Background: The role of inflammatory reactions in the pathogenesis of chronic venous insufficiency and the persistence of venous ulcerations is still not totally clear and remains a hotly debated topic. An investigation of the intensity and distribution of ICAM-1 expression and different inflammatory cells should help clarify whether inflammatory processes are limited locally to the area of the ulcer or if an upregulation can also be observed in clinically unaffected skin of CVI-III patients, as a sign of a primary inflammatory process.
Patients And Methods: We examined two skin areas in 10 patients with venous ulcerations. One area was at the border of the ulcer and another in clinically unaffected skin (distance from the ulcer: 12.6 +/- 5.1 cm). In addition skin specimens were obtained from the perimalleolar skin of 10 healthy controls. Our histological and immunohistochemical examinations were focused on inflammatory cells (B and T lymphocytes, macrophages, and mast cells) and on the adhesion molecule ICAM-1.
Results: A very strong expression of ICAM-1 could be seen at the border of the ulcer. This tissue also showed a dense infiltration, mainly by T lymphocytes and macrophages. In some cases the tissue was infiltrated by an increased number of mast cells. This is the typical picture of a chronic inflammatory reaction. Compared to healthy controls, the clinically unaffected skin of patients showed not an increased expression of ICAM-1 and only in some cases we could find a slight perivascular infiltrate of T lymphocytes.
Conclusions: These data imply that the upregulation of endothelial adhesion molecules (ICAM-1) and dermal infiltration by T lymphocytes and macrophages in CVI-III patients is limited to the region of the ulcer, or at least to skin areas with a severe microangiopathy, and is part of a secondary elimination of necrotic issue (an 'injury and repair' process). These local chronic inflammatory reactions are certainly an important factor in the persistence and recurrence of venous ulcerations.
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