Abstract
Clinical recognition of drug-induced vasculitic and lupus-like syndromes is very important because continued use of the offending drug can lead to irreversible and life-threatening vasculitic organ damage (e.g. end-stage renal disease or pulmonary haemorrhage). Withdrawal of the drug often leads to spontaneous recovery, meaning that immunosuppressive therapy can be avoided. The presence of myeloperoxidase–antineutrophil cytoplasmic antibodies, IgM anticardiolipin antibody, and antihistone antibodies in combination was found to be characteristic of drug-induced vasculitic syndromes caused by the antithyroid drugs propylthiouracil and methimazol. Clinically, skin vasculitis and arthralgias predominated and renal vasculitis was rare.
Highlights
The differential diagnosis between drug-induced and idiopathic vasculitic conditions may be difficult in the individual patient
The report by Branka Bonaci-Nikolic and coworkers [1] included in this issue of Arthritis Research and Therapy is a good example of clinical research aimed at identifying details that can aid in distinguishing between seemingly related syndromes, such as idiopathic vasculitides (IVs) and druginduced vasculitides (DIVs)
Cutaneous vasculitis was found to be most common in the DIV patients, being present in 63%, whereas it was found in only 25% of the IV patients
Summary
The differential diagnosis between drug-induced and idiopathic vasculitic conditions may be difficult in the individual patient. The study included 72 consecutive patients who had been found to be positive for antineutrophil cytoplasmic antibodies (ANCAs) directed at proteinase-3 or myeloperoxidase Twentynine of these patients suffered from Wegener’s granulomatosis, 23 from microscopic polyangiitis, four from Churg–Strauss syndrome, and 16 from a DIV caused by either propylthiouracil or methimazol. DIV patients were mostly positive for myeloperoxidase–ANCAs and were positive for ANAs and antihistone antibodies, and had high levels of IgM anticardiolipin antibodies and low C4 values. Others have observed a characteristic development of ANAs and antihistone antibodies as well as myeloperoxidase–ANCAs in such patients, the latter being likely to be caused by drug-induced damage directed at the neutrophils that process the drug [6]
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