Conclusion

We have tried to summarize some of the important findings of the last years with regard to PVR pathogenesis. Some other factors, e.g. collagens, fibrinogen, and mucopolysaccharides have not been discussed. The numerous studies on the pathogenesis of PVR have been prompted by the impression that a merely surgical approach to the treatment of PVR with traction retinal detachment may not be the optimal solution for this important clinical problem. Experimental studies as well as the analysis of clinical specimens can reveal essential features of PVR that may be amenable for an adjunctive pharmacologic treatment. Currently, the anthracycline antibiotic daunomycin, applied as an intra-operative infusion, seems to improve the general outcome of vitrectomy in patients suffering from posttraumatic PVR. This drug has been shown to be a potent inhibitor of both fibroblast and pigment epithelium proliferation in vitro (Wiedemann et al. 1985a; Weller et al. 1987). This drug does affect early events such as chemotaxis (Verdoorn et al. 1986), but serves mainly as an antimitogenic agent. Therefore, we additionally use steroids to suppress the initial macrophage-mediated inflammation in traumatic PVR (Wiedemann et al. 1987). As the contraction of cellular periretinal membranes is a devastating step in the disease process, drugs interfering with microtubule assembling e.g. colchicine may prove to be a valuable addition to the above mentioned agents. Encouraging results in an experimental study using oral colchicine have recently been presented (Lemor et al. 1986). We would suggest, however, that a very early pharmacologic intervention would be preferable and hypothesize that an interference with the local initial macrophage activation could efficiently reduce subsequent cell migration and proliferation without imposing any danger to the function of the retina which tends to be a problem with the common antiinflammatory and antiproliferative agents.