Histopathologic and immunopathologic study of pyoderma gangrenosum

Abstract

Sixty-three patients with pyoderma gangrenosum were seen and studied at the Mayo Clinic from 1971 to 1980. Biopsies from the erythematous border or necrotic edge of the pyoderma gangrenosum lesions usually demonstrated a characteristic pathogenic morphologic evolution. The early lesions revealed mild to moderate perivascular lymphocytic infiltrate associated with endothelial swelling. The fully developed lesions demonstrated necrosis in addition to a dense lymphocytic infiltration surrounding as well as involving the blood vessels. Extravasation of erythrocytes and thrombosis sometimes were seen. Ulceration, infarction, and abscess formation were found in the later stages of evolution. Direct immunofluorescence results were positive in the blood vessels of 36 of 65 (55%) specimens. IgM, C3, and fibrin were found in the papillary and reticular dermal vessels. IgG and IgA were only occasionally present. Pyoderma gangrenosum appears to be a reactive process that is manifested as a vasculitis. Biopsy material from the advancing active erythematous border has early characteristic dermatopathologic findings of lymphocytic vasculitis. Cutaneous vascular immune deposits suggest an immune pathogenesis of either an immune complex disease or lymphocytotoxic reaction.

Effective Strategies for the Management of Pyoderma Gangrenosum

“…Correlating well with the possibility of an aberrant T cell response driving PG, T cell clonal expansions have been reported in patients with PG, 11,12 and lymphocytes are present in early PG lesion. 13 Thus, clonally expanded T cells may secrete TNF, which, in turn, drives overexpression of IL-8. The IL-8 secreted in response to the TNF is produced by a variety of cell types, including lesional dermal fibroblasts.…”

Pyoderma-gangraenosum-Like Ulcers Associated with Lupus Anticoagulant

“…Some authors have found that there is no involvement of blood vessels in pyoderma gangraenosum whereas others have reported varying degrees of vascular damage, particularly endothelial swelling, vessel wall frag mentation and fibrinoid necrosis with leukocytoclasis [23,24]. It is interesting to note that Su et al [25] found an asso ciation between thrombosis/vessel infarction and the pres ence of fibrinoid necrosis/vasculitis when the biopsy speci men was sampled away from the erythematous border of the ulcer.…”

Pyoderma gangrenosum, diagnostic and therapeutic difficulties – two cases imitating breast cancer

“…Zwykle proponuje się terapię systemową połączoną z leczeniem miejscowym, stosując zewnętrznie m.in. GKS w połączeniu z antybiotykami, takrolimus, CsA, 10-procentową sulfasalazynę, azotan srebra, 1-procentowy kromoglikan sodowy [4,[7][8][9][10][11]. W terapii pierwszego rzutu wielu autorów proponuje GKS systemowe, prednizon w dawce 0,5-1,0 mg/kg m.c./dobę lub MP w dawce 0,8 mg/kg m.c./dobę doustnie, a w szybko postępu-jącym procesie chorobowym pulsy MP po 500 mg dożylnie przez 3-5 dni.…”