Biopsy specimen findings in patients with previous lower extremity cellulitis after saphenous venectomy for coronary artery bypass graft surgery
Identifieur interne : 00BB58 ( Main/Exploration ); précédent : 00BB57; suivant : 00BB59Biopsy specimen findings in patients with previous lower extremity cellulitis after saphenous venectomy for coronary artery bypass graft surgery
Auteurs : Larry M. Baddour ; Paul B. Googe ; Scott L. StevensSource :
- Journal of the American Academy of Dermatology [ 0190-9622 ] ; 1997.
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–α 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. (J Am Acad Dermatol 1997;37:246-9.)
Url:
DOI: 10.1016/S0190-9622(97)80132-6
Affiliations:
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Baddour</name><affiliation><wicri:noCountry code="subField">Knoxville</wicri:noCountry></affiliation></author><author><name sortKey="Googe, Paul B" sort="Googe, Paul B" uniqKey="Googe P" first="Paul B." last="Googe">Paul B. Googe</name><affiliation><wicri:noCountry code="subField">Knoxville</wicri:noCountry></affiliation></author><author><name sortKey="Stevens, Scott L" sort="Stevens, Scott L" uniqKey="Stevens S" first="Scott L." last="Stevens">Scott L. Stevens</name><affiliation><wicri:noCountry code="subField">Knoxville</wicri:noCountry></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of the American Academy of Dermatology</title><title level="j" type="abbrev">YMJD</title><idno type="ISSN">0190-9622</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1997">1997</date><biblScope unit="volume">37</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="supplement">P1</biblScope><biblScope unit="page" from="246">246</biblScope><biblScope unit="page" to="249">249</biblScope></imprint><idno type="ISSN">0190-9622</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0190-9622</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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–α 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. (J Am Acad Dermatol 1997;37:246-9.)</div></front></TEI><affiliations><list></list><tree><noCountry><name sortKey="Baddour, Larry M" sort="Baddour, Larry M" uniqKey="Baddour L" first="Larry M." last="Baddour">Larry M. Baddour</name><name sortKey="Googe, Paul B" sort="Googe, Paul B" uniqKey="Googe P" first="Paul B." last="Googe">Paul B. Googe</name><name sortKey="Stevens, Scott L" sort="Stevens, Scott L" uniqKey="Stevens S" first="Scott L." last="Stevens">Scott L. Stevens</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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