Klüken N, Zabel M
Phlebologie. 1986 Jul-Sep;39(3):561-6.
Milian's respectively aetiological and pathogenic hypotheses, based on the infectious origin of this disease, such as tuberculosis or syphilis, have not been confirmed. In almost every case there has proved to be chronic venous deficiency. The histomorphological deterioration shows, as well as the characteristic signs of cutaneous atrophy, the vessel affection developing towards dilation, but also the parietal processes moving towards obliteration. These processes do not correspond to vasculitis, as described by Ruiter. For this reason, we do not go along with those authors associating these histological deteriorations with vasculitis. And we therefore justify our claim that white atrophy cannot be considered as an angiolopathy.
基于本病感染源(如结核病或梅毒)的米利安病因学和发病机制假说尚未得到证实。几乎在每一个病例中都证实存在慢性静脉功能不全。组织形态学恶化表现为皮肤萎缩的特征性体征,血管病变发展为扩张,同时血管壁病变发展为闭塞。这些过程与鲁伊特所描述的血管炎并不相符。因此,我们不同意那些将这些组织学恶化与血管炎联系起来的作者的观点。因此,我们有理由认为白色萎缩不能被视为一种血管病。