Ragni E, Haab F, Delmas V, Costa P
Service d'Urologie, Hôpital Nord, Assistance Publique-Hôpitaux de Marseille, Chemin des Bourrelly, 13015 Marseille, France.
Prog Urol. 2009 Dec;19(13):926-31. doi: 10.1016/j.purol.2009.09.036. Epub 2009 Nov 14.
The physiopathology of urogenital prolapse is multifactorial, a combination of the interaction between constitutional and acquired factors resulting in the weakening of perineal support. Genetic modifications contribute to the occurrence of prolapse (proof level 2). Differences relating to types of collagen and their proportions, the construction of smooth muscle fibres and nervous structures, have been described between women with and without prolapse. But the relationship of cause and effect is not always clear. It would appear that the reduction in the expression of the elastine gene and the perturbation of metabolism may be at the origin of the cause of a prolapse. However, the intense activity of tissue remodeling is probably the consequence of biomechanical pressure born by the prolapse. Muscular or neuropathic lesions of the levator ani have been widely researched and documented. In the case of prolapse, these were isolated exceptions and most often associated with dehiscence of support tissue.
泌尿生殖系统脱垂的生理病理学是多因素的,是体质因素和后天因素相互作用的结果,导致会阴支持组织减弱。基因改变促成了脱垂的发生(证据级别为2)。在有脱垂和无脱垂的女性之间,已描述了与胶原蛋白类型及其比例、平滑肌纤维结构和神经结构有关的差异。但因果关系并不总是清晰的。似乎弹性蛋白基因表达的降低和代谢紊乱可能是脱垂病因的根源。然而,组织重塑的活跃活动可能是脱垂所承受的生物力学压力的结果。肛提肌的肌肉或神经病变已得到广泛研究和记录。在脱垂病例中,这些是个别例外情况,且大多与支持组织的裂开有关。