ArticleMedicine2019
A case report dysregulated neutrophil extracellular traps in a patient with propylthiouracil-induced anti-neutrophil cytoplasmic antibody-associated vasculitis.
Article in Medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 8 citations in OpenAlex.
- Propylthiouracil-induced myeloperoxidase antineutrophil cytoplasmic antibody-associated leukocytoclastic vasculitis.JCEM case reports · 2026Article
- Role of Neutrophils in Systemic Vasculitides.Frontiers in immunology · 2020Review
- Propylthiouracil-Induced Antineutrophil Cytoplasmic Antibodies-Associated Vasculitis with Renal and Lung Involvement.Case reports in nephrology and dialysisArticle
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
rationaleNeutrophil extracellular traps (NETs) are immune defence systems that release extracellular chromatin and myeloid granules including myeloperoxidase (MPO) to kill pathogens. An experimental animal study recently demonstrated that disordered NETs induced by propylthiouracil (PTU) could contribute to the production of MPO anti-neutrophil cytoplasmic antibody (ANCA) and the development of ANCA-associated vasculitis (AAV). However, the role of dysregulated NETs in the pathogenesis of human AAV remains unclear. PATIENT CONCERNS: We report a 19-year-old woman with Graves' disease on PTU presented fever, polyarthralgia, and lung hemorrhage with high titer of MPO-ANCA. This patient had a variety of atypical ANCAs and disordered NETs in vitro. DIAGNOSES: A diagnosis of PTU-induced AAV (PTU-AAV).
interventionsThe PTU was discontinued and she was treated with immunosuppressants and plasmapheresis for reducing pathogenic autoantibodies. OUTCOMES: Clinical manifestations including fever, polyarthralgia, and lung hemorrhage were on remission with a decrease of dysregulated NETs. LESSONS: The clinical course of this PTU-AAV case indicated that dysregulated NETs would play a role in the development of ANCA and the pathogenesis of AAV.
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