作者
Maki Fukuzono,Katsuhito Sasaki,Yuki Ichimura,Sae Inoue,Riko Iwasaki,H Imai,Akimasa Saito,Noriko Kubota,Ryota Tanaka,Yoshiyuki Nakamura,Yasuhiro Fujisawa,Manabu Fujimoto,Toshifumi Nomura,Naoko Okiyama
摘要
Dear Editor, Anti-synthetase syndrome (ASS) is a heterogeneous autoimmune disease characterized by the presence of autoantibodies against aminoacyl transfer RNA synthetases (ARS) with clinical features, including interstitial lung disease (ILD), arthritis, myositis, Raynaud’s phenomenon, fever, and/or mechanic’s hands. Eight types of anti-ARS antibodies have been identified: anti-histidyl, threonyl, alanyl, glycyl, isoleucyl, asparaginyl, phenylalanyl, and tyrosyl transfer RNA synthetase antibodies termed anti-Jo-1, PL-7, PL-12, EJ, OJ, KS, Zo, and Ha antibodies, respectively. Although the clinical features are similar in patients with these anti-ARS antibodies, there are some specific characteristics in each subgroup [1, 2]. Anti-PL-7 antibodies have been found in only 3–4% of all patients with idiopathic inflammatory myopathies [polymyositis (PM) and DM]. A European cohort of 18 patients with anti-PL-7 antibody-positive ASS revealed a high incidence of ILD, myositis, arthritis and pericardial effusion [3]. In a Japanese cohort of 7 patients with anti-PL-7 antibody-positive...