Intravitreal ranibizumab was helpful for either vitrectomized or non-vitrectomized eyes with DME in short-term follow-up. Anatomical and functional improvements were greater in non-vitrectomized patients than in vitrectomized cases.

PURPOSE. We evaluated the anti-inflammatory effect of bortezomib (Velcade), a proteasome inhibitor, on endotoxin-induced uveitis (EIU) in rats and lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. METHODS. EIU was induced by footpad injection of LPS intoLewis rats. MG-132 (10 mg/kg), or high-dose (0.2 mg/kg) or low-dose (0.05 mg/kg) bortezomib was given 30 minutes before LPS injection in each treatment group. The rats were sacrificed 24 hours later to observe the inflammatory response in tissues. The expression levels of fractalkine, MCP-1, ICAM-1, and iNOS were evaluated by PCR and Western blot analysis. Immunohistochemical (IHC) studies were used to demonstrate the expression of pro-inflammatory mediators and nuclear factor-kappa B (NF-jB) p65 in the iris and ciliary body. The DNA-binding activity of NF-jB was evaluated using an electrophoretic mobility shift assay (EMSA). An in vitro study using RAW 264.7 cells was performed to verify the results.RESULTS. Pretreatment with high-dose bortezomib significantly attenuated the inflammatory response of EIU. Reduced expression of inflammatory mediators always was observed in the high-dose bortezomib and MG-132 groups, but invariably was not noted in the low-dose bortezomib group. Decreased DNA-binding activity of NF-jB was noted in those rats pretreated with high-dose bortezomib or MG-132. In vitro study demonstrated the dose-dependent anti-inflammatory effects of bortezomib in LPS-stimulated RAW cells, consistent with the results obtained in vivo.CONCLUSIONS. Bortezomib inhibits EIU, probably by inhibiting the activation of NF-jB, which in turn, down-regulates the expression of the associated inflammatory genes. Proteasome inhibition may be a potential treatment strategy for uveitis. (Invest Ophthalmol Vis Sci. 2012;53:3682-3694)

Fifty-two eyes of 52 patients with treatment-naïve macular edema associated with perfused branch retinal vein occlusion were retrospectively reviewed. Twenty-seven cases received PRN intravitreal bevacizumab, and 25 cases were treated by PRN intravitreal aflibercept with monthly follow-ups for 12 months. Both aflibercept and bevacizumab were effective in reduction of macular thickness and improvement of visual acuity for the participants. Both antivascular endothelial growth factor agents had similar efficacy and duration of treatment for these eyes with macular edema secondary to branch retinal vein occlusion during a 12-month period. No serious systemic or ocular adverse events were reported.

PurposeTo evaluate the protective effects of bortezomib (Velcade) on ischemia-reperfusion (IR) injury in the rat retina.MethodsThe rats were randomized to receive treatment with saline, low-dose bortezomib (0.05 mg/kg), or high-dose bortezomib (0.2 mg/kg) before the induction of IR injury. Electroretinography (ERG) was used to assess functional changes in the retina. The expression of inflammatory mediators (iNOS, ICAM-1, MCP-1, TNF-α), anti-oxidant proteins (heme oxygenase, thioredoxin, peroxiredoxin), and pro-apoptotic proteins (p53, bax) were quantified by PCR and western blot analysis. An immunofluorescence study was performed to detect the expression of iNOS, oxidative markers (nitrotyrosine, 8-OHdG, acrolein), NF-κB p65, and CD 68. Apoptosis of retinal cells was labeled with in situ TUNEL staining. Neu-N staining was performed in the flat-mounted retina to evaluate the density of retinal ganglion cells.ResultsERG showed a decreased b-wave after IR injury, and pretreatment with bortezomib, especially the high dosage, reduced the functional impairment. Bortezomib successfully reduced the elevation of inflammatory mediators, anti-oxidant proteins, pro-apoptotic proteins and oxidative markers after IR insult in a dose-dependent manner. In a similar fashion, NF-κB p65- and CD 68-positive cells were decreased by bortezomib treatment. Retinal cell apoptosis in each layer was attenuated by bortezomib. The retinal ganglion cell density was markedly decreased in the saline and low-dose bortezomib groups but was not significantly changed in the high-dose bortezomib group.ConclusionsBortezomib had a neuro-protective effect in retinal IR injury, possibly by inhibiting the activation of NF-κB related to IR insult and reducing the inflammatory signals and oxidative stress in the retina.

Massive blood transfusion (MBT) increased mortality and morbidity after cardiac surgery. However, a mid-term follow-up study on repair surgery of acute type A aortic dissection (AAAD) with MBT was lacking. This study aimed to assess the impact of perioperative MBT on late outcomes of surgical repair for AAAD.There were 3209 adult patients firstly received repair surgery for AAAD between 2005 and 2013, were identified using Taiwan National Health Insurance Research Database. Primary interest variable was MBT, defined as transfused red blood cell (RBC) ≥10 units.The outcomes contained in-hospital mortality, surgical-related complications, all-cause mortality, respiratory failure, and chronic kidney disease (CKD) during follow-up period. Higher in-hospital mortality (37.7% vs 11.6%; odds ratio, 4.00; 95% confidence interval [CI], 3.30–4.85), all-cause mortality (26.1% vs 13.0%; hazard ratio [HR], 1.66; 95% CI, 1.36–2.04), and perioperative complications were noted in the MBT group. A subdistribution hazard model revealed higher cumulative incidence of CKD (13.9% vs 6.5%; HR, 1.95; 95% CI, 1.47–2.60) and respiratory failure (7.1% vs 2.7%; HR, 2.34; 95% CI, 1.52–3.61) for the MBT cohort. A dose-dependent relationship between amount of transfused RBC (classified as tertiles) and cumulative incidence of all-cause mortality, incident CKD, and respiratory failure was found (P of trend test <.001).Patients with MBT had worse late outcomes following surgical repair of AAAD. The cumulative incidence of all-cause mortality, incident CKD, and respiratory failure increased with the amount of transfused RBC in a dose-dependent manner.

ObjectivesBleeding is a common problem during adult extracorporeal membranes oxygenation (ECMO) support, requiring blood transfusion for correction of volume depletion and coagulopathy. The goal of this study is to investigate the long-term outcomes for adults under support of ECMO with massive blood transfusion (MBT).DesignRetrospective nationwide cohort study.SettingData were provided from Taiwan National Health Insurance Research Database (NHIRD).Participants and interventionsTotally 2757 adult patients were identified to receive MBT (red blood cell ≥10 units) during ECMO support from 2000 to 2013 via Taiwan NHIRD.Main outcome measuresThe outcomes included in-hospital major complications/mortality, all-cause mortality, cardiovascular death, newly onset end-stage renal disease and respiratory failure during the follow-up period.ResultsPatients with MBT had higher in-hospital mortality (65.6% vs 52.1%; OR 1.74; 95% CI 1.53 to 1.98) and all-cause mortality during the follow-up (47.0% vs 35.8%; HR 1.46; 95% CI 1.25 to 1.71) than those without MBT. Not only higher incidences of post ECMO sepsis, respiratory failure and acute kidney injury, but also longer duration of ECMO support, ventilator use and intensive care unit stay were demonstrated in the MBT group. Moreover, a subdistribution hazard model presented higher cumulative of respiratory failure (19.8% vs 16.2%; subdistribution HR 1.36; 95% CI 1.07 to 1.73) for the MBT cohort. Positive dose–dependent relationship was found between the amount of transfused red blood cell product and in-hospital mortality. In the MBT subgroup analysis for the impact of transfused ratio (fresh frozen plasma/packed red blood cell) on in-hospital mortality, ratio ≥1.0 had higher mortality.ConclusionsPatients with MBT during ECMO support had worse long-term outcomes than non-MBT population. The transfused amount of red blood cell had positive dose–dependent effect on in-hospital mortality.

. Purpose:  This study aimed to evaluate treatment effects of intravitreal gas for macular hole with localized retinal detachment (RD) in highly myopic eyes and to examine how the vitreomacular relationship and other factors may influence treatment outcomes. Methods:  Twenty highly myopic patients with macular holes and localized posterior RD, treated initially with intravitreal injection of C3F8, were prospectively studied. Recurrent disease was treated with repeated gas injection or vitrectomy according to the extent of detachment. Length of follow‐up was ≥ 12 months. Vitreomacular conditions were determined before and within 2 months after gas injection by standard optical coherence tomography. Demographics, refractive errors, axial length, the extent of chorioretinal (CR) atrophy and visual acuity were recorded. Results:  The success rate after primary gas injection was 70%. The remaining 30% of patients achieved anatomic success after further treatment, including vitrectomy with gas or silicone oil tamponade and/or scleral buckling. All cases achieved anatomic success after a mean of 1.4 surgeries. Univariate analysis showed that the patterns of the posterior vitreoretinal relationship did not differ significantly between those successfully treated with gas only (group 1) and those requiring vitrectomy (group 2) (p = 1.000). Logistic regression showed no statistically significant differences in any characteristics between groups 1 and 2. Conclusions:  Intravitreal gas tamponade alone may achieve anatomic success in more than two‐thirds of highly myopic patients with macular holes and localized RD. Patients with different clinical characteristics and vitreoretinal relationships seem to have similar opportunities to achieve reattachment through this relatively non‐invasive surgery.

Focal laser photocoagulation was helpful for the management of ruptured or leaky RAM. Combined focal laser and intravitreal anti-VEGF agents could better reduce macular exudation caused by RAM. Additionally, Nd:YAG laser was a safe and effective method to remove the sub-ILM hemorrhage caused by RAM.