RESUMEN
Following the market authorization of interleukin (IL)-17 inhibitors, a growing number of cases of IL-17 inhibitor-induced paradoxical psoriasis (PsO) have been reported. Our objectives were to present two cases of IL-17 inhibitor-induced paradoxical PsO and to systematically review the literature for similar cases, summarizing and presenting the relevant data. A systematic literature review of previously presented cases of paradoxical PsO induced by IL-17 inhibitors was conducted. We presented two patients with axial spondyloarthritis (axSpA) and paradoxical PsO induced by secukinumab (SEC). One patient's psoriatic lesions responded well to adjuvant topical treatment, while the other patient required a combination of topical treatment and cyclosporine Α for successful treatment. SEC was continued in both cases. We also identified 35 patients with IL-17 inhibitor-induced paradoxical PsO in the literature review. The most frequent types of paradoxical PsO were palmoplantar pustular and plaque PsO, while the median latency period was 11 weeks. Approximately one-third of patients continued IL-17 inhibitor treatment with adjunctive therapy, primarily topical, which produced satisfactory results in most patients. Almost two-thirds of the patients discontinued the IL-17 inhibitor, with the majority of patients switching to another biological agent with a different mechanism of action or initiating other systemic antipsoriatic treatments, resulting in mainly satisfactory outcomes. Therefore, paradoxical PsO induced by IL-17 inhibitors appears to respond well in both patients who continue IL-17 inhibitors with adjunctive treatment and those who discontinue IL-17 inhibitors while switching to a different class of biological agent or initiating other systemic antipsoriatic treatments.
RESUMEN
Cases of systemic lupus erythematosus (SLE) following psoriatic arthritis (PsA) or vice versa are uncommon. Due to the complexity of autoimmune diseases and the rarity of such cases, comprehensive global data on the co-occurrence of these conditions are limited. Moreover, the pathophysiology concerning the coexistence of SLE and PsA has yet to be fully understood. Interestingly, the progression of both diseases appears to be significantly influenced by the key interleukin (IL) 17, particularly IL-17A. Here, we report 7 cases of SLE and PsA coexistence. In 5 of these cases, PsA occurred before the development of SLE, while in the remaining 2 cases, SLE was diagnosed before PsA. The PsA was characterized mainly by peripheral arthritis without any axial involvement, while the manifestations of SLE varied, with 3 developing systematic severe manifestations. Therapeutic challenges were posed in all cases, as treating one condition could worsen the other. Finally, we review the literature providing the current knowledge on the coexistence of these conditions. Overall, all reported cases emphasize the importance of personalized treatment and careful monitoring for patients with both SLE and PsA.
