one eye was more pronounced than after 7 days; topical flunarizine had a slight counteracting effect, but could not prevent the decrease in the levels of these peptides. Reduction in SP levels after 28 and 56 days was fully counteracted by flunarizine. By enabling a pronounced influx of Ca²+ ions into peptide-expressing cells, NMDA leads to cell death. Since each of these peptides exerts neuroprotective properties in the central nervous system, the drop in their levels caused by acute insult (e.g. NMDA excitotoxicity) or chronic insult (e.g. glaucoma) may cause a breakdown of endogenous neuroprotection in the retina given that these peptides feature neuroprotective properties in the retina as well.

Substance P and secretoneurin in vitreous aspirates of patients with various vitreoretinal diseases.

By means of highly sensitive radioimmunoassays, the levels of substance P (SP) and secretoneurin (SN) were detected in vitreous aspirates of patients with macular holes which served as controls, in patients with nonproliferative diabetic retinopathy (DR), active proliferative diabetic retinopathy (active PDR), inactive PDR, rhegmatogenous retinal detachment and proliferative vitreoretinopathy (PVR). Furthermore, SN-like immunoreactivities were characterized by reversed phase-HPLC. The concentration of SN was more than 20-fold higher in macular holes when compared with SP and reversed phase HPLC revealed evidence that the vitreous levels of SN represent authentic SN. SN was significantly decreased in patients with nonproliferative DR, active PDR and inactive PDR by more than 70% which seems to result from a reduced expression and/or secretion from the cilary epithelium and a reduced release from the retina both due to diabetes mellitus. By contrast SP was increased in rhegmatogenous retinal detachment most obviously due to an enhanced outflow of the peptide through retinal breaks. Despite their proangiogenic activities, SP and SN are unlikely to be involved in the pathogenesis of neovascularizations in DR because of their unchanged and reduced levels, respectively, but the low levels of both peptides may facilitate the regression of vasoproliferations following laser photocoagulation.

Peptidergic nerves in the eye, their source and potential pathophysiological relevance.

Over the last five decades, several neuropeptides have been discovered which subsequently have been found to be highly conserved during evolution, to be widely distributed both in the central and peripheral nervous system and which act as neurotransmitters and/or neuromodulators. In the eye, the first peptide to be explored was substance P which was reported to be present in the retina but also in peripherally innervated tissues of the eye. Substance P is certainly the best characterized peptide which has been found in sensory neurons innervating the eye. Functionally, it has been shown to act trophically on corneal wound healing and to participate in the irritative response in lower mammals, a model for neurogenic inflammation, where it mediates the noncholinergic nonadrenergic contraction of the sphincter muscle. Over the last three decades, the interest has extended to investigate the presence and distribution of other neuropeptides including calcitonin gene-related peptide, vasoactive intestinal polypeptide, neuropeptide Y, pituitary adenylate cyclase-activating polypeptides, cholecystokinin, somatostatin, neuronal nitric oxide, galanin, neurokinin A or secretoneurin and important functional results have been obtained for these peptides. This review focuses on summarizing the current knowledge about neuropeptides in the eye excluding the retina and retinal pigment epithelium and to elucidate their potential functional significance.

Neurokinin A and neurokinin B in the human retina.

Very recently, the authors found levels of neurokinin (NK) A-like immunoreactivities in the human retina which were more than five times higher than those of substance P (SP). The present study aimed to find out how many of these immunoreactivities can be attributed to NKA and NKB and then the exact distribution pattern of both NKA and NKB was evaluated in the human retina and compared with that of SP. For this purpose, NKA-like immunoreactivities were characterized in the human retina by reversed phase HPLC followed by radioimmunoassay using the K12 antibody which recognizes both NKA and NKB. Furthermore, the retinae from both a 22- and 70-year-old donor were processed for double-immunofluorescence NKA/SP and NKB/SP. The results showed that NKA contributes to approximately two thirds and NKB to approximately one third of the immunoreactivities measured with the K12 antibody. NKA was found to be localized in sparse amacrine cells in the proximal inner nuclear layer, in displaced amacrine cells in the ganglion cell layer with processes ramifying in stratum 3 of the inner plexiform layer and also in sparse ganglion cells. By contrast, staining for NKB was only observed in ganglion cells and in the nerve fiber layer. Double-immunofluorescence revealed cellular colocalization of NKA with SP and also of NKB with SP. Thus, the levels of NKA and NKB are more than three and two times higher than those of SP, respectively. Whereas the distribution pattern of NKA is typical for neuropeptides, the localization of NKB exclusively in ganglion cells is atypical and unique.

Experimental model for proliferative vitreoretinopathy by intravitreal dispase: limited by zonulolysis and cataract.

BACKGROUND: The intravitreal injection of dispase has been shown to be a valuable method for induction of experimental PVR. The goal of the present study was to gain additional information about potential side effects associated with this method. METHODS: Twenty-one pigmented rabbits received a single injection of dispase under topical anesthesia to one eye only, contralateral eyes served as untreated control. The animals were injected with doses from 0.045 to 0.065 units of dispase: 8 animals received 0.045 units, 9 animals 0.055 units and 4 animals 0.065 units. RESULTS: Proliferative vitreoretinopathy occurred in 81% of the treated eyes. In 90% cataract formation was observed. Lens luxation was present in 47.3% of the cataract eyes. CONCLUSION: Intravitreal injection of dispase resulted in the reproducible induction of PVR in addition to cataract formation and lens luxation. Whether these effects may all be associated with a toxic reaction or whether the proliferative changes are solely triggered by endogenous reactions similar to the pathomechanism of human PVR and whether the cataract formation and the lens luxation may be avoided by changing the method of injection require further investigation.

Long-term outcome after vitrectomy for diabetic macular edema.

BACKGROUND: To determine the benefit of vitrectomy on eyes with diabetic macular edema. METHODS: A retrospective institutional case series was used including 66 patients (69 eyes) who had undergone pars plana vitrectomy for diabetic macular edema between 1992 and 2000. Prior to surgery, the patients had been treated with laser coagulation as recommended by the Early Treatment Diabetic Retinopathy Study. In the case of persistent macular edema, vitrectomy with removal of the posterior hyaloid in all cases and the inner limiting mem brane in 51 (74%) of all cases was performed. RESULTS: The mean preoperative best-corrected visual acuity improved from 20/320 to 20/80 at the time of best postoperative best-corrected visual acuity (p < 0.0001). The mean increase in Snellen lines was 2.7 +/- 7.9. In 90% of eyes, the macular edema improved. A persistence of the edema was observed in 10%. All eyes had at least 12 months of follow-up with a mean of 55 months and a maximum of 120 months. CONCLUSIONS: Our findings confirm that vitrectomy might represent a therapeutic alternative in the case of persisting diabetic macular edema after laser photocoagulation.

Laser photocoagulation for retinopathy of prematurity: structural and functional outcome.

BACKGROUND: To report the structural and refractive outcome after laser photocoagulation for retinopathy of prematurity (ROP). METHODS: Nineteen consecutive patients who had undergone photocoagulation for ROP between 1997 and 2002 at our clinic were examined for this non-comparative, consecutive, interventional, retrospective case series. A total of 37 eyes received either transscleral or transpupillary laser treatment. Data consisted of grade of ROP pre- and postoperatively, birth weight, perioperative and postoperative complications and refraction. Based on indirect ophthalmoscopy, independent observers graded the extent of ROP and determined the postoperative refraction by retinoscopy. RESULTS: A total of 97% of all eyes responded to laser treatment with regression of ROP. Only one eye out of 37 progressed to stage IV B despite photocoagulation and therefore an encircling procedure was performed. After further progression a vitrectomy was carried out. Perioperative complications included haemorrhages in 22% that resorbed spontaneously and cataract formation in one eye (3%). Postoperative refractive errors at mean ages of 23 +/- 12 months and 45 +/- 14 months were evaluated in 15/19 patients (79%). The spherical equivalents ranged between -8 D and +6 D at the first examination and between -12 D and +7 D at the second examination. In all only 14% of the refracted eyes were myopic. CONCLUSIONS: Photocoagulation for ROP in our patients resulted in regression of threshold ROP. In addition, the analyses of the refractive outcomes demonstrated a predominance of hypermetropia in our patients.