Trophic Ulcers and Microbial Eczema: From Pathogenesis to Treatment

Abstract

The article examines trophic ulcers of the lower extremities as a consequence of impaired arterial, venous, and lymphatic hemodynamics, including microcirculatory disturbances, as well as injuries to the skin, soft tissues, and peripheral nerves. It describes the role of tissue hypoxia, activation of collagenolytic enzymes—particularly cathepsin D—and lysosomal damage in the development of skin necrosis. Patients with ulcers were characterized by a shift of skin pH toward neutrality and markedly increased microbial colonization, including pathogenic microorganisms. Their proteolytic enzymes weaken the skin barrier, promote sensitization, and contribute to microbial eczema, supporting the inclusion of desensitizing and antihistamine agents in comprehensive treatment.