Gostishchev V K, Khokhlov A M
Khirurgiia (Mosk). 1991 Oct(10):100-5.
The work generalized the results of examination of 418 patients with primary varicosity (V) complicated by trophic ulcers. On the basis of the study conducted by the authors, a conception of pathogenesis is suggested, the main links of which are microcirculatory disorders in the system of perforating veins of a closed structure, and deficient resolution of fibrin due to diminished local fibrinolytic activity of the plasma. Insufficient fibrin splitting leads to the formation of paravasal collagen cuffs preventing normal exchange between the capillaries and tissues. Impaired nutrition facilitates spasm of arteries and arterioles, whose genesis magnesium deficit contributes to. Activation of collagenolytic peptidases-cathepsins, D, A, B occurs in the ischemic tissues, which leads to destruction of the skin and the formation of ulcers. The disease is attended by disorders of immunity (secondary immunodeficiency), which reduces the reparative processes and thus promotes the development of a chronic process. A complex approach to the treatment of V in the presence of trophic ulcers is suggested.
该研究概括了418例原发性静脉曲张(V)合并营养性溃疡患者的检查结果。基于作者开展的研究,提出了一种发病机制的概念,其主要环节是闭合结构的穿通静脉系统中的微循环障碍,以及由于血浆局部纤溶活性降低导致的纤维蛋白溶解不足。纤维蛋白分解不足导致血管旁胶原袖套形成,阻碍毛细血管与组织之间的正常交换。营养障碍促使动脉和小动脉痉挛,镁缺乏是其发生的原因之一。缺血组织中胶原olytic肽酶 - 组织蛋白酶D、A、B被激活,导致皮肤破坏和溃疡形成。该疾病伴有免疫紊乱(继发性免疫缺陷),这会降低修复过程,从而促进慢性病程的发展。建议采用综合方法治疗存在营养性溃疡的静脉曲张。