Dear Editors,

Tyrosine kinase 2 (TYK2) is a member of Janus kinase (JAK) family. Although, clinical efficacy of TYK2 inhibitor, deucravacitinib, for psoriatic arthritis (PsA) has been reported [1], the radiological assessment was not conducted in the study. We herein report the first case of radiological improvement in PsA after deucravacitinib treatment.

A 46-year-old Japanese woman with a 25-year history of plaque psoriasis had been treated with 8 mg weekly of methotrexate for the last 2 years for concomitant PsA on the right wrist, fingers, and knee, which developed 3 years before. While her joint symptoms improved, skin lesions were not sufficiently ameliorated. At presentation, she had extensive scaly erythema on the trunk and extremities, with psoriasis area and severity index (PASI) and body surface area (BSA) 14.8% and 28%, respectively (Figure 1A). She was enrolled in POETYK PSO-4 trial (NCT03924427), a prospective, open-label, single-arm, phase 3 trial evaluating efficacy and safety of deucravacitinib for moderate to severe plaque psoriasis and its extension trail POETYK PSO-LTE (NCT04036435). Two years later, her PASI and BSA improved to 1 and 0.5, respectively, without adverse events (Figure 1B). Although joint assessment was not included in the study protocols, clinical and radiographical assessment for joint symptoms was also conducted. Her arthritis remained in clinical remission during the 2 years, and X-ray image showed disappearance of bone erosion in the right third distal interphalangeal joint (DIP) as compared to the findings before the initiation of deucravacitinib treatment (Figures 1C–E).

Deucravacitinib is currently approved for plaque psoriasis but not for PsA. The involvement of TYK2 in the pathophysiology of psoriatic arthritis (PsA) is still to be elucidated. TYK2 medicates intracellular signaling of interferon-α/β, interleukin (IL)-12, IL-23, IL-10 family cytokines (IL-10, IL-26, and IL-22), IL-6, and IL-13, by pairing with JAK1 or JAK2 [2]. On the other hand, IL-23 and its downstream IL-17 are pathogenic cytokines not only in plaque psoriasis but also in PsA [3]. Structural bone damage is a feature of PsA as a result of joint inflammation affecting cartilage and bone. Recently, the efficacy of IL-6 inhibitors for joint/bone repair in inflammatory arthritis draws much attention. In rheumatoid arthritis, an IL-6 inhibitor tocilizumab has been shown to repair bone erosion [4]. Moreover, Kutsuna et al. reported effectiveness of tocilizumab in a patient with progressive and destructive PsA [5]. They confirmed radiological repair of the bone cyst at the lateral humeral condyle in the elbow and repair of the DIP joints [5]. Since deucravacitinib also suppresses IL-6 signaling, inhibition of IL-6 in addition to IL-23 may have contributed to bone erosion repair in our case. Further research is necessary to elucidate the efficacy of deucravacitinib for PsA.