الفهرس 
Pathogenesis of Proliferative VitreoretinopathyOnly 14 pages are availabe for public view
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Abstract
Proliferative vitreoretinopathy is the most common cause of ultimate failure after retinal reattachment. I briefly reviewed the pathology and pathogenesis of PVR, and the different drugs reported which can be used for pharmacological prevention of PVR.
Proliferative vitreoretinopathy remains a difficult problem to solve despite advances in vitreoretinal sugical techniques. There is still a significant incidence of PVR in rhegmatogenous retinal detachment. The ongoing process of proliferation and contraction could result in secondary PVR formation and recurrence.
The main problem of medical therapy in PVR appears to be one of pharmacokinetics, not pharmacodynamics. To achieve an effect, a medication must come in contact wiyh the intended cells for a critical minimal time.
The use of adjunctive treatments to prevent cellular proliferation holds promise for the prevention of PVR or recurrences after surgery. It seems unlikely that focusing therapy on one particular target will be sufficient to stop the entire cascade of cellular events leading to PVR. Rather multiple adjunctive agents targeting at different stages of the process are needed.
Various medications as steroids, heparin, 5-fluorouracil and daunomycin are most commonly used agents.
Other medications as retinoids, taxol, colchicines and matrix metalloproteinases inhibitors proved to be effective in preventing proliferation and helping in preventing recurrence of retinal detachment.
Corticosteriods were the first agents to be tested for their modifying effect on vitreoretinal fibrosis. Dexamethasone, triamcinolone and methyl prednisolone decreased the incidence of retinal detatchment alone or in combination with either 5-fluorouracil, daunomycin or heparin.
Fluoropyrimidines were the first antimetabolites used to prevent intraocular proliferation. Adjuvant 5-FU and LMWH durind vitrectomy proved to be safe and effective in cases with higher grades of PVR, hypotony, and traumatic PVR cases.
Daunorubicin, an anthracycline cytotoxic antibiotic showed a significant effect in reducing PVR as it affects cell proliferation and migration. Also retinoids played an important role in the differentiation and proliferation by inhibiting cell-meditated contraction of the RPE cells.
Taxol derived from the tree Taxus brevifolia, promoted rather than inhibited the assembly of microtubules, and stabilized them once they are formed, which could be responsible for the inhibition of cellular contraction, migration and proliferation.
Hepain and LMWH, proved to be effective in reducing PVR alone or in combination with either steroids, 5-FU or daunomycin.
The simplest method to increase a therapy’s value lies in the combination of various medications.