Die Rolle der Inflammation beim diabetischen Makulaödem

2015 ◽  
Vol 1 (2) ◽  
pp. 80-81
Keyword(s):  
Macular Edema ◽  
Diabetic Macular Edema ◽  
Immunosorbent Assay ◽  
Enzyme Linked Immunosorbent Assay ◽  
Pentraxin 3 ◽  
Laser Flare ◽  
Laser Flare Meter

Der Gehalt des Glaskörpers an vaskulärem endothelialem Wachstumsfaktor (VEGF), löslichem VEGF-Rezeptor 2 (sVEGFR-2), löslichem interzellulärem Adhäsionsmolekül 1 (sICAM-1), Monozyten-chemotaktischem Protein 1 (MCP-1) und Pentraxin 3 (PTX3) wurde bei 36 Patienten mit diabetischem Makulaödem (DMÖ) und 15 Patienten mit Makulaforamen (MF) mittels Enzymimmunoassay (enzyme-linked immunosorbent assay) bestimmt. Die Tyndall-Werte wurden mit einem Laser-Flare-Meter ermittelt und das Makulaödem mittels optischer Kohärenztomografie untersucht. Der Gehalt des Glaskörpers an VEGF, sVEGFR-2, sICAM-1, MCP-1 und PTX3 war bei den Patienten mit DMÖ signifikant höher als bei denen mit MF. Zwischen dem Glaskörper-Gehalt an sVEGFR-2 und den Konzentrationen von sICAM-1, MCP-1 und PTX3 bestand eine signifikante Korrelation. Der Tyndall-Wert korrelierte signifikant mit dem Glaskörper-Gehalt an sVEGFR-2, sICAM-1, MCP-1 und PTX3. Diese Ergebnisse deuten darauf hin, dass Entzündungsfaktoren bei DMÖ-Patienten eine erhöhte Gefäßpermeabilität induzieren und zur Unterbrechung der Blut-Kammerwasser-Schranke führen könnten. Übersetzung aus Noma H, et al: Role of inflammation in diabetic macular edema. Ophthalmologica 2014;232:127-135 (DOI: 10.1159/000364955)

scholarly journals Measurement of plasminogen activator inhibitor 1 in biologic fluids with a murine monoclonal antibody-based enzyme-linked immunosorbent assay

Blood ◽  
1988 ◽  
Vol 71 (1) ◽  
pp. 220-225 ◽  
Author(s):  
PJ Declerck ◽  
MC Alessi ◽  
M Verstreken ◽  
EK Kruithof ◽  
I Juhan-Vague ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Immunosorbent Assay ◽  
Healthy Subjects ◽  
Plasminogen Activator Inhibitor ◽  
Enzyme Linked Immunosorbent Assay ◽  
Plasminogen Activator Inhibitor 1 ◽  
Platelet Poor Plasma ◽  
Activator Inhibitor ◽  
Pai 1

An enzyme-linked immunosorbent assay for plasminogen activator inhibitor-1 (PAI-1) in biologic fluids was developed on the basis of two murine monoclonal antibodies raised against PAI-1 purified from HT- 1080 fibrosarcoma cells. The lower limit of sensitivity of the assay in plasma is 2 ng/mL. The assay is 12 times less sensitive toward the PAI- 1/human tissue-type plasminogen activator (t-PA) complex as compared with free PAI-1. The intraassay, interassay, and interdilution coefficients of variation are 5.2%, 8.0%, and 7.1%, respectively. The level of PAI-1 in platelet-poor plasma of healthy subjects is 18 +/- 10 ng/mL (mean +/- SD, n = 45). In platelet-rich plasma after freezing and thawing, 92% of PAI-1 antigen is released from platelets, whereas only 8% is found in the corresponding platelet-poor plasma. In platelet-poor plasma from healthy subjects, a linear correlation (r = 0.80) was found between PAI activity and PAI-1 antigen. In plasma approximately two thirds of the PAI-1 antigen was functionally active, whereas only 5% of the PAI-1 antigen released from platelets was active. During pregnancy a progressive increase of PAI-1 antigen levels up to three- to sixfold the control value was observed. In plasma of patients with recurrent deep vein thrombosis, PAI-1 levels were 44 +/- 20 ng/mL (mean +/- SD, n = 7), during a clinically silent phase. Four of these patients had a level above 38 ng/mL (mean +/- 2 SD of normal). The present assay, based on stable and reproducible reagents, allows the specific determination of PAI-1 antigen in biologic fluids. It may facilitate interlaboratory comparisons and be useful for further investigations of the role of PAI-1 in clinical conditions associated with impaired fibrinolysis and/or a tendency to thrombosis and investigations of the role of PAI-1 in platelets.

Surgical Therapy in Diabetic Macular Edema and Diabetic Intravitreal Hemorrhage

2018 ◽  
pp. 194-201
Keyword(s):  
Risk Factors ◽  
Macular Edema ◽  
Diabetic Macular Edema ◽  
Surgical Therapy ◽  
Current Literature ◽  
Preventive Measures ◽  
Timing Of Surgery ◽  
Intravitreal Injections ◽  
Complications Of Diabetes

Diabetic macular edema and diabetic intravitreal hemorrhage are frequent complications of diabetes. In selected cases of diabetic macular edema which is primarily treated with intravitreal injections, surgery may be performed. In this review, the role of surgery in diabetic macular edema will be discussed in light of the current literature. Moreover, changes in the timing of surgery in diabetic intravitreal hemorrhage since DRVS and risk factors and the efficacy of preventive measures for post vitrectomy intravitreal hemorrhage will be discussed.

Evolving Role of Regional Depot Corticosteroids in Management of Diabetic Macular Edema

Retina ◽  
2017 ◽  
Vol 37 (12) ◽  
pp. 2201-2207
Author(s):  
Stephen J. Kim ◽  
Ingrid U. Scott
Keyword(s):  
Macular Edema ◽  
Diabetic Macular Edema

The current role of steroids in diabetic macular edema

2020 ◽  
Vol 15 (1) ◽  
pp. 11-26
Author(s):  
Maria Vittoria Cicinelli ◽  
Michele Cavalleri ◽  
Rosangela Lattanzio ◽  
Francesco Bandello
Keyword(s):  
Macular Edema ◽  
Diabetic Macular Edema ◽  
Current Role

scholarly journals Measurement of plasminogen activator inhibitor 1 in biologic fluids with a murine monoclonal antibody-based enzyme-linked immunosorbent assay

Blood ◽  
1988 ◽  
Vol 71 (1) ◽  
pp. 220-225 ◽  
Author(s):  
PJ Declerck ◽  
MC Alessi ◽  
M Verstreken ◽  
EK Kruithof ◽  
I Juhan-Vague ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Immunosorbent Assay ◽  
Healthy Subjects ◽  
Plasminogen Activator Inhibitor ◽  
Enzyme Linked Immunosorbent Assay ◽  
Plasminogen Activator Inhibitor 1 ◽  
Platelet Poor Plasma ◽  
Activator Inhibitor ◽  
Pai 1

Abstract An enzyme-linked immunosorbent assay for plasminogen activator inhibitor-1 (PAI-1) in biologic fluids was developed on the basis of two murine monoclonal antibodies raised against PAI-1 purified from HT- 1080 fibrosarcoma cells. The lower limit of sensitivity of the assay in plasma is 2 ng/mL. The assay is 12 times less sensitive toward the PAI- 1/human tissue-type plasminogen activator (t-PA) complex as compared with free PAI-1. The intraassay, interassay, and interdilution coefficients of variation are 5.2%, 8.0%, and 7.1%, respectively. The level of PAI-1 in platelet-poor plasma of healthy subjects is 18 +/- 10 ng/mL (mean +/- SD, n = 45). In platelet-rich plasma after freezing and thawing, 92% of PAI-1 antigen is released from platelets, whereas only 8% is found in the corresponding platelet-poor plasma. In platelet-poor plasma from healthy subjects, a linear correlation (r = 0.80) was found between PAI activity and PAI-1 antigen. In plasma approximately two thirds of the PAI-1 antigen was functionally active, whereas only 5% of the PAI-1 antigen released from platelets was active. During pregnancy a progressive increase of PAI-1 antigen levels up to three- to sixfold the control value was observed. In plasma of patients with recurrent deep vein thrombosis, PAI-1 levels were 44 +/- 20 ng/mL (mean +/- SD, n = 7), during a clinically silent phase. Four of these patients had a level above 38 ng/mL (mean +/- 2 SD of normal). The present assay, based on stable and reproducible reagents, allows the specific determination of PAI-1 antigen in biologic fluids. It may facilitate interlaboratory comparisons and be useful for further investigations of the role of PAI-1 in clinical conditions associated with impaired fibrinolysis and/or a tendency to thrombosis and investigations of the role of PAI-1 in platelets.

Role of Inflammation in Diabetic Macular Edema

2014 ◽  
Vol 232 (3) ◽  
pp. 127-135 ◽  
Author(s):  
Hidetaka Noma ◽  
Tatsuya Mimura ◽  
Kanako Yasuda ◽  
Masahiko Shimura
Keyword(s):  
Macular Edema ◽  
Diabetic Macular Edema
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