Safety of Receiving Anti-Vascular Endothelial Growth Factor Intravitreal Injection in Office-Based vs Operating Room Settings: A Meta-analysis.

IMPORTANCE: Compared with the operating room (OR), office-based intravitreal injection (IVI) is considered a more cost-effective and convenient approach, yet clinical outcomes of IVIs with anti-vascular endothelial growth factor (VEGF) agents in different settings (office-based vs OR) have not been systematically evaluated. OBJECTIVE: To evaluate the safety outcomes of IVI with anti-VEGF agents in the OR vs office-based setting. DATA SOURCES: PubMed, Embase, Cochrane Library, Web of Science, and ClinicalTrials.gov were searched from inception to July 2020. STUDY SELECTION: Eligible studies reporting on patients who received IVIs with anti-VEGF drugs with a clearly stated injection setting of the office or OR. DATA EXTRACTION AND SYNTHESIS: Two reviewers independently screened studies, extracted data, and assessed risk of bias. A meta-analysis was conducted to determine the rates of endophthalmitis (EO) and culture-positive EO. MAIN OUTCOMES AND MEASURES: Rates of EO and culture-positive EO following anti-VEGF IVIs in the OR and office-based setting. RESULTS: Thirty-one studies with a total of 1 275 815 injections were included. Comparative analysis suggested no difference between rates of EO after IVIs performed in the office and OR settings (odds ratio, 3.06; 95% CI, 0.07-139.75; P = .57; I2 = 80%) were identified, yet a higher rate of culture-positive EO was found in the office setting (odds ratio, 21.52; 95% CI, 2.39-193.55; P = .006; I2 = 0%). The pooled rates of EO following anti-VEGF IVIs were 0.03% (95% CI, 0.03-0.04) and 0.02% (95% CI, 0.01-0.04) in office and OR settings, respectively, and the pooled rates of culture-positive EO were 0.01% (95% CI, 0.01-0.02) and 0.01% (95% CI, 0-0.02). The pooled rates of other ocular and systemic adverse events were low. CONCLUSIONS AND RELEVANCE: The rate of clinically suspected or culture-positive EO following anti-VEGF IVIs was low whether the procedure was performed in the office or OR setting. Bacterial spectrum could differ between the 2 settings. This meta-analysis could not determine if it is more appropriate to give treatment in the OR for safety reasons in low-income compared with higher-income regions in the world.

Antivascular endothelial growth factors in the treatment of macular oedema secondary to central retinal vein occlusion: a meta-analysis.

BACKGROUND: Macular oedema secondary to central retinal vein occlusion is a major cause of vision loss. Intraocuclar anti-vascular endothelial growth factor injection is a promising treatment but lacks clinical evidence of its safety and efficacy. DESIGN: Meta-analysis. PARTICIPANTS: Patients from previously reported randomized, controlled trials comparing intravitreal anti-vascular endothelial growth factor versus sham injections. METHODS: A comprehensive search in MEDLINE, CENTRAL, and EMBASE was conducted for reports published by April 2013. A meta-analysis of the retrieved data was conducted in RevMan 5.2 software. MAIN OUTCOME MEASURES: Primary outcome measures were changes in best-corrected visual acuity and central retinal thickness from baseline. Secondary outcome measures were the proportion of eyes changing 15 or more letters on the Early Treatment in Diabetic Retinopathy Study chart, the proportion with neovascularization and changes in the 25-item Visual Function Questionnaire. Severe adverse events were summarized to assess safety. RESULTS: Six trials involving a total of 940 eyes were included in the meta-analysis. The mean difference in 6-month changes in best-corrected visual acuity and central retinal thickness for the anti-vascular endothelial growth factor group were 15.2 Early Treatment Diabetic Retinopathy Study letters (P < 0.00001) and -242.2 µm (P < 0.00001), respectively. Severe adverse event incidence was similar between the groups. CONCLUSIONS: Intravitreal anti-vascular endothelial growth factor injections were safe and effective for macular oedema secondary to central retinal vein occlusion. The efficacy was rapid and robust. Further trials are needed to determine the detailed indications and therapeutic regimens of anti-vascular endothelial growth factor treatments.

Glucocorticoid effects on the beta-adrenergic receptor-adenylyl cyclase system of human airway epithelium.

BACKGROUND: Activation of the beta(2)-adrenergic receptor (beta(2)AR) system expressed by human airway epithelial cells elicits a variety of cyclic adenosine monophosphate (cAMP)-dependent processes that help determine airway caliber and the intensity of airway inflammation in asthma. Glucocorticoids, mainstays in the treatment of asthma, profoundly affect the expression and function of the beta(2)-adrenergic receptor-adenylyl cyclase (beta(2)AR-AC) system in a variety of cell types. However, the effects of glucocorticoids on the beta(2)AR-AC system expressed by human airway epithelial cells are unstudied. OBJECTIVE: We examined the effects of dexamethasone (DEX) on beta(2)AR gene expression and the function of the beta(2)AR-AC system in cultured human airway epithelial cells. METHODS: Studies were performed in normal airway epithelial cells and BEAS-2B cells. Beta(2)AR gene expression was assessed from measurements of beta-adrenergic receptor density, beta(2)AR mRNA, and the activity of a full-length beta(2)AR promoter-luciferase reporter construct. The function of the beta(2)AR-AC system was assessed from cAMP production in response to the beta(2)-agonist isoproterenol and the expression of the stimulatory G protein G(alpha)s. RESULTS: DEX had no effect on beta-adrenergic receptor density or on the beta(1)/beta(2) ratio over a wide range of concentrations and exposure times. However, DEX significantly but transiently enhanced beta(2)AR mRNA levels (approximately 1.5-fold) and beta(2)AR promoter activity (approximately 1.5-fold), indicating increased beta(2)AR gene transcription. DEX also dose-dependently enhanced cAMP responses to isoproterenol but not to forskolin, a direct activator of adenylyl cyclase. DEX-induced changes in cAMP production were associated with small (approximately 15%) increases in G(alpha)s expression. CONCLUSIONS: These data indicate that glucocorticoids only transiently enhance beta(2)AR gene transcription and fail to increase steady-state levels of beta(2)AR protein in human airway epithelial cells. Nonetheless, glucocorticoid-induced effects on the beta(2)AR-AC system of human airway epithelial cells contribute to the beneficial effects of corticosteroids in asthma by enhancing the functional response to beta(2)-agonists.