Brief Report: Takayasu Arteritis and Ulcerative Colitis: High Rate of Co‐Occurrence and Genetic Overlap
2015; Wiley; Volume: 67; Issue: 8 Linguagem: Inglês
10.1002/art.39157
ISSN2326-5205
AutoresChikashi Terao, Takayoshi Matsumura, Hajime Yoshifuji, Yohei Kirino, Yasuhiro Maejima, Yoshikazu Nakaoka, Meiko Takahashi, Eisuke Amiya, Natsuko Tamura, Toshiki Nakajima, Tomoki Origuchi, Tetsuya Horita, Mitsuru Matsukura, Yuta Kochi, Akiyoshi Ogimoto, Motohisa Yamamoto, Hiroki Takahashi, Shingo Nakayamada, Kazuyoshi Saito, Yoko Wada, Ichiei Narita, Yasushi Kawaguchi, Hisashi Yamanaka, Koichiro Ohmura, Tatsuya Atsumi, Kazuo Tanemoto, Tetsuro Miyata, Masataka Kuwana, Issei Komuro, Yasuharu Tabara, Atsuhisa Ueda, Mitsuaki Isobe, Tsuneyo Mimori, Fumihiko Matsuda,
Tópico(s)Renal Diseases and Glomerulopathies
ResumoObjective Takayasu arteritis (TAK) is a systemic vasculitis affecting large arteries and large branches of the aorta. Ulcerative colitis (UC) is a prevalent autoimmune colitis. Since TAK and UC share HLA–B*52:01 and IL12B as genetic determinants, and since there are case reports of the co‐occurrence of these diseases, we hypothesized that UC is a common complication of TAK. We undertook this study to perform a large‐scale analysis of TAK, both to evaluate the prevalence of concurrent cases of TAK and UC and to identify and estimate susceptibility genes shared between the 2 diseases. Methods We analyzed a total of 470 consecutive patients with TAK from 14 institutions. We characterized patients with TAK and UC by analyzing clinical manifestations and genetic components. Genetic overlapping of TAK and UC was evaluated with the use of UC susceptibility single‐nucleotide polymorphisms by comparing risk directions and effect sizes between susceptibility to the 2 diseases. Results Thirty of 470 patients with TAK had UC (6.4% [95% confidence interval 4.3–9.0]). This percentage was strikingly higher than that expected from the prevalence of UC in Japan. Patients with TAK complicated with UC developed TAK at an earlier stage of life ( P = 0.0070) and showed significant enrichment of HLA–B*52:01 compared to TAK patients without UC ( P = 1.0 × 10 −5 ) (odds ratio 12.14 [95% confidence interval 2.96–107.23]). The 110 non‐HLA markers of susceptibility to UC significantly displayed common risk directions with susceptibility to TAK ( P = 0.0054) and showed significant departure of permutation P values from expected P values ( P < 1.0 × 10 −10 ). Conclusion UC is a major complication of TAK. These 2 diseases share a significant proportion of their genetic background, and HLA–B*52:01 may play a central role in their co‐occurrence.
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