Our patient was a 46-year-old man who had been diagnosed with plaque psoriasis 27 years earlier and reported no previous axial or peripheral joint signs. Over the preceding years he had responded poorly to narrowband ultraviolet-B phototherapy, methotrexate, cyclosporine, etanercept, adalimumab, ustekinumab, and infliximab. At the time of the consultation he had numerous generalized plaques (psoriasis area and severity index [PASI], 10). Treatment was started with subcutaneous ixekizumab at the usual dose. After the first dose of 160 mg, the patient reported generalized migratory arthralgias that intensified and became disabling after the second dose of 80 mg, prompting an emergency visit to the rheumatology service. Physical examination revealed pain and marked limitation of cervical spinal cord mobility with no involvement of the lumbar or sacroiliac spinal cord (normal response in the Schober test and negative response to sacroiliac manipulation), pain and limited mobility of the scapular and pelvic girdles, pain and mild swelling of the carpal joints, and pain without swelling in the ankles, knees, and the small joints of the fingers. The painful joint count (PJC28) was 10 (carpal joints, knees, shoulders, and second and third bilateral metacarpophalangeal joints), and the swollen joint count (SJC28) was 2 (carpal joints). Based on these findings, the patient was diagnosed with paradoxical arthritis. With the patient's consent ixekizumab treatment was discontinued, and he was treated with a tapering dose of oral prednisone (20 mg/d) for 10 days, resulting in almost complete resolution of the joint problems. Upon reaching the end of the corticosteroid regimen, the patient was treated with secukinumab at the usual dose (300 mg). After 10 months of coordinated monitoring by the dermatology and rheumatology services, the patient's psoriasis had markedly improved (PASI, 1), with no adverse effects or joint symptoms.

Ixekizumab is a humanized IgG4 monoclonal antibody that acts to neutralize IL-17A, and in clinical trials has shown high efficacy in patients with plaque psoriasis1 and psoriatic arthritis,2 with an acceptable safety profile3 and no adverse effects on joints. In the present case, the coincidence of ixekizumab injections and the sudden onset of joint symptoms in a patient with no history of arthritis, together with the progressive disappearance of these symptoms after ixekizumab discontinuation, suggest a causal relationship between ixekizumab and this adverse effect. The literature describes several cases of so-called paradoxical psoriatic arthritis coinciding with the use of biological treatments for plaque psoriasis, including efalizumab,4 etanercept, adalimumab,5 infliximab, and ustekinumab,6 but none involving IL-17 inhibitors. The appearance of paradoxical psoriatic arthritis in this case underscores the pathogenic complexity of this disease.

In conclusion, despite the absence from the literature of any reports of adverse joint effects caused by ixekizumab, we describe a case of paradoxical arthritis that was associated with ixekizumab treatment, discontinuation of which was ultimately required. Long-term follow-up studies will be necessary to determine the frequency and causality of this adverse effect.