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A Case of Heparin-Induced Thrombocytopenia That Developed in the Therapeutic Course of Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis

BACKGROUND: Heparin-induced thrombocytopenia (HIT) causes thrombocytopenia via an immunological mechanism, resulting in severe organ injury due to arterial-venous thrombosis. HIT often develops in hemodialysis patients owing to heparin use. Anti-neutrophil cytoplasmic antibody-associated vasculitis...

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Autores principales: Nonaka, Taketoshi, Harada, Makoto, Sumi, Masahiko, Ishii, Wataru, Ichikawa, Tohru, Kobayashi, Mamoru
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6679837/
https://www.ncbi.nlm.nih.gov/pubmed/31428502
http://dx.doi.org/10.1155/2019/2724304
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author Nonaka, Taketoshi
Harada, Makoto
Sumi, Masahiko
Ishii, Wataru
Ichikawa, Tohru
Kobayashi, Mamoru
author_facet Nonaka, Taketoshi
Harada, Makoto
Sumi, Masahiko
Ishii, Wataru
Ichikawa, Tohru
Kobayashi, Mamoru
author_sort Nonaka, Taketoshi
collection PubMed
description BACKGROUND: Heparin-induced thrombocytopenia (HIT) causes thrombocytopenia via an immunological mechanism, resulting in severe organ injury due to arterial-venous thrombosis. HIT often develops in hemodialysis patients owing to heparin use. Anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV) is a systemic vasculitis, and cases of AAV complicated with HIT are rare. In addition, it mostly occurs in patients undergoing hemodialysis. CASE PRESENTATION: An 87-year-old woman presented with rapidly progressive renal failure and severe leg edema. She was diagnosed with AAV and treated with glucocorticoid and heparin calcium to prevent deep vein thrombosis. Eight days after the start of heparin calcium, her platelet count decreased and the anti-platelet factor 4-heparin complex antibody was strongly positive (>5.0 U/mL; the cutoff point of the anti-platelet factor 4-heparin complex antibody evaluated by the latex turbidity assay is 1.0 U/mL). She was diagnosed with HIT and treated with argatroban. Subsequently, her platelet counts increased gradually. CONCLUSION: We encountered a case of HIT that developed prior to the induction of hemodialysis in the clinical course of AAV. When AAV clinical course presents thrombocytopenia, the possibility of HIT should be considered.
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spelling pubmed-66798372019-08-19 A Case of Heparin-Induced Thrombocytopenia That Developed in the Therapeutic Course of Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis Nonaka, Taketoshi Harada, Makoto Sumi, Masahiko Ishii, Wataru Ichikawa, Tohru Kobayashi, Mamoru Case Rep Rheumatol Case Report BACKGROUND: Heparin-induced thrombocytopenia (HIT) causes thrombocytopenia via an immunological mechanism, resulting in severe organ injury due to arterial-venous thrombosis. HIT often develops in hemodialysis patients owing to heparin use. Anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV) is a systemic vasculitis, and cases of AAV complicated with HIT are rare. In addition, it mostly occurs in patients undergoing hemodialysis. CASE PRESENTATION: An 87-year-old woman presented with rapidly progressive renal failure and severe leg edema. She was diagnosed with AAV and treated with glucocorticoid and heparin calcium to prevent deep vein thrombosis. Eight days after the start of heparin calcium, her platelet count decreased and the anti-platelet factor 4-heparin complex antibody was strongly positive (>5.0 U/mL; the cutoff point of the anti-platelet factor 4-heparin complex antibody evaluated by the latex turbidity assay is 1.0 U/mL). She was diagnosed with HIT and treated with argatroban. Subsequently, her platelet counts increased gradually. CONCLUSION: We encountered a case of HIT that developed prior to the induction of hemodialysis in the clinical course of AAV. When AAV clinical course presents thrombocytopenia, the possibility of HIT should be considered. Hindawi 2019-07-22 /pmc/articles/PMC6679837/ /pubmed/31428502 http://dx.doi.org/10.1155/2019/2724304 Text en Copyright © 2019 Taketoshi Nonaka et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Case Report
Nonaka, Taketoshi
Harada, Makoto
Sumi, Masahiko
Ishii, Wataru
Ichikawa, Tohru
Kobayashi, Mamoru
A Case of Heparin-Induced Thrombocytopenia That Developed in the Therapeutic Course of Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis
title A Case of Heparin-Induced Thrombocytopenia That Developed in the Therapeutic Course of Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis
title_full A Case of Heparin-Induced Thrombocytopenia That Developed in the Therapeutic Course of Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis
title_fullStr A Case of Heparin-Induced Thrombocytopenia That Developed in the Therapeutic Course of Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis
title_full_unstemmed A Case of Heparin-Induced Thrombocytopenia That Developed in the Therapeutic Course of Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis
title_short A Case of Heparin-Induced Thrombocytopenia That Developed in the Therapeutic Course of Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis
title_sort case of heparin-induced thrombocytopenia that developed in the therapeutic course of anti-neutrophil cytoplasmic antibody-associated vasculitis
topic Case Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6679837/
https://www.ncbi.nlm.nih.gov/pubmed/31428502
http://dx.doi.org/10.1155/2019/2724304
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