Venous stasis causes release of interleukin 1beta (IL-1beta), interleukin 6 (IL-6) and tumor necrosis factor alpha (TNFalpha) by monocyte-macrophage

Abstract

Background: many studies have investigated between venous stasis, functions of the vascular and perivascular anastomotic structure, venous endothelium and circulating leukocytes.

Setting: patients with varicose veins (n = 15) and a healthy control group (n = 15).

Methods: the authors investigated some soluble mediators of monocytes-macrophages, which induce inflammation. They determined interleukin 1beta (IL-1beta) and interleukin 6 (IL-6) and tumor necrosis factor alpha (TNFalpha) levels at rest and after induced venous occlusion (using an inflated cuff to 60 mmHg for 25 minutes).

Results: their results revealed elevated baseline production in the former and that induced venous occlusion further augmented the levels of all cytokines in the study series, especially in patients with varicose veins.

Conclusion: The authors believe that the study shows functional activation of monocyte-macrophages related to venous stasis as a consequence of venous hypertension. Cell response damages the endothelial structure and may represent an important element in the pathophysiology of chronic venous insufficiency.