Therapeutic approach to chronic venous insufficiency and its complications: Place of Daflon (R) 500 mg

Early manifestations of chronic venous insufficiency (CVI) are edema, hyper pigmentation, and lipodermatosclerosis, Late complications are cutaneous ul ceration and delayed healing. The specific hallmarks of this inflammation i nclude CD68-positive infiltration into the dermal tissue, monocytes, and ly mphocytes and enhanced endothelial permeability. This may lead to "fibrin c uff" formation. In addition, membrane adhesion molecules are present and cy tokine expression is seen. In one experimental model of mesenteric venous hypertension, the inflammato ry process was detected in its earliest stages. This was evident in the for m of neutrophilic leukocyte adhesion to venular endothelium as well as migr ation of cells across the endothelium and basement membrane into the inters titial space. Simultaneously, parenchymal cell death was detected. This sug gests that the mechanism that triggers the inflammatory reaction is venous hypertension, This may cause venous distension and a shift in fluid shear s tress. Our observations suggest that patients with venous insufficiency dem onstrate circulatory humoral stimulators for leukocyte activation. Otherwis e, there is evidence that the inflammatory reaction is limited to the regio n of the venous ulceration or at least to the skin areas with severe microa ngiopathy. It may be that activated leukocytes traverse perivascular cuffs and release active transforming growth factor-P, (TGF-PI) which has been fo und to be elevated exclusively in areas of clinically active CVL Surgical i ntervention markedly decreases the number of dysfunctional vein segments an d allows pharmacologic agents to protect normal structures from continuing damage, Daflon((R)) 500 mg, the purified micronized flavonoid fraction containing 9 0% diosmin and 10% hesperidin, acts favorably in venous ulcer treatment by inhibiting the synthesis of prostaglandins and free radicals. It decreases bradykinin-induced microvascular leakage and may act favorably to inhibit l eukocyte activation, trapping, and migration. Clinically, edema is reduced, ulcer healing is accelerated, and leukocyte trapping diminished. The actio n of micronized purified flavonoid fraction is beginning to be better under stood, and as further knowledge is gained, better pharmacologic control of CVI is a tantalizing promise.