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Psoriasis Review

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The IPC Psoriasis Review provides practicing physicians with an authoritative research review that targets a range of key psoriasis publications most relevant to current clinical practice. The newsletter leverages the collective research and clinical expertise of IPC’s Councilors to identify the most important publications in psoriasis from the past year and provide a concise editorial commentary on the value of these publications.


Efficacy and safety of risankizumab in moderate-to-severe plaque psoriasis (UltIMMa-1 and UltIMMa-2): results from two double-blind, randomised, placebo-controlled and ustekinumab-controlled phase 3 trials.

Risankizumab is a humanized IgG1 monoclonal antibody that binds to the p19 subunit of interleukin-23. It therefore inhibits this cytokine, which plays a key role in psoriatic inflammation. The aim of this study was to compare the efficacy and safety of risankizumab with placebo and with ustekinumab in moderate to severe chronic plaque psoriasis. Two replicate, multi-center, phase 3 studies across 14 countries involved 506 and 491 patients who were randomly assigned (3:1:1) to risakizumab 150 mg, ustekinumab 45 or 90 mg, or placebo for the initial double-blind 16 weeks. At week 16, the placebo group switched to risankizumab and the other patients continued on their original drug up to week 52. A Psoriasis Area and Severity Index (PASI) score of 90 was achieved at 16 weeks by 75.3% in the first study and 74.8% in the second study of patients on risakizumab, by 42% and 47.5% respectively, of patients on ustekinumab, and by 4.9% and 2.0% of patients on placebo. Confidence intervals were reported and demonstrated clear differences between the treatment groups. Secondary outcome measures included the Dermatology Life Quality Index (DLQI)* and the Psoriasis Symptom Scale (PSS), which scores the severity of pain, redness, itching, and burning. A DLQI score of 0 or 1 was achieved at week 16 by 66% and 67% of patients on risakizumab, by 43% and 46% on ustekinumab, and by 8% and 4% patients on placebo. A PSS score of 0 was achieved at 16 weeks by 29% and 31% of patients on risakizumab, 15% and 15% patients on ustekinumab, and 2% and 0% patents on placebo. Treatment-emergent adverse events were similar across patients treated with risakizumab, ustekinumab, and placebo.

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IL-1 and IL-36 are dominant cytokines in generalized pustular psoriasis


This study from the Journal of Allergy and Clinical Immunology investigated the expression of IL-1 and IL-36 in generalized pustular psoriasis (GPP). The various cytokines involved in psoriasis were examined by gene expression studies in paraffin-embedded sections from lesional skin. GPP was compared with psoriasis vulgaris (PV). Significant contributions of IL-17A, TNF, IL-1, IL-36, and interferons in both diseases were detected in both variants, but GPP had higher IL-36 and IL-1 expression and lower IL-17A and IFN-g mRNA expression than PV lesions. The investigators detected prominent IL-36 expression by keratinocytes proximal to neutrophilic pustules and it was also shown that proteases from neutrophils activated IL-36. The protease inhibitors serpin A1 and A3, which are inhibitors of elastase and cathepsin G, were also detected in both diseases and inhibited IL-36. These findings explain why many standard treatments for PV, such as acitretin, cyclosporine and even TNF-α blockers, do not seem to work well in GPP. The data from this paper provides a basis for targeted effective drug therapy in GPP, which is characterized by periodic neutrophil infiltration into the skin and development of pustules. There was a strongly enhanced expression of the neutrophil chemokines CXCL1, CXCL2, and CXCL8 (IL-8) in GPP, which enhanced the induction of neutrophils into the epidermis. Compared to PV, there were between 5 to 15 more transcripts of these chemokines, thus establishing a clear difference in the pathomechanism of the two conditions. IL-1 has three isoforms, IL-35 alpha, beta, and gamma. They drive the keratinocyte inflammatory process and synergize with the rest of the inflammation in the skin. TNF-α is a central mediator in chronic plaque psoriasis as evidenced by the effectiveness of therapies that block TNF-α activity. Infliximab has most commonly been used for GPP and PV among the TNF-α blockers. This is because of the inhibition of the synergy between TNF-α and IL-36 and other cytokines. This study also detected increased IL-17A activity in GPP lesions, opening up an area of targeted therapy for GPP.

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