{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,9,25]],"date-time":"2023-09-25T06:43:55Z","timestamp":1695624235503},"reference-count":15,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2016,10,24]],"date-time":"2016-10-24T00:00:00Z","timestamp":1477267200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100005968","name":"Leukemia Research Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100005968","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Dermatology"],"published-print":{"date-parts":[[2017,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Livedoid vasculopathy (<jats:styled-content style=\"fixed-case\">LV<\/jats:styled-content>) is a chronic disease with recurrent reticularis and ulcers, mainly affecting the feet and lower legs. The pathogenesis of <jats:styled-content style=\"fixed-case\">LV<\/jats:styled-content> has not been yet thoroughly understood, but thrombosis is thought to play a major role because fibrin deposition within both the wall and lumen of affected vessels is pathologically detected. A 68\u2010year\u2010old woman first presented to our hospital in 2004 with a 6\u2010year history of a reticular rash and ulceration on the lower legs. Screening tests for vasculitis and collagen disease were mostly normal, leading to diagnosis of <jats:styled-content style=\"fixed-case\">LV<\/jats:styled-content>. After failed treatment with steroid and aspirin, she was started on warfarin, to which she had a favorable response. However, she had to be admitted to the hospital because complication of swelling and infection in her left lower leg in 2004 + 10. Contrast\u2010enhanced computed tomography showed thrombosis in the left popliteal artery. Screening tests for thrombotic tendency revealed that protein S activity was low (27%) although total protein S antigen was within normal range (73%). Analysis of protein S\u2010alpha gene revealed 155 Lys&gt;Glu mutation in exon <jats:styled-content style=\"fixed-case\">VI<\/jats:styled-content>, which was reported in 1994 and named as protein S Tokushima. Thus, we conclude that protein S deficiency could contribute to <jats:styled-content style=\"fixed-case\">LV<\/jats:styled-content>.<\/jats:p>","DOI":"10.1111\/1346-8138.13652","type":"journal-article","created":{"date-parts":[[2016,10,24]],"date-time":"2016-10-24T08:58:47Z","timestamp":1477299527000},"page":"198-201","source":"Crossref","is-referenced-by-count":2,"title":["Livedoid vasculopathy and popliteal artery occlusion in a patient with protein S deficiency"],"prefix":"10.1111","volume":"44","author":[{"given":"Takayuki","family":"Nakayama","sequence":"first","affiliation":[{"name":"Department of Transfusion Medicine Aichi Medical University Nagakute Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kentaro","family":"Mizutani","sequence":"additional","affiliation":[{"name":"Department of Dermatology Aichi Medical University Nagakute 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