Document Detail


Macular edema--rationale for therapy.
MedLine Citation:
PMID:  20703043     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Blood-retinal barrier breakdown with macular edema is caused by many diseases, which modulate--via different growth factors--the integrity of the tight junctions. Starling's law predicts furthermore that macular edema will develop if the hydrostatic pressure gradient between capillary and retinal tissue is increased, for example in the presence of elevated blood pressure, or if the osmotic pressure gradient is decreased, for example when protein accumulates excessively in the extracellular space within the retina. The rationale for clinical treatment of macular edema is based on the understanding and the inhibition of these pathophysiological mechanisms. On the medical side, nonsteroidal anti-inflammatory drugs inhibit the production of prostaglandins and leukotrienes, and modulate fluid movement coupled to chloride movement. Corticosteroids block cyclooxygenase and interleukin, downregulate vascular endothelial growth factor (VEGF) and decrease the phosphorylation of occludin, thereby increasing the tightness of the blood-retinal barrier. Carbonic anhydrase inhibitors are thought to modulate the polarized distribution of carbonic anhydrase at the level of the retinal pigment epithelium via extracellular pH gradients and thus the fluid resorption from the retina into the choroid. Anti-VEGF agents restore occludin proteins in the blood-retinal barrier and reduce protein kinase C activation. On the surgical side, the beneficial effect of vitrectomy with release of traction on the macula is explained by an increase in tissue pressure and a lowering of the hydrostatic pressure gradient, reducing the water flux from blood vessels into retinal tissue. The therapeutic action of vitrectomy in nontractional edema is thought to be based on two mechanisms: increased oxygen transport between the anterior and posterior segments of the eye and the removal of growth factors which are secreted in large amounts into the vitreous during proliferative vasculopathies.
Authors:
Thomas J Wolfensberger; Zdenek J Gregor
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Publication Detail:
Type:  Journal Article; Review     Date:  2010-08-10
Journal Detail:
Title:  Developments in ophthalmology     Volume:  47     ISSN:  1662-2790     ISO Abbreviation:  Dev Ophthalmol     Publication Date:  2010  
Date Detail:
Created Date:  2010-08-12     Completed Date:  2011-01-04     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8010321     Medline TA:  Dev Ophthalmol     Country:  Switzerland    
Other Details:
Languages:  eng     Pagination:  49-58     Citation Subset:  IM    
Copyright Information:
2010 S. Karger AG, Basel
Affiliation:
Jules Gonin Eye Hospital, Lausanne, Switzerland. thomas.wolfensberger@fa2.ch
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MeSH Terms
Descriptor/Qualifier:
Blood-Retinal Barrier / drug effects,  physiology
Carbonic Anhydrase Inhibitors / therapeutic use*
Cyclooxygenase Inhibitors / therapeutic use*
Glucocorticoids / therapeutic use*
Humans
Macular Edema / metabolism,  physiopathology,  therapy*
Prostaglandin Antagonists / therapeutic use*
Protein Kinase C / antagonists & inhibitors
Treatment Outcome
Vascular Endothelial Growth Factor A / drug effects,  metabolism
Vitrectomy / methods*
Chemical
Reg. No./Substance:
0/Carbonic Anhydrase Inhibitors; 0/Cyclooxygenase Inhibitors; 0/Glucocorticoids; 0/Prostaglandin Antagonists; 0/Vascular Endothelial Growth Factor A; EC 2.7.11.13/Protein Kinase C

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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