Abstract
Pyoderma gangrenosum (PG) is a rare, neutrophilic dermatosis with extracutaneous manifestations and associated systemic disorders, including inflammatory bowel diseases, arthritis and haematological malignancies. The pathogenesis of PG is still not fully understood. The cutaneous lesions are often polymorphic and include papules, nodules, sterile pustules with erythematous induration, which quickly evolve into necrotic painful ulcerations. PG can also affect lungs, spleen, liver, pancreas, kidneys, bones and eyes. The treatment of PG is long and challenging and involves the use of sytemic corticoteroids, immunosupressive drugs and biological therapies with concomitant pain management and wound care.
Highlights
Pyoderma gangrenosum (PG) is a rare, ulcerative neutrophilic dermatosis with possible extracutaneous manifestations. It is often associated with underlying systemic disorders, including inflammatory bowel diseases, arthritis, and hematological malignancies
Activation of leukocytes, as well as growth factors, including granulocyte-macrophage colony-stimulating factor (GM-CSF) can stimulate the disease, which is connected with the disfunction of neutrophils and uncontrolled infiltration leading to tissue destructions
Over-expression of TNF-α, IL-17, IL-1β, IL-8 and increased synthesis of matrix metalloproteinases (MMPs) have been found in PG, which play a significant role in the development of the inflammatory processes and cause damage to the tissue (2, 5-8)
Summary
Pyoderma gangrenosum (PG) is a rare, ulcerative neutrophilic dermatosis with possible extracutaneous manifestations. It is often associated with underlying systemic disorders, including inflammatory bowel diseases, arthritis, and hematological malignancies. PG was first described in 1930 by Brunsting, Goeckerman and O'Leary. They presented the theory, that PG had an infectious background with streptococcal or staphylococcal etiology. The concomitance of pyoderma gangrenosum with systemic diseases suggests immunologic and inflammatory pathologic response and genetic background. Activation of leukocytes, as well as growth factors, including granulocyte-macrophage colony-stimulating factor (GM-CSF) can stimulate the disease, which is connected with the disfunction of neutrophils and uncontrolled infiltration leading to tissue destructions
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