Microcirculation and venous ulcers: a review

Area of Science:

• Dermatology
• Vascular Biology
• Immunology

Background:

• Chronic venous insufficiency (CVI) is characterized by skin lesions and ulceration.
• Histological and immunocytochemical analyses suggest an inflammatory process underlies CVI.
• The superficial vascular network is a primary target in the inflammatory reaction.

Purpose of the Study:

• To explore the inflammatory mechanisms driving chronic venous insufficiency and venous leg ulcer formation.
• To identify potential therapeutic targets for CVI by understanding the role of leukocyte activation.

Main Methods:

• Histological and immunocytochemical analyses of venous leg ulcers.
• Examination of hemodynamic forces (venous hypertension, stasis, shear stress) and their role in leukocyte activation.
• Review of inflammatory mediators released during leukocyte activation.

Main Results:

• Inflammatory processes lead to fibrosclerotic and liposclerotic remodeling of skin and subcutaneous tissue.
• Leukocyte activation, involving integrin expression and release of inflammatory molecules, is central to CVI.
• Hemodynamic forces contribute significantly to leukocyte activation and subsequent CVI manifestations like venous dermatitis and ulceration.

Conclusions:

• Venous leg ulcer formation is linked to a self-perpetuating inflammatory response.
• Targeting leukocyte activation presents a promising therapeutic strategy for managing CVI.
• Pentoxifylline and flavonoids are being investigated for their anti-inflammatory effects in CVI treatment.