epidermal-growth-factor and Macular-Edema

To determine differences in inflammatory markers expressed in diabetic macular edema (DME) patients with and without obstructive sleep apnea (OSA).. This was a prospective, cross-sectional study. Patients with treatment naive DME were enrolled in the study. They were stratified into 2 groups based on Apnea Hypopnea Index (AHI) from overnight polysomnography: OSA + (AHI ≥ 15) and OSA - (AHI<15). Multiplex immunoassay was performed for aqueous and serum cytokines including VEGF, placental growth factor (PGF), ICAM, IL2, IL3, IL6, IL8, IL10, IL17, vascular cell adhesion molecule-1 (VCAM1), monocyte attractant protein-1 (MCP1), epidermal growth factor (EGF) and platelet derived growth factor (PDGF). Statistical significance was defined as p < 0.004 using Bonferroni correction.. 32 DME positive patients were enrolled in the study; of which 17 patients were OSA + and 15 OSA-. The OSA + cohort had significantly higher levels of serum EGF (p = 0.003), and trended towards higher levels of most serum cytokines including ICAM and IL6. OSA- cohort had significantly higher levels of aqueous IL17 compared to the OSA + cohort (2.97 ± 1.7 vs. 1.4 ± 0.46 pg/mL, p = 0.004). There were no significant differences in other aqueous cytokines.. OSA + group trended towards higher levels of most serum inflammatory markers, suggesting a greater pro-inflammatory state. However, they did not have significantly greater level of aqueous cytokines.

Topics: Biomarkers; Cross-Sectional Studies; Cytokines; Diabetes Mellitus; Diabetic Retinopathy; Epidermal Growth Factor; Female; Humans; Inflammation Mediators; Interleukin-6; Macular Edema; Placenta Growth Factor; Prospective Studies; Sleep Apnea, Obstructive

To assess the safety of intravitreally applied epidermal growth factor (EGF).. The clinical interventional, prospective, single-centre, case series study included patients with age-related macular degeneration-related geographic atrophy (GA), in whom the eye with the worse best-corrected visual acuity (BCVA) underwent a single, or repeated, intravitreal injection of EGF (0.75 µg in 50 µL). At baseline and afterwards, the eyes underwent ophthalmological examinations.. The study included seven patients (mean age:70.0±12.2 years (range: 54-86 years), with five patients receiving a single injection and two patients receiving two intravitreal injections in an interval of 4 weeks. Mean duration of follow-up was 97±97 days (median:35 days; range: 7-240 days). Mean BCVA was lower at baseline than at study end (1.41±0.44 logMAR vs 0.97±0.12 logMAR; p=0.03). Mean size of the GA lesions did not differ significantly between baseline and study end (29 212±22 887 pixels vs 29 300±22 905 pixels; p=0.59) nor did the mean perimetric mean defect (-10.3±5.9 dB vs 12.0±8.8 dB; p=0.35) or the electroretinographical b-wave amplitude (44.53±31.7 µV vs 64.5±25.5 µV; p=0.12). After a second injection 4 weeks after the first injection, one of two patients developed a cystoid macular oedema in association with an induced incomplete posterior vitreous detachment. It persisted for 3 weeks. Visual acuity in this eye improved from 1.0 logMAR at baseline to 0.80 logMAR at study end.. Except for one eye with temporary, self-resolving cystoid macular oedema, single and repeated intravitreal applications of EGF (0.75 µg) in patients with GA did not lead to intraocular inflammations or any observed intraocular side effect.. ISRCTN12733334.

Topics: Aged; Aged, 80 and over; Angiogenesis Inhibitors; Antibodies, Monoclonal, Humanized; Bevacizumab; Epidermal Growth Factor; Humans; Macular Degeneration; Macular Edema; Middle Aged; Prospective Studies; Tomography, Optical Coherence; Vascular Endothelial Growth Factor A

This study evaluates diabetic macular-edema (DME) patients for the effect of intravitreal bevacizumab (IVB) \ injection on macular thickness and proangiogenic biomarkers in serum and vitreous.. Forty DME patients were analyzed for macular thickness (MT). Twelve proangiogenic biomarkers in serum \ and vitreous were analyzed before and after IVB.. Significant decrease in MT with vitreal vascular endothelial growth factor-A (VEGF-A) was observed as expected after IVB, \ while serum VEGF-A did not follow a decreasing trend in contrast to VEGF-C, which decreased both in serum and vitreous. Other \ vitreal factors like bone morphogenetic protein-9 (BMP9) and fibroblast growth factor (FGF) were also significantly decreased, while \ endothelial growth factor (EGF) increased following IVB. Before IVB, significant negative correlations were vitreous BMP9 with serum \ FGF, vitreous human growth factor (HGF) and interleukin-8 (IL-8) with serum endothelin, and vitreous and serum FGF and serum \ placental growth factor (PLGF) with EGF. After IVB, negative correlations in serum vs. vitreous were found for both HGF and PLGF \ with BMP9, and angiopoietin with FGF. Cube average thickness was negatively correlated with serum FGF and positively correlated \ with vitreous PLGF and endothelin.. Vascular endothelial growth factors are not the only factors that cause macular edema in diabetic patients. The effect of IVB \ on different proangiogenic biomarkers indicated a complex interplay of other factors in DME.

Topics: Adult; Aged; Angiogenesis Inhibitors; Angiopoietins; Bevacizumab; Biomarkers; Diabetic Retinopathy; Endothelins; Epidermal Growth Factor; Female; Fibroblast Growth Factors; Hepatocyte Growth Factor; Humans; Intercellular Signaling Peptides and Proteins; Interleukin-8; Intravitreal Injections; Macula Lutea; Macular Edema; Male; Middle Aged; Neovascularization, Pathologic; Placenta Growth Factor; Vascular Endothelial Growth Factor A; Vitreous Body

Diabetes mellitus is a disease with considerable morbidity and mortality worldwide. Breakdown of the blood-retinal barrier and leakage from the retinal vasculature leads to diabetic macular edema, an important cause of vision loss in patients with diabetes. Although epidemiologic studies and randomized clinical trials suggest that glycemic control plays a major role in the development of vascular complications of diabetes, insulin therapies for control of glucose metabolism cannot prevent long-term retinal complications. The phenomenon of temporary paradoxical worsening of diabetic macular edema after insulin treatment has been observed in a number of studies. In prospective studies on non-insulin-dependent (type 2) diabetes mellitus patients, a change in treatment from oral drugs to insulin was often associated with a significant increased risk of retinopathy progression and visual impairment. Although insulin therapies are critical for regulation of the metabolic disease, their role in the retina is controversial. In this study with diabetic mice, insulin treatment resulted in increased vascular leakage apparently mediated by betacellulin and signaling via the epidermal growth factor (EGF) receptor. In addition, treatment with EGF receptor inhibitors reduced retinal vascular leakage in diabetic mice on insulin. These findings provide unique insight into the role of insulin signaling in mediating retinal effects in diabetes and open new avenues for therapeutics to treat the retinal complications of diabetes mellitus.

Topics: ADAM Proteins; ADAM10 Protein; Amyloid Precursor Protein Secretases; Animals; Betacellulin; Blood Vessels; Capillary Permeability; Diabetic Retinopathy; Endothelial Cells; Epidermal Growth Factor; ErbB Receptors; Female; Humans; Insulin; Intercellular Signaling Peptides and Proteins; Macular Edema; Membrane Proteins; Mice; Mice, Inbred C57BL; Protective Agents; Protein Kinase Inhibitors; Retina; Retinal Pigment Epithelium; Signal Transduction; Tight Junctions