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Primary Retinal Detachment

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204<br />

10 <strong>Retinal</strong> <strong>Detachment</strong> Repair: Outlook for the Future<br />

Fig. 10.15. Proliferative vitreoretinopathy<br />

Finally, let us not forget drug treatment and pharmacotherapy<br />

in the area of retinal detachment. One of the main nemeses of<br />

retinal detachment surgeons is proliferative vitreoretinopathy<br />

(PVR) (Fig. 10.15). This is the result of a biological process gone<br />

awry. Cellular elements already in the eye and, in some cases in the<br />

blood, proliferate, lay down collagen, and cause collagen contraction.<br />

This biological process results in membrane formation, recurrent<br />

retinal detachment, and macular pucker. There has been<br />

widespread study of the classical antiproliferatives to reduce the<br />

risk of PVR or to limit it. These drugs, such as 5FU and Daunomycin,<br />

are intrinsically toxic. We will soon be using the techniques<br />

of molecular biology and intelligent drug design to create more<br />

sophisticated anti-proliferative drugs. Such drugs may take the<br />

shape of the hammerhead ribozyme, which cleaves mRNA involved<br />

in proliferation and other processes (Fig. 10.16). These types<br />

of drugs are similar to antisense, but unlike antisense are recycled<br />

intracellularly [9]. Thus, they may be able to be applied into the<br />

eye and remain active in cells for months or longer. There will<br />

be other ways to block this biological process, including acting on<br />

inflammation, proliferative pathways, and cytokine pathways. The

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