{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,9,15]],"date-time":"2023-09-15T05:03:31Z","timestamp":1694754211085},"reference-count":18,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2018,4,6]],"date-time":"2018-04-06T00:00:00Z","timestamp":1522972800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"FUNADERSP"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Acad Dermatol Venereol"],"published-print":{"date-parts":[[2018,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Erythroderma is a severe manifestation of pemphigus foliaceus (<jats:styled-content style=\"fixed-case\">PF<\/jats:styled-content>), a blistering disease mediated by IgG autoantibodies against desmoglein 1. Increasing evidence supports the contribution of angiogenic mediators in the pathogenesis of erythroderma.<\/jats:p><\/jats:sec><jats:sec><jats:title>Objective<\/jats:title><jats:p>To evaluate the <jats:italic>in situ<\/jats:italic> expression of vascular endothelial growth factor (<jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content>) and endoglin in patients with <jats:styled-content style=\"fixed-case\">PF<\/jats:styled-content> with erythroderma.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Formalin\u2010fixed paraffin\u2010embedded skin samples obtained from patients with erythrodermic <jats:styled-content style=\"fixed-case\">PF<\/jats:styled-content> (<jats:italic>n<\/jats:italic> = 19; 12 patients with endemic <jats:styled-content style=\"fixed-case\">PF<\/jats:styled-content>), non\u2010erythrodermic <jats:styled-content style=\"fixed-case\">PF<\/jats:styled-content> (<jats:italic>n<\/jats:italic> = 17), pemphigus vulgaris (<jats:styled-content style=\"fixed-case\">PV<\/jats:styled-content>;<jats:italic> n<\/jats:italic> = 10), psoriasis (<jats:italic>n<\/jats:italic> = 10) and healthy individuals (<jats:styled-content style=\"fixed-case\">HI<\/jats:styled-content>;<jats:italic> n<\/jats:italic> = 10) were processed in an automated immunohistochemistry platform utilizing anti\u2010<jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> and anti\u2010endoglin as primary antibodies. Reactivity was evaluated both manually (0 = negative; 1+ = mild; 2+ = intense) and through an automated microvessel analysis algorithm.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Vascular endothelial growth factor expression in erythrodermic <jats:styled-content style=\"fixed-case\">PF<\/jats:styled-content> was higher than in non\u2010erythrodermic <jats:styled-content style=\"fixed-case\">PF<\/jats:styled-content> (<jats:italic>P<\/jats:italic> = 0.034) and in <jats:styled-content style=\"fixed-case\">HI<\/jats:styled-content> (<jats:italic>P<\/jats:italic> = 0.004), and similar to psoriasis (<jats:italic>P<\/jats:italic> = 0.667) and <jats:styled-content style=\"fixed-case\">PV<\/jats:styled-content> (<jats:italic>P<\/jats:italic> = 0.667). In non\u2010erythrodermic <jats:styled-content style=\"fixed-case\">PF<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> VEGF<\/jats:styled-content> positivity was similar to <jats:styled-content style=\"fixed-case\">HI<\/jats:styled-content> (<jats:italic>P<\/jats:italic> = 0.247), and lower than psoriasis (<jats:italic>P<\/jats:italic> = 0.049) and <jats:styled-content style=\"fixed-case\">PV<\/jats:styled-content> (<jats:italic>P<\/jats:italic> = 0.049). Both erythrodermic and non\u2010erythrodermic <jats:styled-content style=\"fixed-case\">PF<\/jats:styled-content> presented similar endoglin expression (<jats:italic>P<\/jats:italic> = 0.700). In addition, endoglin positivity during erythrodermic <jats:styled-content style=\"fixed-case\">PF<\/jats:styled-content> was similar to psoriasis (<jats:italic>P<\/jats:italic> = 0.133) and lower than <jats:styled-content style=\"fixed-case\">PV<\/jats:styled-content> (<jats:italic>P<\/jats:italic> = 0.0009). Increased expression of <jats:italic>in situ<\/jats:italic><jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> suggests that healing processes are triggered in response to tissue damage led by autoantibodies in <jats:styled-content style=\"fixed-case\">PF<\/jats:styled-content>, especially during erythroderma. Reduced endoglin positivity suggests that an unbalanced angiogenesis may occur during erythrodermic <jats:styled-content style=\"fixed-case\">PF<\/jats:styled-content>. Further studies may help to confirm if the regulation of <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> and endoglin expression in patients with <jats:styled-content style=\"fixed-case\">PF<\/jats:styled-content> can contribute to control the healing process and enable disease remission.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Overexpression of <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> in erythrodermic <jats:styled-content style=\"fixed-case\">PF<\/jats:styled-content> as well as in <jats:styled-content style=\"fixed-case\">PV<\/jats:styled-content> and psoriasis points out a dysregulated repair process in severe forms of these diseases and suggests <jats:styled-content style=\"fixed-case\">VEGF<\/jats:styled-content> and endoglin could act as prognostic markers and future therapeutic targets to enable proper healing in <jats:styled-content style=\"fixed-case\">PF<\/jats:styled-content>.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jdv.14903","type":"journal-article","created":{"date-parts":[[2018,2,28]],"date-time":"2018-02-28T13:46:40Z","timestamp":1519825600000},"page":"1954-1958","update-policy":"http:\/\/dx.doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Exploring the <i>in situ<\/i> expression of vascular endothelial growth factor and endoglin in pemphigus foliaceus variants and pemphigus vulgaris"],"prefix":"10.1111","volume":"32","author":[{"given":"D.","family":"Miyamoto","sequence":"first","affiliation":[{"name":"Department of Dermatology University of S\u00e3o Paulo Medical School S\u00e3o Paulo S\u00e3o Paulo Brazil"},{"name":"MUHC \u2010 McGill University Ocular Pathology Laboratory Montreal Quebec Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C.W.","family":"Maruta","sequence":"additional","affiliation":[{"name":"Department of Dermatology University of S\u00e3o Paulo Medical School S\u00e3o Paulo S\u00e3o Paulo Brazil"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C.G.","family":"Santi","sequence":"additional","affiliation":[{"name":"Department of Dermatology University of S\u00e3o Paulo Medical School S\u00e3o Paulo S\u00e3o Paulo Brazil"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P.","family":"Zoroquiain","sequence":"additional","affiliation":[{"name":"MUHC \u2010 McGill University Ocular Pathology Laboratory Montreal Quebec Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A.B.T.","family":"Dias","sequence":"additional","affiliation":[{"name":"MUHC \u2010 McGill University Ocular Pathology Laboratory Montreal Quebec Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J.J.","family":"Mansure","sequence":"additional","affiliation":[{"name":"Department of Urology McGill University Montreal Quebec 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