G Sais1, A Vidaller, A Jucglá, E Condom, J Peyrí. 1. Department of Dermatology, Ciutat Sanitària i Universitària de Bellvitge, Universitat de Barcelona, Spain.
Abstract
OBJECTIVES: To investigate the sequential expression of adhesion molecules on endothelium and inflammatory cells in cutaneous leukocytoclastic vasculitis, and the relation of these adhesive molecules with clinical and histologic variables. DESIGN: An immunohistochemical analysis (streptavidin-biotin-peroxidase technique) of 42 vasculitic lesions of up to 96 hours was performed using a panel of monoclonal antibodies specific for different adhesion molecules. Twenty normal skin samples and 3 perilesional specimens served as control samples. A clinical protocol was also performed, and patients were followed up for 1 to 5 years. SETTING: A clinicopathologic research unit of a university hospital. PATIENTS: Forty-two patients, 21 women and 21 men, aged 22 to 79 years, with cutaneous leukocytoclastic vasculitis. INTERVENTIONS: Three skin biopsy specimens of vasculitic lesions from each patient were obtained for histopathologic examination on paraffin, direct immunofluorescence, and immunohistochemical analysis on cryostatic tissue sections. MAIN OUTCOME MEASURES: The histologic characteristics and the immunohistochemical-stained specimens were evaluated by 3 independent investigators, using a semiquantitative method. RESULTS: Increased endothelial expression of very late activation antigen-1, HLA-DR, and intercellular adhesion molecule-1 was observed. The induction of E-selectin expression was more marked in recent lesions (P < .001) and correlated with the proportion of infiltrating neutrophils (P = .03). Endothelial expression of vascular cell adhesion molecule-1 was restricted to developed lesions. Most infiltrating cells were neutrophils expressing Mac-1. In 1 patient, lymphocyte function associated antigen-1 expression was also up-regulated. No significant increase in CD3, CD8, or CD71 immunoreactivity was found. An up-regulation of perivascular cells expressing HLA-DR and vascular cell adhesion molecule-1 was observed in vasculitic lesions. This cellular staining correlated with long-term evolution of the disease (P = .04). CONCLUSIONS: Adhesion molecules are sequentially upregulated in cutaneous leukocytoclastic vasculitis. The results of this study support the possible involvement of E-selectin in mediating recruitment of neutrophils expressing Mac-1.
OBJECTIVES: To investigate the sequential expression of adhesion molecules on endothelium and inflammatory cells in cutaneous leukocytoclastic vasculitis, and the relation of these adhesive molecules with clinical and histologic variables. DESIGN: An immunohistochemical analysis (streptavidin-biotin-peroxidase technique) of 42 vasculitic lesions of up to 96 hours was performed using a panel of monoclonal antibodies specific for different adhesion molecules. Twenty normal skin samples and 3 perilesional specimens served as control samples. A clinical protocol was also performed, and patients were followed up for 1 to 5 years. SETTING: A clinicopathologic research unit of a university hospital. PATIENTS: Forty-two patients, 21 women and 21 men, aged 22 to 79 years, with cutaneous leukocytoclastic vasculitis. INTERVENTIONS: Three skin biopsy specimens of vasculitic lesions from each patient were obtained for histopathologic examination on paraffin, direct immunofluorescence, and immunohistochemical analysis on cryostatic tissue sections. MAIN OUTCOME MEASURES: The histologic characteristics and the immunohistochemical-stained specimens were evaluated by 3 independent investigators, using a semiquantitative method. RESULTS: Increased endothelial expression of very late activation antigen-1, HLA-DR, and intercellular adhesion molecule-1 was observed. The induction of E-selectin expression was more marked in recent lesions (P < .001) and correlated with the proportion of infiltrating neutrophils (P = .03). Endothelial expression of vascular cell adhesion molecule-1 was restricted to developed lesions. Most infiltrating cells were neutrophils expressing Mac-1. In 1 patient, lymphocyte function associated antigen-1 expression was also up-regulated. No significant increase in CD3, CD8, or CD71 immunoreactivity was found. An up-regulation of perivascular cells expressing HLA-DR and vascular cell adhesion molecule-1 was observed in vasculitic lesions. This cellular staining correlated with long-term evolution of the disease (P = .04). CONCLUSIONS: Adhesion molecules are sequentially upregulated in cutaneous leukocytoclastic vasculitis. The results of this study support the possible involvement of E-selectin in mediating recruitment of neutrophils expressing Mac-1.