Drug-induced vasculitis
Vascular injury due to drugs is recognized as a distinct entity under the Chapel Hill Consensus Conference 2012 definitions for vasculitis. Drug-induced vasculitis (DIV) may affect various types of vessels. Isolated cutaneous leukocytoclastic vasculitis is most commonly seen in association with anti...
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| Format: | Article |
| Language: | English |
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SAGE Publishing
2019-01-01
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| Series: | Indian Journal of Rheumatology |
| Subjects: | |
| Online Access: | http://www.indianjrheumatol.com/article.asp?issn=0973-3698;year=2019;volume=14;issue=5;spage=3;epage=9;aulast=Misra |
| _version_ | 1826910386643795968 |
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| author | Durga Prasanna Misra Pallavi Patro Aman Sharma |
| author_facet | Durga Prasanna Misra Pallavi Patro Aman Sharma |
| author_sort | Durga Prasanna Misra |
| collection | DOAJ |
| description | Vascular injury due to drugs is recognized as a distinct entity under the Chapel Hill Consensus Conference 2012 definitions for vasculitis. Drug-induced vasculitis (DIV) may affect various types of vessels. Isolated cutaneous leukocytoclastic vasculitis is most commonly seen in association with antibiotics and nonsteroidal anti-inflammatory drugs. Drug-induced antineutrophil cytoplasmic antibodies (ANCA)-associated vasculitis has been classically associated with cocaine (alone or contaminated with levamisole), antithyroid drugs (propylthiouracil, methimazole, carbimazole) and hydralazine; minocycline often mimics medium-vessel vasculitis, with ANCA positivity. Drug-induced large-vessel vasculitis remains rare; however, it has been reported with anticancer agents targeting immune pathways, including immune checkpoint inhibitors. Cerebral vasculitis has been associated with oral or topical sympathomimetic drug use. Operational pathogenetic mechanisms in DIV include immune complex deposition, abnormal generation of neutrophil extracellular traps, and bypassing of normal immune checkpoints like that between programmed cell death ligand 1 on dendritic cells and programmed cell death 1 on T-lymphocytes. DIV can have an unpredictable course, and a significant proportion of patients require immunosuppressive therapy in addition to drug withdrawal. |
| first_indexed | 2024-04-11T23:22:44Z |
| format | Article |
| id | doaj.art-f5f20396b2cd48759635fb3a08b0cca3 |
| institution | Directory Open Access Journal |
| issn | 0973-3698 0973-3701 |
| language | English |
| last_indexed | 2025-02-17T09:58:37Z |
| publishDate | 2019-01-01 |
| publisher | SAGE Publishing |
| record_format | Article |
| series | Indian Journal of Rheumatology |
| spelling | doaj.art-f5f20396b2cd48759635fb3a08b0cca32025-01-02T04:45:17ZengSAGE PublishingIndian Journal of Rheumatology0973-36980973-37012019-01-011453910.4103/0973-3698.272156Drug-induced vasculitisDurga Prasanna MisraPallavi PatroAman SharmaVascular injury due to drugs is recognized as a distinct entity under the Chapel Hill Consensus Conference 2012 definitions for vasculitis. Drug-induced vasculitis (DIV) may affect various types of vessels. Isolated cutaneous leukocytoclastic vasculitis is most commonly seen in association with antibiotics and nonsteroidal anti-inflammatory drugs. Drug-induced antineutrophil cytoplasmic antibodies (ANCA)-associated vasculitis has been classically associated with cocaine (alone or contaminated with levamisole), antithyroid drugs (propylthiouracil, methimazole, carbimazole) and hydralazine; minocycline often mimics medium-vessel vasculitis, with ANCA positivity. Drug-induced large-vessel vasculitis remains rare; however, it has been reported with anticancer agents targeting immune pathways, including immune checkpoint inhibitors. Cerebral vasculitis has been associated with oral or topical sympathomimetic drug use. Operational pathogenetic mechanisms in DIV include immune complex deposition, abnormal generation of neutrophil extracellular traps, and bypassing of normal immune checkpoints like that between programmed cell death ligand 1 on dendritic cells and programmed cell death 1 on T-lymphocytes. DIV can have an unpredictable course, and a significant proportion of patients require immunosuppressive therapy in addition to drug withdrawal.http://www.indianjrheumatol.com/article.asp?issn=0973-3698;year=2019;volume=14;issue=5;spage=3;epage=9;aulast=Misrahydralazineimmune checkpoint inhibitorleukocytoclastic vasculitislevamisoleminocyclinepropylthiouracil |
| spellingShingle | Durga Prasanna Misra Pallavi Patro Aman Sharma Drug-induced vasculitis Indian Journal of Rheumatology hydralazine immune checkpoint inhibitor leukocytoclastic vasculitis levamisole minocycline propylthiouracil |
| title | Drug-induced vasculitis |
| title_full | Drug-induced vasculitis |
| title_fullStr | Drug-induced vasculitis |
| title_full_unstemmed | Drug-induced vasculitis |
| title_short | Drug-induced vasculitis |
| title_sort | drug induced vasculitis |
| topic | hydralazine immune checkpoint inhibitor leukocytoclastic vasculitis levamisole minocycline propylthiouracil |
| url | http://www.indianjrheumatol.com/article.asp?issn=0973-3698;year=2019;volume=14;issue=5;spage=3;epage=9;aulast=Misra |
| work_keys_str_mv | AT durgaprasannamisra druginducedvasculitis AT pallavipatro druginducedvasculitis AT amansharma druginducedvasculitis |