Abstract

Aetiopathogenesis and therapy for Peyronie's disease are summarized below. AETIOPATHOGENESIS: (a) Plaque fibroblasts and their products provoke an immune response; (b) there are chromosomal differences between plaques and normal albuginea; (c) plaque fibroblasts are immortalized cells; (d) plaque fibroblasts demonstrate an impaired mitochondrial activity. These patterns provoke inflammation and they compel us to regard Peyronie's disease as being more similar to keloids than to scars. THERAPY: Medical therapy plays a pivotal role in the management of Peyronie's disease and should be performed prior to any surgery. Intraplaque collagenase, intraplaque verapamil, intraplaque interferon, oral acetyl-L-carnitine, oral propionyl-L-carnitine and oral colchicine have proved effective in Peyronie's disease. With the exception of collagenase, these drugs have displayed a number of activities whose final result is to improve immune response, to inhibit inflammation and to inhibit fibroblast metabolism and replication. Therefore, the primitive replicative (rather than reactive) nature of the disease is confirmed; this knowledge may be of help in the identification of new non-surgical therapies for Peyronie's disease.