目的探討下肢慢性靜脈功能不全（CVI）時(shí)細(xì)胞因子水平和粘附分子表達(dá)與皮膚損傷的關(guān)系。方法采用酶聯(lián)免疫吸附法（ELISA法）檢測血漿TNFα、IL1β和IL2R水平，免疫組織化學(xué)法（SP法）檢測血漿白細(xì)胞粘附分子（ECICAM1、PMNCD18及PMNCD11b）的表達(dá)，并在電鏡下觀察32例CVI患者和8例正常對照組下肢皮膚標(biāo)本的超微結(jié)構(gòu)改變。結(jié)果①CVI Class 2～3級血漿TNFα和IL1β水平分別為（194.66±221.90)pmol/L和（100.60±19.43）pmol/L，明顯高于對照組的（34.38±9.74）pmol/L和（67.62±17.20）pmol/L（P＜0.05），Class 2～3級和1級血漿IL2R水平分別為（149.79±85.77）pmol/L和（98.22±38.55）pmol/L，與對照組的（94.67±13.01）pmol/L相比較，差異無顯著性意義（P gt;0.05）； ②Class 2～3級ECICAM1、PMNCD18和PMNCD11b表達(dá)陽性率分別為（0.70±0.14）%、（0.12±0.03）%和（0.16±0.02）%，明顯高于對照組的（0.15±0.09）%、（0.04±0.01）%和（0.05±0.01）%(P＜0.05)； ③相關(guān)分析顯示ICAM1表達(dá)與CD11b和CD18表達(dá)呈顯著正相關(guān)，r值分別為0.845 4和0.563 9 (P＜0.05)； ④電鏡超微結(jié)構(gòu)見中性粒細(xì)胞（PMN）與ECs粘附導(dǎo)致皮膚微血管病變。結(jié)論CVI下肢靜脈系統(tǒng)瘀血和高壓可能激活單核細(xì)胞分泌釋放TNFα、IL1β等細(xì)胞因子，上調(diào)ICAM1和CD11b/CD18表達(dá)，并介導(dǎo)PMN粘附于ECs，導(dǎo)致ECs和組織損傷，可能是靜脈潰瘍重要的發(fā)病機(jī)理之一。
引用本文： 喬正榮,時(shí)德. 下肢慢性靜脈功能不全發(fā)病機(jī)理的臨床研究. 中國普外基礎(chǔ)與臨床雜志, 2003, 10(3): 249-252. doi: 復(fù)制
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- 3. Carlos TM, Harlan JM. Membrane proteins involved in phagocyte adherence to endothelium [Ｊ]. Immunol Rev, 1990; 114(2)∶5.
- 4. Makgoba MW, Bernard A, Sanders ME. Cell adhesion/signalling: biology and clinical applications [Ｊ]. Eur J Clin Invest, 1992; 22(7)∶443.
- 5. Bennett CF， Crook ST. Regulation of endothelial cell adhesion molecule expression with antisense oligonucleotides [Ｊ]. Adv Pharmacols, 1994; 28（1）∶1.
- 6. Claudy AL, Mirshahi M, Soria C, et al. Detection of undegraded fibrin and tumor necrosis factoralpha in venous leg ulcers [Ｊ]. J Am Acad Dermatol, 1991; 25(4)∶623.
- 7. Ksander GA, Sawamura SJ, Ogawa Y, et al. The effect of platelet releasate on wound healing in animal models [Ｊ]. J Am Acad Dermatol, 1990; 22(5 Pt 1)∶781.
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