Peyronie hastalığı patofizyolojisi

Peyronie hastalığı (PH) peniste tunika albuginea’nın (TA) progresif lokalize fibrotik hastalığıdır. Fibröz, elastik olmayan skar formasyonu ve kalsifiye plak oluşumuyla sonuçlanan bir yara iyileşme bozukluğu olarak da kabul edilmektedir. Klinik olarak bu plaklar, peniste eğrilik, kısalma ve daralma gibi deformitelere ve ağrıya neden olabilir. Peyronie hastalığı için etiyolojik faktörlerin tam spektrumu bilinmemesine rağmen, travma, bozulmuş fibrin klirensi, otoimmün ve genetik faktörler dahil olmak üzere birçok etiyolojik mekanizma ileri sürülmüştür. Penise tekrarlayan mikrotravmalar ile bilaminar yapıdaki TA’nın delaminasyonunun ve sonrasındaki enflamatuvar sürecin peyronie plaklarının gelişimine neden olduğu düşünülmektedir. Travma sonrası enflamatuar süreç, myofibroblast persistansına ve sonrasında anormal kollajen birikiminine neden olur. Beraberinde anormal fibrin birikimi ve elastik liflerin düzensiz bir hal almasıyla, karakteristik tunikal fibröz plak ve skar oluşumu gerçekleşir ve enflamatuar süreç tamamlanır. PH’nin patogenezi hayvan modellerinde, hücre kültürlerinde ve klinik çalışmalarda ortaya konulmaya çalışılmıştır. Bu hastalığın etyopatolojisinin daha iyi anlaşılması tedavi stratejilerinin geliştirilmesi için önemlidir.

The pathophysiology of peyronie’s disease

Peyronie’s disease (PD) is a progressive localized fibrotic disease of tunica albuginea (TA) in the penis. It is also considered as a wound healing disorder with fibrous and non-elastic scar formation and calcified plaque formation. Clinically, these plaques can cause deformities such as curvature, shortening and contraction of the penis and pain. Although the complete spectrum of etiologic factors for PD is unknown, multiple mechanisms have been proposed including trauma, impaired fibrin clearance, autoimmune and genetic factors. It is thought that delamination of bilaminar TA in the penis with repetitive microtrauma and subsequent inflammatory process may cause the development of the Peyronie plaques. The post-traumatic inflammatory process causes myofibroblast persistence and subsequent abnormal collagen accumulation. Accompanying abnormal fibrin accumulation and irregular form of elastic fibers, characteristic tunical fibrous plaque and scar formation occur and the inflammatory process is completed. Pathogenesis of PD has been tried to be demonstrated in animal models, cell cultures and clinical studies. A better understanding of the etiopathology of this disease is important for the development of treatment strategies.

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