gms | German Medical Science

Vorgeschichte: Takayasu Arthritis (TAK) is a systemic vasculitis affecting the large arteries [1]. First line approach is the use of high dose Glucocorticoids which can be combined with disease-modifying anti-rheumatic drugs. Other immunosuppressants including biological agents targeting tumor necrosis factor (TNF)-alpha or the interleukin (IL)-6 receptor are used to treat patients with refractory TAK [2]. Previous studies have shown some effect using the IL-12/23 antibody ustekinumab in refractory TAK [3].

We present the case of a 20-year-old woman emigrated from Afghanistan in whom refractory TAK was successfully treated with ustekinumab after failure of multiple biologic approaches.

In October 2016 she was diagnosed with TAK according to the classification criteria of TAK based on age under 40 years, claudication of extremities, blood pressure difference of more than 10 mmHg between arms and documented inflammation of the carotic arteries seen in MRI [4].

After initial treatment using high dose Glucocorticoids in combination with methotrexate without sufficient response treatment with infliximab was initiated in December 2016. In March 2017 the MRI showed only a mixed response and therapy was switched to tocilizumab. Unfortunately the patient flared after two months. A course with intravenous cyclophosphamide from July until November 2017 failed. From December 2017 throughout July 2018 treatment with adalimumab led to stable disease before in August 2018 therapy had to be switched to tocilizumab due to newly activity. In March 2019 after five administrations of tocilizumab the patient still complained about carotidynia while the MRI showed persistent inflammation. Given that the patient received two doses of rituximab without achieving clinical improvement and persisting elevation of all inflammatory parameters. Additional throughout the entire treatment the patients received courses with high dose intravenous Glucocorticoids and additionally low-dose Prednisolon.

In October 2019 the patient received 90 mg ustekinumab, followed by 90 mg 4 and 16 weeks later. Therapy was well tolerated and the patient reported an improvement of carotidynia. Inflammation parameters normalized and the MRI showed a reduction in inflammation. Mentionable the patient did not receive any additional intravenous Glucocorticoids.

This case demonstrates that the interleukin-12/23 antibody ustekinumab can be effective and safe in treating refractory TAK.

Disclosures: Beratertätigkeit für Janssen-Cilag