Lamisil Induced Dermatomyositis
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Auteurs : K. Seilstad ; D. Hearne [États-Unis] ; K. Gupta ; C. MagroSource :
- Journal of Cutaneous Pathology [ 0303-6987 ] ; 2005-01.
Abstract
Background: Dermatomyositis, a connective tissue disease syndrome where antibodies to the endothelium of the microvasculature of the skin, muscle and lung are implicated in lesional propagation, is characterized by photodistributed erythema, heliotrope rash, Gottron’s papules, muscle weakness and interstitial pulmonary fibrosis. Endotheliotropic viruses and underlying neoplasia are among the inciting triggers. Uncommonly drugs, namely the lipid lowering agents, have been implicated in dermatomyositis. Case Report: The patient, a 57‐year‐old male, developed a photodistributed rash and muscle weakness following treatment with the antifungal medication Lamisil. A skin biopsy was performed, showing an atrophying interface dermatitis with pandermal mucinosis and striking vasculopathic changes including endothelial cell necrosis with denudement and basement membrane zone reduplication. Direct immunofluorescent testing showed prominent staining of C5b‐9 along the dermal‐ epidermal junction and within the vasculature. Conclusion: We have shown a temporal association between use of Lamisil and the development of dermatomyositis. Terbinafine, the active agent in Lamisil, promotes apoptosis of human endothelial cells in culture. Enhanced endothelial cell apoptosis results in the displacement of various cellular antigens creating a state of neo‐antigenicity; its attendant sequelae has held to be one of antiendothelial cell antibody formation, a defining pathogenetic event in the evolution of dermatomyositis.
Url:
DOI: 10.1111/j.0303-6987.2005.320gt.x
Affiliations:
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Magro</name><affiliation><wicri:noCountry code="no comma">Department of Pathology and the Department of Internal Medicine</wicri:noCountry></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Journal of Cutaneous Pathology</title><title level="j" type="alt">JOURNAL OF CUTANEOUS PATHOLOGY</title><idno type="ISSN">0303-6987</idno><idno type="eISSN">1600-0560</idno><imprint><biblScope unit="vol">32</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="116">116</biblScope><biblScope unit="page" to="116">116</biblScope><biblScope unit="page-count">1</biblScope><publisher>Blackwell Publishing Ltd/Inc.</publisher><pubPlace>Oxford, UK; Malden, USA</pubPlace><date type="published" when="2005-01">2005-01</date></imprint><idno type="ISSN">0303-6987</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0303-6987</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Background: Dermatomyositis, a connective tissue disease syndrome where antibodies to the endothelium of the microvasculature of the skin, muscle and lung are implicated in lesional propagation, is characterized by photodistributed erythema, heliotrope rash, Gottron’s papules, muscle weakness and interstitial pulmonary fibrosis. Endotheliotropic viruses and underlying neoplasia are among the inciting triggers. Uncommonly drugs, namely the lipid lowering agents, have been implicated in dermatomyositis. Case Report: The patient, a 57‐year‐old male, developed a photodistributed rash and muscle weakness following treatment with the antifungal medication Lamisil. A skin biopsy was performed, showing an atrophying interface dermatitis with pandermal mucinosis and striking vasculopathic changes including endothelial cell necrosis with denudement and basement membrane zone reduplication. Direct immunofluorescent testing showed prominent staining of C5b‐9 along the dermal‐ epidermal junction and within the vasculature. Conclusion: We have shown a temporal association between use of Lamisil and the development of dermatomyositis. Terbinafine, the active agent in Lamisil, promotes apoptosis of human endothelial cells in culture. Enhanced endothelial cell apoptosis results in the displacement of various cellular antigens creating a state of neo‐antigenicity; its attendant sequelae has held to be one of antiendothelial cell antibody formation, a defining pathogenetic event in the evolution of dermatomyositis.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Ohio</li></region></list><tree><noCountry><name sortKey="Gupta, K" sort="Gupta, K" uniqKey="Gupta K" first="K" last="Gupta">K. Gupta</name><name sortKey="Magro, C" sort="Magro, C" uniqKey="Magro C" first="C" last="Magro">C. Magro</name><name sortKey="Seilstad, K" sort="Seilstad, K" uniqKey="Seilstad K" first="K" last="Seilstad">K. Seilstad</name></noCountry><country name="États-Unis"><region name="Ohio"><name sortKey="Hearne, D" sort="Hearne, D" uniqKey="Hearne D" first="D" last="Hearne">D. Hearne</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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