摘要 ：目的：毛细血管密度减少导致组织缺氧被认为是系统性硬化症的标志，它可诱导血管生成。本研究的目的是研究调节血管生成的介质，并将其水平与血清学和临床指标进行相关性分析。

        方法：用ELISA方法测定系统性硬化症患者和正常对照组的血管内皮生长因子、成纤维细胞生长因子-2、内皮抑素、血小板反应素-1和可溶性血管细胞和细胞间黏附分子(sICAM-1和sVCAM-1)。

        结果：在促血管生成和抗血管生成介质中，内皮抑素在系统性硬化症患者的水平显著高于对照组。由于蛋白酶参与内皮抑素的产生，弹性蛋白酶在SSc患者中显著升高，而组织蛋白酶L在两组间无显著差异。可溶性黏附分子sICAM-1、sVCAM-1水平显著增加，且其水平平行。sICAM-1与炎症标志物CRP及ESR呈正相关，sVCAM-1与上述炎症标志物无相关。

        结论：内皮抑素、蛋白酶和可溶性黏附分子(sICAM-1和sVCAM-1)可能参与系统性硬化症的发病机制。且slCAM-1和CRP、ESR正相关，提示slCAM-1可能为评估疾病炎症状态的生物标记物。

        附原文：abstractAIM:Reduced capillary density is considered the hallmark ofsystemic sclerosis (SSc) leads to tissue hypoxia, a condition that usuallyinduces angiogenesis. The objective of our study is to investigate mediatorsregulating angiogenesis in SSc and to correlate their levels with serologicaland clinical parameters.METHODS: vascularendothelial growth factor, fibroblast growth factor-2, endostatin,thrombospondin-1 and soluble vascular cell and intracellular adhesion molecules(sICAM-1 and sVCAM-1) were measured in sera of SSc and normal subjects byenzyme-linked immunosorbent assay.RESULTS:Among the pro- and anti-angiogenic mediators, endostatin wassignificantly higher in SSc than in the control subjects. Out of the proteasesinvolved in endostatin production, elastase but not cathepsin-L, wassignificantly increased in SSc patients. The soluble adhesion molecules sICAM-1and sVCAM-1 were significantly increased and they occur in parallel. sICAM-1,but not sVCAM-1 positively correlates with the inflammatory markers C-reactiveprotein (CRP) and erythrocyte sedimentation rate (ESR).CONCLUSIONS: Endostatin, elastase and the soluble adhesionmolecules (sICAM-1 and sVCAM-1) are potentially involved in the pathogenesis ofSSc. Moreover, the significant correlation observed between sICAM-1 and CRP andESR indicates that sICAM-1 might be a useful biomarker of the inflammatorystate of the disease.

        引自：Curtiss P,SchwagerZ,CobosG, et al.A Systematic Review and Meta-Analysis of theEffects of Topical Nitrates in the Treatment of Primary and Secondary Raynaud's Phenomenon.J Am AcadDermatol.2018Feb 2. pii:S0190-9622(18)30172-5. doi: 10.1016/j.jaad.2018.01.043.[Epub ahead of print]