L M Baddour1, P B Googe, S L Stevens. 1. Department of Medicine, Graduate School of Medicine, University of Tennessee Medical Center at Knoxville, USA.
Abstract
BACKGROUND: No previous study has examined the immune and inflammatory mechanisms involved in the pathogenesis of lower extremity cellulitis after saphenous venectomy for coronary artery bypass graft surgery. OBJECTIVE: Our purpose was to determine the histopathologic, immunologic, and inflammatory findings in skin biopsy specimens from saphenous venectomy limbs of patients with previous bouts of cellulitis. METHODS: Biopsy specimens were obtained from five patients with previous episodes of cellulitis. Specimens of the contralateral lower extremity of each patient were obtained for controlled comparisons. RESULTS: Histopathologic findings did not provide evidence that could account for the tendency for cellulitis to develop. Moreover, the distribution of CD1a, HLA-DR, intercellular adhesion molecule-1, and lymphocyte function-associated antigen type 1 were similar in specimens from the postvenectomy and contralateral legs. No tumor necrosis factor-alpha expression was found in specimens from the lower extremities. CONCLUSION: The mechanisms responsible for the production of this disorder do not involve the mediators studied.
BACKGROUND: No previous study has examined the immune and inflammatory mechanisms involved in the pathogenesis of lower extremity cellulitis after saphenous venectomy for coronary artery bypass graft surgery. OBJECTIVE: Our purpose was to determine the histopathologic, immunologic, and inflammatory findings in skin biopsy specimens from saphenous venectomy limbs of patients with previous bouts of cellulitis. METHODS: Biopsy specimens were obtained from five patients with previous episodes of cellulitis. Specimens of the contralateral lower extremity of each patient were obtained for controlled comparisons. RESULTS: Histopathologic findings did not provide evidence that could account for the tendency for cellulitis to develop. Moreover, the distribution of CD1a, HLA-DR, intercellular adhesion molecule-1, and lymphocyte function-associated antigen type 1 were similar in specimens from the postvenectomy and contralateral legs. No tumor necrosis factor-alpha expression was found in specimens from the lower extremities. CONCLUSION: The mechanisms responsible for the production of this disorder do not involve the mediators studied.