H1N1 influenza (swine flu)-associated thrombotic microangiopathy with a markedly high plasma ratio of von Willebrand factor to ADAMTS13.
Identifieur interne : 000442 ( Ncbi/Curation ); précédent : 000441; suivant : 000443H1N1 influenza (swine flu)-associated thrombotic microangiopathy with a markedly high plasma ratio of von Willebrand factor to ADAMTS13.
Auteurs : Rui Akiyama [Japon] ; Isao Komori ; Ryugo Hiramoto ; Ayami Isonishi ; Masanori Matsumoto ; Yoshihiro FujimuraSource :
- Internal medicine (Tokyo, Japan) [ 1349-7235 ] ; 2011.
Descripteurs français
- KwdFr :
- Adolescent, Facteur de von Willebrand (biosynthèse), Facteur de von Willebrand (métabolisme), Femelle, Grippe humaine (), Grippe humaine (diagnostic), Grippe humaine (sang), Humains, Microangiopathies thrombotiques (diagnostic), Microangiopathies thrombotiques (sang), Microangiopathies thrombotiques (étiologie), Protéine ADAMTS13, Protéines ADAM (antagonistes et inhibiteurs), Protéines ADAM (sang), Sous-type H1N1 du virus de la grippe A, Études rétrospectives.
- MESH :
- antagonistes et inhibiteurs : Protéines ADAM.
- biosynthèse : Facteur de von Willebrand.
- diagnostic : Grippe humaine, Microangiopathies thrombotiques.
- métabolisme : Facteur de von Willebrand.
- sang : Grippe humaine, Microangiopathies thrombotiques, Protéines ADAM.
- étiologie : Microangiopathies thrombotiques.
- Adolescent, Femelle, Grippe humaine, Humains, Protéine ADAMTS13, Sous-type H1N1 du virus de la grippe A, Études rétrospectives.
English descriptors
- KwdEn :
- ADAM Proteins (antagonists & inhibitors), ADAM Proteins (blood), ADAMTS13 Protein, Adolescent, Female, Humans, Influenza A Virus, H1N1 Subtype, Influenza, Human (blood), Influenza, Human (complications), Influenza, Human (diagnosis), Retrospective Studies, Thrombotic Microangiopathies (blood), Thrombotic Microangiopathies (diagnosis), Thrombotic Microangiopathies (etiology), von Willebrand Factor (biosynthesis), von Willebrand Factor (metabolism).
- MESH :
- chemical , antagonists & inhibitors : ADAM Proteins.
- chemical , biosynthesis : von Willebrand Factor.
- chemical , blood : ADAM Proteins.
- chemical , metabolism : von Willebrand Factor.
- chemical : ADAMTS13 Protein.
- blood : Influenza, Human, Thrombotic Microangiopathies.
- complications : Influenza, Human.
- diagnosis : Influenza, Human, Thrombotic Microangiopathies.
- etiology : Thrombotic Microangiopathies.
- Adolescent, Female, Humans, Influenza A Virus, H1N1 Subtype, Retrospective Studies.
Abstract
We describe an 18-year-old woman infected with H1N1 influenza followed by thrombotic microangiopathy. During the acute phase, her plasma levels of von Willebrand factor (VWF) were remarkably elevated, whereas those of ADAMTS13 were reduced without its inhibitors, generating a markedly high ratio of VWF to ADAMTS13 in circulation. A retrospective analysis established the following hypothesis: an influenza-mediated cytokine storm induced an enhanced release of unusually large VWF multimers (UL-VWFM) from vascular endothelial cells, generating platelet thrombi in microcirculatures under high shear stress. Plasma exchange removed UL-VWFM and cytokines, and rescued her life. This report sheds a light on a hitherto unrecognized influenza complication.
DOI: 10.2169/internalmedicine.50.4620
PubMed: 21422695
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pubmed:21422695Le document en format XML
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<term>Female</term>
<term>Humans</term>
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<term>Influenza, Human (blood)</term>
<term>Influenza, Human (complications)</term>
<term>Influenza, Human (diagnosis)</term>
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<term>Thrombotic Microangiopathies (diagnosis)</term>
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<term>Facteur de von Willebrand (métabolisme)</term>
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<term>Protéines ADAM (sang)</term>
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<term>Thrombotic Microangiopathies</term>
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<term>Humains</term>
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<term>Sous-type H1N1 du virus de la grippe A</term>
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<front><div type="abstract" xml:lang="en">We describe an 18-year-old woman infected with H1N1 influenza followed by thrombotic microangiopathy. During the acute phase, her plasma levels of von Willebrand factor (VWF) were remarkably elevated, whereas those of ADAMTS13 were reduced without its inhibitors, generating a markedly high ratio of VWF to ADAMTS13 in circulation. A retrospective analysis established the following hypothesis: an influenza-mediated cytokine storm induced an enhanced release of unusually large VWF multimers (UL-VWFM) from vascular endothelial cells, generating platelet thrombi in microcirculatures under high shear stress. Plasma exchange removed UL-VWFM and cytokines, and rescued her life. This report sheds a light on a hitherto unrecognized influenza complication.</div>
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