摘要 ：目的：毛細血管密度減少導致組織缺氧被認為是係統性硬化症的標誌，它可誘導血管生成。本研究的目的是研究調節血管生成的介質，並將其水平與血清學和臨床指標進行相關性分析。
方法：用ELISA方法測定係統性硬化症患者和正常對照組的血管內皮生長因子、成纖維細胞生長因子-2、內皮抑素、血小板反應素-1和可溶性血管細胞和細胞間黏附分子(sICAM-1和sVCAM-1)。
結果：在促血管生成和抗血管生成介質中，內皮抑素在係統性硬化症患者的水平顯著高於對照組。由於蛋白酶參與內皮抑素的產生，彈性蛋白酶在SSc患者中顯著升高，而組織蛋白酶L在兩組間無顯著差異。可溶性黏附分子sICAM-1、sVCAM-1水平顯著增加，且其水平平行。sICAM-1與炎症標誌物CRP及ESR呈正相關，sVCAM-1與上述炎症標誌物無相關。
結論：內皮抑素、蛋白酶和可溶性黏附分子(sICAM-1和sVCAM-1)可能參與係統性硬化症的發病機製。且slCAM-1和CRP、ESR正相關，提示slCAM-1可能為評估疾病炎症狀態的生物標記物。
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]
