title: An immunohistopathologic study in cutaneous necrotizing vasculitis.
abstract: In order to investigate the importance of timing in the immunophenotypical characteristics of the inflammatory infiltrate and in the adhesion molecules expression in cutaneous necrotizing vasculitis (CNV) we carried on an immunohistopathologic study. An avidin-biotin-streptavidin peroxidase technique was performed on 21 lesional skin biopsy specimens obtained sequentially at 0 to 24, 72 and 120 hours from seven patients with a CNV presenting as palpable purpura. A panel of monoclonal antibodies specific for inflammatory cells (T lymphocytes, polymorphonuclear leukocytes, macrophages, dendritic cells) and different adhesion molecules (E-selectin, ICAM-1, VCAM-1, LFA-1, VLA-4) was used. Moreover, HECA-450 monoclonal antibody was used to identify cutaneous lymphocyte antigen (CLA) in the inflammatory infiltrate. In all cases, polymorphonuclear leukocytes predominated in the early phase of CNV and their number decreased significantly with time (p = 0.0001). The T lymphocytes were present from the beginning and their number remained stable or increased slightly in time (p = 0.1), thus becoming predominant in the perivascular infiltrate in older lesions. Macrophages were scattered on interstitium since the early phase and they showed a time-dependent increase (p = 0.0003). E-selectin (ELAM-1) expression was detected at the first biopsy and it decreased depending on the age of the evolving vasculitis (p = 0.0033). The expression of CLA decreased also with time in 5 of the 7 cases (p = 0.0001). Our study supports the existence of an unique histopathologic pattern in CNV, in which the inflammatory infiltrate varies with time at the expense of the number of polymorphonuclear cells and macrophages.
authors.affiliation: Department of Dermatology, Hospital Universitari Germans Trias i Pujol, Badalona, Spain.
authors.forename: I
authors.initials: I
authors.lastname: Bielsa
authors.forename: J M
authors.initials: JM
authors.lastname: Carrascosa
authors.forename: G
authors.initials: G
authors.lastname: Hausmann
authors.forename: C
authors.initials: C
authors.lastname: Ferrándiz
mesh_terms: D000911:Antibodies, Monoclonal / Q000276:immunology; D015415:Biomarkers / Q000032:analysis; D015815:Cell Adhesion Molecules / Q000378:metabolism; D002452:Cell Count; D003713:Dendritic Cells / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007124:Immunoenzyme Techniques; D008264:Macrophages / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D009336:Necrosis; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D011693:Purpura / Q000209:etiology / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D017445:Skin Diseases, Vascular / Q000150:complications / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D013997:Time Factors; D014657:Vasculitis / Q000150:complications / Q000276:immunology / Q000378:metabolism / Q000473:pathology*
chemical_list: D000911:Antibodies, Monoclonal; D015415:Biomarkers; D015815:Cell Adhesion Molecules