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IL-17 and IL-23 inhibitors have shown successful results in improving skin lesions in the treatment of moderate-to-severe plaque psoriasis. However, psoriasis is a chronic inflammatory disease characterized by systemic inflammation including joints in addition to skin lesions. Therefore, in this retrospective and observational cohort study, we aimed to evaluate the effect of IL-17 inhibitors (secukinumab and ixekizumab) and IL-23 inhibitors (risankizumab and guselkumab) on systemic inflammation in psoriasis.

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Obesity is a metabolic disease that is marked by excessive fat accumulation and is objectively defined as a body mass index (BMI) ≥30 kg/m2. Obesity is associated with several other comorbidities, including psoriasis, which is a chronic autoimmune skin disease. Adipocytes produce pro-inflammatory signaling molecules, namely adipokines and classic cytokines, that drive increased inflammation axnd may contribute to the pro-inflammatory pathways driving psoriasis disease pathogenesis.

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We present a case of a patient with longstanding psoriasis vulgaris who developed an atopic dermatitis-like eruption following long-term IL-17A inhibitor therapy. Following many years of excellent disease control with secukinumab and later ixekizumab, he developed a de novo eczematous eruption, which showed spongiotic dermatitis upon biopsy. The patient was successfully treated for both psoriasis and atopic dermatitis with upadacitinib, a Janus kinase inhibitor.

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the present multicenter retrospective study aimed to evaluate the efficacy and safety of intra-class switching between interleukin-17A (IL-17A) inhibitors, specifically from ixekizumab to secukinumab, in patients with plaque psoriasis. this study included 11 patients (6 male, 5 female) who had previously received ixekizumab and then were switched to secukinumab. Patients' PASI, DLQI, and pain VAS (in those with psoriatic arthritis) were evaluated at weeks 16, 24, 54, and 98.

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