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Necrotic leg ulcers induced by vitamin K antagonists: five cases
Vitamin K antagonists (VKAs) are widely used in thromboembolic diseases. We report five cases of necrotic leg ulcers having a particularly severe course and in which withdrawal of VKA treatment alone enabled healing. Five patients presented with necrotic leg ulcers clinically evocative of necrotic a...
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Published in: | Annales de dermatologie et de vénéréologie 2011-10, Vol.138 (10), p.657-663 |
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creator | Bezier, M Perceau, G Reguiai, Z Remy-Leroux, V Tchen, T Durlach, A Grange, F Nguyen, P Bernard, P |
description | Vitamin K antagonists (VKAs) are widely used in thromboembolic diseases. We report five cases of necrotic leg ulcers having a particularly severe course and in which withdrawal of VKA treatment alone enabled healing.
Five patients presented with necrotic leg ulcers clinically evocative of necrotic angiodermatitis or vasculitis. Histological features were variable, including inconstantly inflammatory lesions (leukocytoclastic vasculitis) and microthrombosis. None of the patients had laboratory signs of autoimmune disease. Healing occurred in all patients only after withdrawal of VKA therapy (fluindione or acenocoumarol). Associated vascular diseases included superficial venous, distal arterial insufficiency and postphlebitic disease. In three cases, thrombotic factors were observed: hyperhomocysteinaemia or heterozygous Factor V Leiden mutation.
Although the causative role of VKAs is based solely on chronological criteria, this potential side effect deserves publication because of its practical therapeutic consequences. The physiopathological mechanisms accounting for the role of VKAs, including immunoallergic phenomena and, above all, microcirculatory thrombotic processes, are hypothetical and not universally accepted. |
doi_str_mv | 10.1016/j.annder.2011.06.008 |
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Five patients presented with necrotic leg ulcers clinically evocative of necrotic angiodermatitis or vasculitis. Histological features were variable, including inconstantly inflammatory lesions (leukocytoclastic vasculitis) and microthrombosis. None of the patients had laboratory signs of autoimmune disease. Healing occurred in all patients only after withdrawal of VKA therapy (fluindione or acenocoumarol). Associated vascular diseases included superficial venous, distal arterial insufficiency and postphlebitic disease. In three cases, thrombotic factors were observed: hyperhomocysteinaemia or heterozygous Factor V Leiden mutation.
Although the causative role of VKAs is based solely on chronological criteria, this potential side effect deserves publication because of its practical therapeutic consequences. The physiopathological mechanisms accounting for the role of VKAs, including immunoallergic phenomena and, above all, microcirculatory thrombotic processes, are hypothetical and not universally accepted.</description><identifier>ISSN: 0151-9638</identifier><identifier>DOI: 10.1016/j.annder.2011.06.008</identifier><identifier>PMID: 21978501</identifier><language>fre</language><publisher>France</publisher><subject>Acenocoumarol - adverse effects ; Acenocoumarol - therapeutic use ; Activated Protein C Resistance - complications ; Activated Protein C Resistance - genetics ; Aged ; Aged, 80 and over ; Anticoagulants - adverse effects ; Anticoagulants - therapeutic use ; Diabetic Angiopathies - complications ; Factor V - genetics ; Female ; Humans ; Hyperhomocysteinemia - complications ; Leg Ulcer - chemically induced ; Leg Ulcer - etiology ; Leg Ulcer - pathology ; Male ; Necrosis ; Phenindione - adverse effects ; Phenindione - analogs & derivatives ; Phenindione - therapeutic use ; Polyarteritis Nodosa - chemically induced ; Polyarteritis Nodosa - pathology ; Postoperative Complications - chemically induced ; Postoperative Complications - prevention & control ; Purpura - chemically induced ; Thrombophilia - complications ; Varicose Ulcer - chemically induced ; Varicose Ulcer - pathology ; Vasculitis, Leukocytoclastic, Cutaneous - chemically induced ; Vasculitis, Leukocytoclastic, Cutaneous - pathology ; Vitamin K - antagonists & inhibitors</subject><ispartof>Annales de dermatologie et de vénéréologie, 2011-10, Vol.138 (10), p.657-663</ispartof><rights>Copyright © 2011 Elsevier Masson SAS. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21978501$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bezier, M</creatorcontrib><creatorcontrib>Perceau, G</creatorcontrib><creatorcontrib>Reguiai, Z</creatorcontrib><creatorcontrib>Remy-Leroux, V</creatorcontrib><creatorcontrib>Tchen, T</creatorcontrib><creatorcontrib>Durlach, A</creatorcontrib><creatorcontrib>Grange, F</creatorcontrib><creatorcontrib>Nguyen, P</creatorcontrib><creatorcontrib>Bernard, P</creatorcontrib><title>Necrotic leg ulcers induced by vitamin K antagonists: five cases</title><title>Annales de dermatologie et de vénéréologie</title><addtitle>Ann Dermatol Venereol</addtitle><description>Vitamin K antagonists (VKAs) are widely used in thromboembolic diseases. We report five cases of necrotic leg ulcers having a particularly severe course and in which withdrawal of VKA treatment alone enabled healing.
Five patients presented with necrotic leg ulcers clinically evocative of necrotic angiodermatitis or vasculitis. Histological features were variable, including inconstantly inflammatory lesions (leukocytoclastic vasculitis) and microthrombosis. None of the patients had laboratory signs of autoimmune disease. Healing occurred in all patients only after withdrawal of VKA therapy (fluindione or acenocoumarol). Associated vascular diseases included superficial venous, distal arterial insufficiency and postphlebitic disease. In three cases, thrombotic factors were observed: hyperhomocysteinaemia or heterozygous Factor V Leiden mutation.
Although the causative role of VKAs is based solely on chronological criteria, this potential side effect deserves publication because of its practical therapeutic consequences. The physiopathological mechanisms accounting for the role of VKAs, including immunoallergic phenomena and, above all, microcirculatory thrombotic processes, are hypothetical and not universally accepted.</description><subject>Acenocoumarol - adverse effects</subject><subject>Acenocoumarol - therapeutic use</subject><subject>Activated Protein C Resistance - complications</subject><subject>Activated Protein C Resistance - genetics</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Anticoagulants - adverse effects</subject><subject>Anticoagulants - therapeutic use</subject><subject>Diabetic Angiopathies - complications</subject><subject>Factor V - genetics</subject><subject>Female</subject><subject>Humans</subject><subject>Hyperhomocysteinemia - complications</subject><subject>Leg Ulcer - chemically induced</subject><subject>Leg Ulcer - etiology</subject><subject>Leg Ulcer - pathology</subject><subject>Male</subject><subject>Necrosis</subject><subject>Phenindione - adverse effects</subject><subject>Phenindione - analogs & derivatives</subject><subject>Phenindione - therapeutic use</subject><subject>Polyarteritis Nodosa - chemically induced</subject><subject>Polyarteritis Nodosa - pathology</subject><subject>Postoperative Complications - chemically induced</subject><subject>Postoperative Complications - prevention & control</subject><subject>Purpura - chemically induced</subject><subject>Thrombophilia - complications</subject><subject>Varicose Ulcer - chemically induced</subject><subject>Varicose Ulcer - pathology</subject><subject>Vasculitis, Leukocytoclastic, Cutaneous - chemically induced</subject><subject>Vasculitis, Leukocytoclastic, Cutaneous - pathology</subject><subject>Vitamin K - antagonists & inhibitors</subject><issn>0151-9638</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><recordid>eNo1j71OwzAURj2AaCm8AULemBKu7cSxmUBV-REVLDBHzs1t5SpxQpxU6ttTiTJ9y9Gncxi7EZAKEPp-l7oQahpSCUKkoFMAc8bmIHKRWK3MjF3GuAMQ0qj8gs2ksIXJQczZ4wfh0I0eeUNbPjVIQ-Q-1BNSzasD3_vRtT7wd-7C6LZd8HGMD3zj98TRRYpX7HzjmkjXp12w7-fV1_I1WX--vC2f1kkvMhgTV0tVSYtSYQHOod1khqymzGKBxdFRE5Kucgd4VMvQyiIDBVJUORWajFqwu7_ffuh-Jopj2fqI1DQuUDfF0lhtlFRZfiRvT-RUtVSX_eBbNxzK_2j1C73aWEw</recordid><startdate>201110</startdate><enddate>201110</enddate><creator>Bezier, M</creator><creator>Perceau, G</creator><creator>Reguiai, Z</creator><creator>Remy-Leroux, V</creator><creator>Tchen, T</creator><creator>Durlach, A</creator><creator>Grange, F</creator><creator>Nguyen, P</creator><creator>Bernard, P</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>201110</creationdate><title>Necrotic leg ulcers induced by vitamin K antagonists: five cases</title><author>Bezier, M ; Perceau, G ; Reguiai, Z ; Remy-Leroux, V ; Tchen, T ; Durlach, A ; Grange, F ; Nguyen, P ; Bernard, P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p140t-ad23b29c23c70aac9f48e96e49c7c79636ece6b5a0c9784c927403021b5e76e83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>fre</language><creationdate>2011</creationdate><topic>Acenocoumarol - adverse effects</topic><topic>Acenocoumarol - therapeutic use</topic><topic>Activated Protein C Resistance - complications</topic><topic>Activated Protein C Resistance - genetics</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Anticoagulants - adverse effects</topic><topic>Anticoagulants - therapeutic use</topic><topic>Diabetic Angiopathies - complications</topic><topic>Factor V - genetics</topic><topic>Female</topic><topic>Humans</topic><topic>Hyperhomocysteinemia - complications</topic><topic>Leg Ulcer - chemically induced</topic><topic>Leg Ulcer - etiology</topic><topic>Leg Ulcer - pathology</topic><topic>Male</topic><topic>Necrosis</topic><topic>Phenindione - adverse effects</topic><topic>Phenindione - analogs & derivatives</topic><topic>Phenindione - therapeutic use</topic><topic>Polyarteritis Nodosa - chemically induced</topic><topic>Polyarteritis Nodosa - pathology</topic><topic>Postoperative Complications - chemically induced</topic><topic>Postoperative Complications - prevention & control</topic><topic>Purpura - chemically induced</topic><topic>Thrombophilia - complications</topic><topic>Varicose Ulcer - chemically induced</topic><topic>Varicose Ulcer - pathology</topic><topic>Vasculitis, Leukocytoclastic, Cutaneous - chemically induced</topic><topic>Vasculitis, Leukocytoclastic, Cutaneous - pathology</topic><topic>Vitamin K - antagonists & inhibitors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bezier, M</creatorcontrib><creatorcontrib>Perceau, G</creatorcontrib><creatorcontrib>Reguiai, Z</creatorcontrib><creatorcontrib>Remy-Leroux, V</creatorcontrib><creatorcontrib>Tchen, T</creatorcontrib><creatorcontrib>Durlach, A</creatorcontrib><creatorcontrib>Grange, F</creatorcontrib><creatorcontrib>Nguyen, P</creatorcontrib><creatorcontrib>Bernard, P</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Annales de dermatologie et de vénéréologie</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bezier, M</au><au>Perceau, G</au><au>Reguiai, Z</au><au>Remy-Leroux, V</au><au>Tchen, T</au><au>Durlach, A</au><au>Grange, F</au><au>Nguyen, P</au><au>Bernard, P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Necrotic leg ulcers induced by vitamin K antagonists: five cases</atitle><jtitle>Annales de dermatologie et de vénéréologie</jtitle><addtitle>Ann Dermatol Venereol</addtitle><date>2011-10</date><risdate>2011</risdate><volume>138</volume><issue>10</issue><spage>657</spage><epage>663</epage><pages>657-663</pages><issn>0151-9638</issn><abstract>Vitamin K antagonists (VKAs) are widely used in thromboembolic diseases. We report five cases of necrotic leg ulcers having a particularly severe course and in which withdrawal of VKA treatment alone enabled healing.
Five patients presented with necrotic leg ulcers clinically evocative of necrotic angiodermatitis or vasculitis. Histological features were variable, including inconstantly inflammatory lesions (leukocytoclastic vasculitis) and microthrombosis. None of the patients had laboratory signs of autoimmune disease. Healing occurred in all patients only after withdrawal of VKA therapy (fluindione or acenocoumarol). Associated vascular diseases included superficial venous, distal arterial insufficiency and postphlebitic disease. In three cases, thrombotic factors were observed: hyperhomocysteinaemia or heterozygous Factor V Leiden mutation.
Although the causative role of VKAs is based solely on chronological criteria, this potential side effect deserves publication because of its practical therapeutic consequences. The physiopathological mechanisms accounting for the role of VKAs, including immunoallergic phenomena and, above all, microcirculatory thrombotic processes, are hypothetical and not universally accepted.</abstract><cop>France</cop><pmid>21978501</pmid><doi>10.1016/j.annder.2011.06.008</doi><tpages>7</tpages></addata></record> |
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subjects | Acenocoumarol - adverse effects Acenocoumarol - therapeutic use Activated Protein C Resistance - complications Activated Protein C Resistance - genetics Aged Aged, 80 and over Anticoagulants - adverse effects Anticoagulants - therapeutic use Diabetic Angiopathies - complications Factor V - genetics Female Humans Hyperhomocysteinemia - complications Leg Ulcer - chemically induced Leg Ulcer - etiology Leg Ulcer - pathology Male Necrosis Phenindione - adverse effects Phenindione - analogs & derivatives Phenindione - therapeutic use Polyarteritis Nodosa - chemically induced Polyarteritis Nodosa - pathology Postoperative Complications - chemically induced Postoperative Complications - prevention & control Purpura - chemically induced Thrombophilia - complications Varicose Ulcer - chemically induced Varicose Ulcer - pathology Vasculitis, Leukocytoclastic, Cutaneous - chemically induced Vasculitis, Leukocytoclastic, Cutaneous - pathology Vitamin K - antagonists & inhibitors |
title | Necrotic leg ulcers induced by vitamin K antagonists: five cases |
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