Drug-induced anti-neutrophil cytoplasmic antibody-associated vasculitis

Abstract

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.

Acute tubulointerstitial nephritis associated with antineutrophil cytoplasmic antibody following cimetidine treatment: a case report

“…Although certain drugs, such as propylthiouracil, may play a role in the pathogenesis of AAV [ 9 , 10 ], the relationship between most drugs and ATIN associated with ANCA is tentative and the pathological mechanisms are unknown. Most cases of drug-induced AAV improve after withdrawal of the suspected drug, but in severe cases, steroids may be required [ 11 ]. It is, therefore, difficult to distinguish between drug-induced AAV and primary AAV based on clinical symptoms, laboratory markers, and pathological findings [ 11 ].…”

“…Most cases of drug-induced AAV improve after withdrawal of the suspected drug, but in severe cases, steroids may be required [ 11 ]. It is, therefore, difficult to distinguish between drug-induced AAV and primary AAV based on clinical symptoms, laboratory markers, and pathological findings [ 11 ].…”

Hydralazine-Induced Antineutrophil Cytoplasmic Antibody-Associated Vasculitis: Asymptomatic and Renal-Restricted Presentation

“…The culprits include anti-thyroid drugs (propylthiouracil, methimazole, carbimazole, and benzylthiouracil), tumor necrosis factor inhibitors (etanercept, infliximab, adalimumab, and golimumab) and hydralazine, rituximab, minocycline, and montelukast. Other drugs that have been shown to have a possible association with ANCA-associated vasculitis include cefotaxime, nitrofurantoin, trimethoprim-sulfamethoxazole, vancomycin, isoniazid, rifampicin, D-penicillamine, sulfasalazine, clozapine, thioridazine, allopurinol, indomethacin, atorvastatin, cocaine/levamisole, denosumab, isotretinoin, and phenytoin [ 6 ]. Because of the low incidence of drug-induced ANCA-associated vasculitis and the beneficial use of the previously mentioned drugs, there is no recommendation to preclude the use of these medications.…”

Localized Forms of Vasculitis

“…Druginduced antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a notable exception, in which a year or more can separate the start of the causative medication and the clinical manifestations [8]. There is a large variety of drugs associated with drug-induced ANCA-associated vasculitis which mainly include anti-thyroid drugs and tumor necrosis factor inhibitors [22]. Notably, it has been suggested that the risk of developing AAV may be related to the duration of treatment with some drugs, such as propylthiouracil [22].…”

“…There is a large variety of drugs associated with drug-induced ANCA-associated vasculitis which mainly include anti-thyroid drugs and tumor necrosis factor inhibitors [22]. Notably, it has been suggested that the risk of developing AAV may be related to the duration of treatment with some drugs, such as propylthiouracil [22]. When the provoking agent persists, such as in hepatitis Crelated cryoglobulinemic vasculitis or rheumatoid arthritis, chronic vasculitis can be observed, with fluctuating lesions or persistent lesions of different ages.…”