Coleridge Smith P D
Department of Surgery, UCL Medical School, Middlesex Hospital, London, UK.
Vasc Med. 1997;2(3):203-13. doi: 10.1177/1358863X9700200306.
Venous ulceration is a common problem in western countries and results in large costs to healthcare systems. A number of hypotheses of the mechanisms of development of venous ulceration have been advanced, but this question has not been fully resolved. In recent years research effort has focused on the microcirculation of the skin and many methods of investigation have been employed to study this. Some of the principal findings described in published work are reviewed in this article. It seems unlikely from the available evidence that venous ulceration is attributable solely to failure of diffusion of oxygen and other small nutritional molecules to the tissues of the skin. The microvascular changes in the skin are characterised by activated endothelium and perivascular inflammatory cells. It is much more likely that leucocytes attach themselves to the cutaneous microcirculation, become activated and produce endothelial injury. Repeated over many months or years, this chronic inflammatory process leads to be tissues changes of lipodermatosclerosis. Although there is evidence of leucocyte involvement in the pathogenesis of venous ulceration, the exact mechanisms remain to be resolved. Improved treatment for patients may be devised once a better understanding of the basic causes of this condition has been reached.
静脉溃疡在西方国家是一个常见问题,给医疗系统带来了巨大成本。关于静脉溃疡发生机制的多种假说已被提出,但这个问题尚未完全解决。近年来,研究工作聚焦于皮肤微循环,并且采用了多种研究方法来对此进行研究。本文对已发表文献中描述的一些主要发现进行了综述。从现有证据来看,静脉溃疡似乎不太可能仅仅归因于氧气和其他小分子营养物质向皮肤组织扩散失败。皮肤的微血管变化以内皮细胞活化和血管周围炎症细胞为特征。白细胞更有可能附着于皮肤微循环,被激活并造成内皮损伤。这种慢性炎症过程反复持续数月或数年,会导致脂膜炎性硬化的组织变化。虽然有证据表明白细胞参与静脉溃疡的发病机制,但确切机制仍有待解决。一旦对这种疾病的根本原因有了更好的理解,就可能为患者设计出更好的治疗方法。