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Drug-induced anti-neutrophil cytoplasmic antibody-associated vasculitis
OBJECTIVE: In recent years, an increasing number of drugs have been proved to be associated with the induction of anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). This article reviews the latest research progress on drug-induced AAV. DATA SOURCES: We conducted a comprehensive...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Wolters Kluwer Health
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6940077/ https://www.ncbi.nlm.nih.gov/pubmed/31856057 http://dx.doi.org/10.1097/CM9.0000000000000539 |
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author | Weng, Cheng-Hua Liu, Zhi-Chun |
author_facet | Weng, Cheng-Hua Liu, Zhi-Chun |
author_sort | Weng, Cheng-Hua |
collection | PubMed |
description | OBJECTIVE: In recent years, an increasing number of drugs have been proved to be associated with the induction of anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). This article reviews the latest research progress on drug-induced AAV. DATA SOURCES: We conducted a comprehensive and detailed search of the PubMed database. The search terms mainly included drug-induced, ANCA, and vasculitis. STUDY SELECTION: We summarized the original articles and reviews on drug-induced AAV in recent years. The extracted information included the definition, epidemiology, associated drugs, pathogenesis, clinical features, diagnosis, treatment, and prognosis of drug-induced AAV. We also focused on the differences between drug-induced AAV and primary vasculitis. RESULTS: The offending drugs leading to drug-induced AAV are almost from pharmacologic categories and we need to be vigilant when using these drugs. The pathogenesis of drug-induced AAV might be multifactorial. The formation of neutrophil extracellular traps is an important mechanism for the development of drug-induced AAV. The clinical features of drug-induced AAV are similar to those of primary AAV. Understanding the difference between drug-induced AAV and primary AAV is helpful to identify drug-induced AAV. Stopping the offending drug at once after diagnosis may be sufficient for those patients with mild symptoms. Immunosuppressive therapy should only be used in patients with vital organs involvement. CONCLUSIONS: Patients with drug-induced AAV usually have a good prognosis if they stop using the offending drug immediately. Recent advances in research on AAV are expected to help us better understand the pathogenesis of drug-induced AAV. |
format | Online Article Text |
id | pubmed-6940077 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Wolters Kluwer Health |
record_format | MEDLINE/PubMed |
spelling | pubmed-69400772020-02-04 Drug-induced anti-neutrophil cytoplasmic antibody-associated vasculitis Weng, Cheng-Hua Liu, Zhi-Chun Chin Med J (Engl) Review Articles OBJECTIVE: In recent years, an increasing number of drugs have been proved to be associated with the induction of anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). This article reviews the latest research progress on drug-induced AAV. DATA SOURCES: We conducted a comprehensive and detailed search of the PubMed database. The search terms mainly included drug-induced, ANCA, and vasculitis. STUDY SELECTION: We summarized the original articles and reviews on drug-induced AAV in recent years. The extracted information included the definition, epidemiology, associated drugs, pathogenesis, clinical features, diagnosis, treatment, and prognosis of drug-induced AAV. We also focused on the differences between drug-induced AAV and primary vasculitis. RESULTS: The offending drugs leading to drug-induced AAV are almost from pharmacologic categories and we need to be vigilant when using these drugs. The pathogenesis of drug-induced AAV might be multifactorial. The formation of neutrophil extracellular traps is an important mechanism for the development of drug-induced AAV. The clinical features of drug-induced AAV are similar to those of primary AAV. Understanding the difference between drug-induced AAV and primary AAV is helpful to identify drug-induced AAV. Stopping the offending drug at once after diagnosis may be sufficient for those patients with mild symptoms. Immunosuppressive therapy should only be used in patients with vital organs involvement. CONCLUSIONS: Patients with drug-induced AAV usually have a good prognosis if they stop using the offending drug immediately. Recent advances in research on AAV are expected to help us better understand the pathogenesis of drug-induced AAV. Wolters Kluwer Health 2019-12-05 2019-12-05 /pmc/articles/PMC6940077/ /pubmed/31856057 http://dx.doi.org/10.1097/CM9.0000000000000539 Text en Copyright © 2019 The Chinese Medical Association, produced by Wolters Kluwer, Inc. under the CC-BY-NC-ND license. http://creativecommons.org/licenses/by-nc-nd/4.0 This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. http://creativecommons.org/licenses/by-nc-nd/4.0 |
spellingShingle | Review Articles Weng, Cheng-Hua Liu, Zhi-Chun Drug-induced anti-neutrophil cytoplasmic antibody-associated vasculitis |
title | Drug-induced anti-neutrophil cytoplasmic antibody-associated vasculitis |
title_full | Drug-induced anti-neutrophil cytoplasmic antibody-associated vasculitis |
title_fullStr | Drug-induced anti-neutrophil cytoplasmic antibody-associated vasculitis |
title_full_unstemmed | Drug-induced anti-neutrophil cytoplasmic antibody-associated vasculitis |
title_short | Drug-induced anti-neutrophil cytoplasmic antibody-associated vasculitis |
title_sort | drug-induced anti-neutrophil cytoplasmic antibody-associated vasculitis |
topic | Review Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6940077/ https://www.ncbi.nlm.nih.gov/pubmed/31856057 http://dx.doi.org/10.1097/CM9.0000000000000539 |
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