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[Pathogenesis of skin pathologic changes and ulceration]

H S Qian1

  • 1Department of Vascular Surgery, Renji Hospital, Shanghai Second Medical University.

Zhonghua Yi Xue Za Zhi
|June 1, 1993
PubMed
Summary

Venous insufficiency causes skin changes and ulcerations due to fibrin deposition blocking oxygen diffusion. Reduced fibrinolysis activity worsens this, hindering fibrin removal and promoting venous ulcer development.

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Area of Science:

  • Vascular Biology
  • Dermatology
  • Pathophysiology

Context:

  • Venous insufficiency is a common condition leading to skin changes and potential ulceration.
  • The microcirculation and tissue oxygenation are critical in the pathogenesis of venous disease.
  • Understanding the role of fibrin and fibrinolysis in venous ulceration is essential.

Purpose:

  • To investigate the relationship between skin pathological changes, transcutaneous oxygen tension (Tcpo2), and fibrinolytic activity in patients with venous insufficiency.
  • To identify the role of pericapillary fibrin deposition in the development of venous ulcerations.

Summary:

  • Studies on 26 patients with venous insufficiency and 15 controls revealed pericapillary fibrin deposition in ulcerated and liposclerotic skin areas.
  • Patients with severe venous disease exhibited lower Tcpo2 levels and reduced fibrinolysis activity (tPA, PAI), correlating with the severity of skin changes.
  • Extravascular fibrin deposition impedes oxygen diffusion, while decreased fibrinolysis impairs fibrin removal, contributing to venous ulcer formation.

Impact:

  • This research highlights extravascular fibrin deposition as a key factor in venous ulcer development.
  • Findings suggest that impaired fibrinolysis exacerbates venous ulceration by preventing the clearance of pericapillary fibrin.
  • The study provides insights into the pathophysiology of venous ulceration, potentially informing therapeutic strategies targeting fibrin deposition and fibrinolysis.

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