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Trichostasis spinulosa arising in isolated collagenoma of the scalp

531 negative six months later, but MPO-ANCA remained elevated (figure 1D). Based on the clinical course and laboratory findings, PTU-induced AAV was diagnosed. Hyperthyroidism recurred eight months after withdrawal of PTU and was treated with methimazole. After 36 months of follow-up, the patient had no recurrence of vasculitis. A unique feature of this clinical course was that PR3-ANCA correlated well with disease activity. PR3-ANCA decreased soon after cessation of PTU, whereas MPO-ANCA titres remained high. Our patient was positive for both MPO-ANCA and PR3ANCA. It has been reported that 22.2-37.5% of patients with anti-thyroid drug-induced AAV show double positivity for MPO-ANCA and PR3-ANCA [7, 8]. The pathomechanism of PTU-induced AAV is not fully understood. One possible explanation for MPO-ANCA production is that PTU could alter the structure of MPO, which acts as a neoantigen [6, 9]. However, the mechanism of PR3-ANCA production remains unknown. PTU-induced MPO-ANCA seropositivity is usually asymptomatic. In a cohort study, 21 of 56 patients (37.5%) receiving long-term treatment with PTU developed MPOANCA seropositivity; PR3-ANCA was not detected in any patients. Among them, 12 (57.1%) had no symptoms [10]. MPO-ANCA seropositivity without vasculitis suggests that MPO-ANCA alone is insufficient to induce PTU-induced AAV. In this study, we focused on the chronological changes in ANCA titres. Several reports have indicated that MPOANCA titres correlate with disease activity, however, others have reported that MPO-ANCA became negative in only four of 15 patients (26.7%) during follow-up after discontinuation of PTU [4]. A recent review of PTU-induced AAV showed that five of six (83.3%) patients who were positive for both MPO-ANCA and PR3-ANCA at diagnosis were negative for PR3-ANCA at the last follow-up visit, however, only 33.3% (2/6) of patients showed negativity for MPO-ANCA at the last follow-up visit [8]. Detailed time course observations for PR3-ANCA titres in our case led us to hypothesize that PR3-ANCA may be a useful marker for disease activity in PTU-induced double ANCA-positive vasculitis. In summary, we report a case of PTU-induced double ANCA-positive vasculitis in which PR3-ANCA titres correlated with disease activity. However, it remains uncertain whether PR3-ANCA is a pathogenic antibody in PTUinduced double ANCA-positive vasculitis. Further reports are necessary to understand the pathomechanism of PTUinduced double ANCA-positive vasculitis.