| Literature DB >> 32540394 |
Ichiro Takeuchi1, Toshinao Kawai2, Meika Nambu2, Ohsuke Migita3, Satoshi Yoshimura4, Kenichi Nishimura5, Takako Yoshioka6, Masao Ogura7, Reiko Kyodo8, Hirotaka Shimizu8, Shuichi Ito5, Motohiro Kato4, Masafumi Onodera2, Kenichiro Hata3, Yoichi Matsubara9, Katsuhiro Arai8.
Abstract
X-linked inhibitor of apoptosis protein (XIAP) deficiency results in monogenic inflammatory bowel disease. To date, no vasculitis associated with XIAP deficiency has been reported. A 10-year-old boy was diagnosed with Crohn's disease and he responded poorly to conventional treatment for Crohn's disease. He was dependent on corticosteroids and parenteral nutrition. To manage severe colitis, he underwent ileostomy followed by ileocolectomy for an ileo-sigmoid fistula. At the age of 15 years, he developed IgA vasculitis and at the age of 17 years, he developed refractory Takayasu arteritis (TAK), which was resistant to corticosteroid and immunosuppressive therapy. Whole-exome sequencing revealed a novel mutation of the splice acceptor site in XIAP (c.1057-1G > A) at the age of 19 years. Allogeneic hematopoietic stem cell transplantation was successful with subsequent withdrawal of intensive immunosuppressive therapy and clinical remission of both enterocolitis and TAK. This case suggests that patients with XIAP deficiency could develop intractable inflammatory disease involving the intestinal tract and blood vessels.Entities:
Keywords: Monogenic inflammatory bowel disease; Takayasu arteritis; Whole-exome sequencing; X-linked inhibitor of apoptosis protein deficiency; X-linked lymphoproliferative disorder type 2
Year: 2020 PMID: 32540394 DOI: 10.1016/j.clim.2020.108495
Source DB: PubMed Journal: Clin Immunol ISSN: 1521-6616 Impact factor: 3.969