Introduction
GCA, inflammatory bowel disease, Takayasu and giant cell arteritis, arthritis, infections, psoriasis, infection, Takayasu arteritis
INFLAMMATORY BOWEL DISEASE, INFLAMMATION, LARGE VESSEL VASCULITIS, INFECTIONS, ARTHRITIS, GIANT CELL ARTERITIS, PSORIASIS, GRANULOMATOUS INFLAMMATION, INFECTION, GCA, TAKAYASU ARTERITIS
Edited by: Ryu Watanabe, Osaka Metropolitan University, JapanReviewed by: Shuji Sumitomo, Kobe City Medical Center General Hospital, Japan; Eamonn Molloy, St Vincent’s University Hospital, IrelandThe Janus kinase (JAK)–STAT signaling pathway is relevant in both Takayasu and giant cell arteritis (GCA), and the use of JAK inhibitors (JAKi) in arthritis, psoriasis, and inflammatory bowel disease is nowadays common. Some evidence of the clinical efficacy of JAKi in GCA exists and a phase III randomized controlled trial (RCT) of upadacitinib is currently recruiting. In 2017, we started using barcitinib in a GCA patient with inadequate response to corticosteroids, and later on, we treated other 14 GCA patients with baricitinib/tofacitinib during intense follow-up. The retrospective data of these 15 individuals are here summarized. GCA was diagnosed based on the ACR criteria and/or imaging techniques combined with increased C-reactive protein (CRP) and/or erythrocyte sedimentation rate (ESR) followed by a good initial response to corticosteroids. JAKi was initiated based on inflammatory activity, with increased CRP, presumably dependent on GCA with clinical symptoms, despite unsatisfying high doses of prednisolone. The mean age at JAKi initiation was 70.1 years and the mean exposure to JAKi was 19 months. From initiation, significant reductions in CRP were seen already at 3 (Giant cell arteritis (GCA) and Takayasu arteritis (TAK) constitute two different types of large vessel vasculitis (Immunomechanistic studies of GCA and TAK have revealed that dendritic cells in the arterial wall attract T cells and macrophages, and subsequently, granulomatous inflammation is formed. Several cytokines are involved in this process, for example, interleukin (IL)-6, IL-17, TNF, and interferon (IFN)-γ (Many cytokines bind to extracellular receptors. Intracellularly, the pro-inflammatory signal of IL-6 and many other cytokines is mediated by the Janus kinase (JAK)/STAT pathway, and JAK–STAT signaling has proved important in both TAK and GCA (The JAKi baricitinib is more selective to JAK1 and JAK2, and baricitinib has been studied in 15 GCA patients in a pilot study with promising results (By tradition, treatment of GCA starts with corticosteroids. High doses are effective, but in some patients, tapering the dose is difficult without getting a rebound of inflammation. In 2017, we started using baricitinib in a GCA patient with inadequate response to corticosteroids and where the abolishment of CRP reaction by TCZ in case of infection would have caused problems. Since then, we have treated other 14 GCA patients (who had failed on corticosteroids and/or TCZ, or where IL-6-blocking regimen with TCZ was considered inappropriate due to increased risk of, or impaired ability to diagnose, infections) with baricitinib or tofacitinib for ≥6 months, and the retrospective data of these patients are summarized herein.