ObjectiveTo explore the relationship among plasma cytokines’ level, adhesion molecules expression and skin damage in patients with chronic venous insufficiency (CVI) of lower extremities.MethodsIn 32 patients with CVI and 8 normal individuals as control, blood TNFα, IL1β and IL2R were assayed with ELISA method; serum endothelial cellintercellular adhesion molecule1(ECICAM1), polymorphonuclearCD18(PMNCD18) and polymorphonuclearCD11b(PMNCD11b) were assayed with immunohistochemical method; and ultrastructure of diseased veins was examined by electroscope.ResultsThe results showed that the level of plasma TNFα and IL1β increased remarkably in Class 2-3 compared with Class 1 and control (P<0.05), IL2R had no difference in Class 1,2,3(P gt;0.05). The index of ECICAM1 and PMNCD11b positively expression increased remarkably in Class 2-3 compared with that in Class 1 and control. The index of PMNCD18 expression in Class 2-3 and Class 1 was greatly higher than that in control (P<0.05). The expression of ICAM1 was positively correlated with that of CD11b/CD18. Electron microcopy showed that the change in microvessel was mainly PMN adhesion with endothelial cells (ECs) and trapped in microvessels.ConclusionThe results suggest that activated monocyte may release TNFα and IL1β, upregulate ICAM1 and CD11b/CD18 expression, and mediate the PMN adhesion to ECs, thus causing ECs and tissue damage. It may be one of important mechanism of venous ulcer.
Citation:
QIAO Zhengrong,SHI De. Clinical Study on the Pathogenesis of Chronic Venous Insufficiency in the Lower Extremities. CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY, 2003, 10(3): 249-252. doi:
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- 1. Porter J, Rutherford RB, Clagett G, et al. Reporting standards in venous disease [J]. J Vasc Surg, 1988; 8(2)∶172.
- 2. Fujita H, Morita I, Murota S. A possible mechanism for vascular endothelial cell injury elicited by activated leukocytes: a significant involvement of adhesion molecules, CD11/CD18, and ICAM1 [J]. Arch Biochem Biophys, 1994; 309(1)∶62.
- 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.
- 8. Barath P, Fishbein MC, Cao J, et al. Detection and localization of tumor necrosis factor in human atheroma [J]. Am J Cardiol, 1990; 65(5)∶297.
- 9. Weyl A, Vanscheidt W, Weiss JM, et al. Expression of the adhesion molecules ICAM1, VCAM1, and Eselectin and their ligands VLA4 and LFA1 in chronic venous leg ulcers [J]. J Am Acad Dermatol, 1996; 34(3)∶418.