Somers K D, Dawson D M
Department of Microbiology and Immunology, Eastern Virginia Medical School, Norfolk, USA.
J Urol. 1997 Jan;157(1):311-5.
Peyronie's disease is a pathological fibrosis characterized by excessive deposition of collagen in the plaque. Although the etiology of Peyronie's disease is unknown, trauma has been hypothesized as the inciting event. In an effort to obtain more insight into the pathogenesis of Peyronie's disease plaque tissue was examined for collagen, elastic fiber, and fibrin content and distribution.
Plaque tissue specimens from 33 patients with Peyronie's disease, control penile tissue and nodular tissue from 8 patients with Dupuytren's contracture were analyzed histochemically for collagen staining and elastic fiber structure and distribution. Plaque tissue from 19 Peyronie's disease patients, control tissue and nodular tissue from Dupuytren's disease were also analyzed for the presence of fibrin by histochemical staining and immunoblotting.
Aberrantly stained collagen was detected in 32 of 33 plaque specimens (97%) and disrupted elastic fibers in 31 of the same specimens (94%). Fibrin deposition was detected histochemically in plaque tissue from 18 of 19 patients (95%) but it was not detectable in normal or scarred tunica from control patients. The presence of authentic fibrin accumulation in plaque tissue was confirmed by immunoblot analysis but fibrin was not detected in dermal tissue extracts from the same patient. Aberrant collagen staining and fibrin deposition were detected in nodular tissue from 7 of 8 Dupuytren's contracture patients (88%) and altered elastic fibers in 5 of the same patients (63%).
Deposition of fibrin in plaque tissue is consistent with the hypothesis that repetitive microvascular injury results in fibrin deposition in the tissue space and has served to provide insights into the pathophysiology of Peyronie's disease. We propose a model that accounts for the clinical and biological features of Peyronie's disease.
佩罗尼氏病是一种病理性纤维化疾病,其特征为斑块中胶原蛋白过度沉积。尽管佩罗尼氏病的病因尚不清楚,但有假说认为创伤是引发该病的事件。为了更深入了解佩罗尼氏病的发病机制,对斑块组织的胶原蛋白、弹性纤维和纤维蛋白含量及分布进行了检查。
对33例佩罗尼氏病患者的斑块组织标本、对照阴茎组织以及8例掌腱膜挛缩症患者的结节组织进行组织化学分析,以检测胶原蛋白染色、弹性纤维结构及分布情况。还对19例佩罗尼氏病患者的斑块组织、对照组织以及掌腱膜挛缩症的结节组织进行组织化学染色和免疫印迹分析,以检测纤维蛋白的存在情况。
在33个斑块标本中的32个(97%)检测到异常染色的胶原蛋白,在相同的31个标本中(94%)检测到弹性纤维破坏。在19例患者中的18例(95%)斑块组织中通过组织化学检测到纤维蛋白沉积,但在对照患者的正常或瘢痕化白膜中未检测到。通过免疫印迹分析证实斑块组织中存在真正的纤维蛋白积聚,但在同一患者的真皮组织提取物中未检测到纤维蛋白。在8例掌腱膜挛缩症患者中的7例(88%)结节组织中检测到异常胶原蛋白染色和纤维蛋白沉积,在相同患者中的5例(63%)检测到弹性纤维改变。
斑块组织中纤维蛋白的沉积与重复性微血管损伤导致组织间隙纤维蛋白沉积的假说一致,这有助于深入了解佩罗尼氏病的病理生理学。我们提出了一个解释佩罗尼氏病临床和生物学特征的模型。