2f:I[703058,["/_next/static/immutable/chunks/3bhq_5eh1d760.js","/_next/static/immutable/chunks/2iy5wruuedsh6.js","/_next/static/immutable/chunks/2pfsjpn6k6zlg.js","/_next/static/immutable/chunks/26c7v3_3uwnwu.js","/_next/static/immutable/chunks/00yc7rcvua6a7.js","/_next/static/immutable/chunks/37ktb71aq3480.js","/_next/static/immutable/chunks/2d50b-7eu4558.js","/_next/static/immutable/chunks/06_yt270h41rg.js","/_next/static/immutable/chunks/2d6noqpp6ehas.js","/_next/static/immutable/chunks/1sx186c93bpzg.js","/_next/static/immutable/chunks/3dc-1n866s65i.js","/_next/static/immutable/chunks/20x2y96ldu5wx.js","/_next/static/immutable/chunks/2w1bvggzb0ga8.js","/_next/static/immutable/chunks/2051ffx3xzio9.js"],"PaperListPageClient"] 30:T6d0,This study investigated the role of IL-17 in Giant Cell Arteritis (GCA), which has remained uncertain despite previous research suggesting a contribution of Th17 cells to the disease. Temporal artery biopsies (TABs) were cultured ex vivo in MATRIGEL® with IL-17, secukinumab, or control IgG, and subsequently analyzed using bulk RNA-sequencing and RT-qPCR. Positive-TABs with GCA features were compared to negative-TABs or used to obtain in vitro cultures of myofibroblasts (MFs). Confocal microscopy analyzed IL-17 receptor expression. MFs and peripheral blood mononuclear cells co-cultures were used to study T-cell polarization. Transcriptomic analysis showed that secukinumab treatment of positive TABs reduced expression of genes linked to vascular inflammation, notably IL6. RT-qPCR analysis confirmed that secukinumab decreased mRNA encoding IL-6, CCL20, and GM-CSF in positive-TABs, while IL-17 upregulated them in negative-TABs. No changes were observed regarding the expression of genes related to vascular remodeling. IL-17 receptor chains were expressed on MFs, and their expression was enhanced by IFN-γ. RT-qPCR and Luminex® analyses confirmed IL-17-driven upregulation of IL-6, CCL20, CCL2, GM-CSF, and VEGF in MFs, which was reversed by secukinumab. Addition of IFN-γ to the culture increased the expression level of IL-17 receptor chains, resulting in a synergistic effect. Additionally, IL-17 pre-treated MFs promoted Th17 polarization. IL-17 exacerbates vascular inflammation in GCA by activating MFs and synergizing with IFN-γ to increase production of pro-inflammatory cytokines (IL-6, GM-CSF), chemokines (CCL20, CCL2), and angiogenic factors (VEGF, indicating that IL-17 is a key contributor to disease pathogenesis.31:Tc6b, Objectives This study investigated the role of IL‐17 in Giant Cell Arteritis (GCA), which has remained uncertain despite previous research suggesting a contribution of Th17 cells to the disease. Methods Temporal artery biopsies (TABs) were cultured ex vivo in MATRIGEL® with IL‐17, secukinumab, or control IgG, and subsequently analyzed using bulk RNA‐sequencing and RT‐qPCR. Positive‐TABs with GCA features were compared to negative‐TABs or used to obtain in vitro cultures of myofibroblasts (MFs). Confocal microscopy analyzed IL‐17 receptor expression. MFs and peripheral blood mononuclear cells co‐cultures were used to study T‐cell polarization. Results Transcriptomic analysis showed that secukinumab treatment of positive TABs reduced expression of genes linked to vascular inflammation, notably IL6 . RT‐qPCR analysis confirmed that secukinumab decreased mRNA encoding IL‐6, CCL20, and GM‐CSF in positive‐TABs, while IL‐17 upregulated them in negative‐TABs. No changes were observed regarding the expression of genes related to vascular remodeling. IL‐17 receptor chains were expressed on MFs, and their expression was enhanced by IFN‐γ. RT‐qPCR and Luminex® analyses confirmed IL‐17‐driven upregulation of IL‐6, CCL20, CCL2, GM‐CSF, and VEGF in MFs, which was reversed by secukinumab. Addition of IFN‐γ to the culture increased the expression level of IL‐17 receptor chains, resulting in a synergistic effect. Additionally, IL‐17 pre‐treated MFs promoted Th17 polarization. Conclusions IL‐17 exacerbates vascular inflammation in GCA by activating MFs and synergizing with IFN‐γ to increase production of pro‐inflammatory cytokines (IL‐6, GM‐CSF), chemokines (CCL20, CCL2), and angiogenic factors (VEGF, indicating that IL‐17 is a key contributor to disease pathogenesis.

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32:T4ab,The study included 4438 unique patients with psoriasis (2717 [61.2%] male; mean [SD] age, 45.0 [14.6] years at the time of their first treatment included in the study), 1039 (23.4%) of whom had comorbid psoriatic arthritis. A total of 3790 treatment series from bionaive patients were analyzed: 2646 were with adalimumab, 377 with secukinumab, and 767 with ustekinumab. The 5-year standardized risk of discontinuing ustekinumab was 0.37 (95% CI, 0.33-0.41), which was significantly lower than the standardized risks for adalimumab (0.51; 95% CI, 0.49-0.54) and secukinumab (0.54; 95% CI, 0.48-0.60). A total of 3403 treatment series from bioexperienced patients were analyzed: 790 were with adalimumab, 376 with bimekizumab, 192 with brodalumab, 218 with guselkumab, 556 with ixekizumab, 78 with risankizumab, 466 with secukinumab, and 727 with ustekinumab. The 2-year standardized absolute risk of discontinuing ustekinumab was 0.39 (95% CI, 0.36-0.43). Only bimekizumab (0.27; 95% CI, 0.20-0.34), guselkumab (0.29; 95% CI, 0.22-0.36), and risankizumab (0.25; 95% CI, 0.15-0.36) were associated with a significantly lower standardized absolute risk of discontinuation compared with ustekinumab.33:Taf0,Drug survival is an important measure to help guide treatment selection. However, clinical evidence for newer biologics, including bimekizumab, is limited. To determine the drug survival of biologics used for treating psoriasis in a routine clinical practice setting. This cohort study was based on data from the DERMBIO registry, which includes all patients treated with biologics for psoriasis in Denmark. All adult patients enrolled in DERMBIO from its inception in May 2007 until June 2025 were assessed for eligibility. Data were extracted in June 2025 and analyzed separately among those without previous biologic exposure (bionaive patients) and those with previous biologic exposure (bioexperienced patients). Adalimumab, secukinumab, and ustekinumab among bionaive patients and adalimumab, bimekizumab, brodalumab, guselkumab, ixekizumab, risankizumab, secukinumab, and ustekinumab among bioexperienced patients. The main outcome was standardized absolute risks of treatment discontinuation at 1, 2, and 5 years. Kaplan-Meier estimator was used to determine crude drug survival estimates and the Aalen-Johansen estimator was used to determine crude cause-specific absolute risks. The study included 4438 unique patients with psoriasis (2717 [61.2%] male; mean [SD] age, 45.0 [14.6] years at the time of their first treatment included in the study), 1039 (23.4%) of whom had comorbid psoriatic arthritis. A total of 3790 treatment series from bionaive patients were analyzed: 2646 were with adalimumab, 377 with secukinumab, and 767 with ustekinumab. The 5-year standardized risk of discontinuing ustekinumab was 0.37 (95% CI, 0.33-0.41), which was significantly lower than the standardized risks for adalimumab (0.51; 95% CI, 0.49-0.54) and secukinumab (0.54; 95% CI, 0.48-0.60). A total of 3403 treatment series from bioexperienced patients were analyzed: 790 were with adalimumab, 376 with bimekizumab, 192 with brodalumab, 218 with guselkumab, 556 with ixekizumab, 78 with risankizumab, 466 with secukinumab, and 727 with ustekinumab. The 2-year standardized absolute risk of discontinuing ustekinumab was 0.39 (95% CI, 0.36-0.43). Only bimekizumab (0.27; 95% CI, 0.20-0.34), guselkumab (0.29; 95% CI, 0.22-0.36), and risankizumab (0.25; 95% CI, 0.15-0.36) were associated with a significantly lower standardized absolute risk of discontinuation compared with ustekinumab. In this cohort study in Denmark, among bionaive patients with psoriasis, ustekinumab had superior drug survival compared with adalimumab and secukinumab, and among bioexperienced patients with psoriasis, bimekizumab, guselkumab, and risankizumab had superior drug survival. These results offer insight into the performance of different biologics in the treatment of psoriasis in a routine clinical practice setting.34:Tfc4, Importance Drug survival is an important measure to help guide treatment selection. However, clinical evidence for newer biologics, including bimekizumab, is limited. Objective To determine the drug survival of biologics used for treating psoriasis in a routine clinical practice setting. Design, Setting, and Participants This cohort study was based on data from the DERMBIO registry, which includes all patients treated with biologics for psoriasis in Denmark. All adult patients enrolled in DERMBIO from its inception in May 2007 until June 2025 were assessed for eligibility. Data were extracted in June 2025 and analyzed separately among those without previous biologic exposure (bionaive patients) and those with previous biologic exposure (bioexperienced patients). Exposures Adalimumab, secukinumab, and ustekinumab among bionaive patients and adalimumab, bimekizumab, brodalumab, guselkumab, ixekizumab, risankizumab, secukinumab, and ustekinumab among bioexperienced patients. Main Outcomes and Measures The main outcome was standardized absolute risks of treatment discontinuation at 1, 2, and 5 years. Kaplan-Meier estimator was used to determine crude drug survival estimates and the Aalen-Johansen estimator was used to determine crude cause-specific absolute risks. Results The study included 4438 unique patients with psoriasis (2717 [61.2%] male; mean [SD] age, 45.0 [14.6] years at the time of their first treatment included in the study), 1039 (23.4%) of whom had comorbid psoriatic arthritis. A total of 3790 treatment series from bionaive patients were analyzed: 2646 were with adalimumab, 377 with secukinumab, and 767 with ustekinumab. The 5-year standardized risk of discontinuing ustekinumab was 0.37 (95% CI, 0.33-0.41), which was significantly lower than the standardized risks for adalimumab (0.51; 95% CI, 0.49-0.54) and secukinumab (0.54; 95% CI, 0.48-0.60). A total of 3403 treatment series from bioexperienced patients were analyzed: 790 were with adalimumab, 376 with bimekizumab, 192 with brodalumab, 218 with guselkumab, 556 with ixekizumab, 78 with risankizumab, 466 with secukinumab, and 727 with ustekinumab. The 2-year standardized absolute risk of discontinuing ustekinumab was 0.39 (95% CI, 0.36-0.43). Only bimekizumab (0.27; 95% CI, 0.20-0.34), guselkumab (0.29; 95% CI, 0.22-0.36), and risankizumab (0.25; 95% CI, 0.15-0.36) were associated with a significantly lower standardized absolute risk of discontinuation compared with ustekinumab. Conclusions and Relevance In this cohort study in Denmark, among bionaive patients with psoriasis, ustekinumab had superior drug survival compared with adalimumab and secukinumab, and among bioexperienced patients with psoriasis, bimekizumab, guselkumab, and risankizumab had superior drug survival. These results offer insight into the performance of different biologics in the treatment of psoriasis in a routine clinical practice setting. 35:T9e5,The cardiovascular impact of biologics used in psoriasis is not fully understood. Several studies have suggested that the inhibition of the T-helper 17 cell pathway could lead to the destabilization of atherosclerotic plaques, leading to major adverse cardiovascular events (MACEs). To assess whether the initiation of interleukin (IL)-17(R)A inhibitors triggers MACEs. In this case-time-control study using the French National Health Insurance database, all individuals who received IL-17(R)A inhibitors (secukinumab, ixekizumab, and brodalumab) from 2016 to 2021, were included and classified according to their cardiovascular risk level. The risk period was defined as the 6 months before the MACE, and the reference period as the 6 months before the risk period. The same design for patients who received tumor necrosis factor (TNF)-α inhibitors (adalimumab or etanercept) for similar indications (psoriasis, psoriatic arthritis, ankylosing spondylitis, or juvenile arthritis), as an active comparator. The data analysis was conducted between April 2023 and August 2024. The initiation of the biologic was screened in both periods. The odds ratios (ORs) for the risk of MACEs were assessed following the initiation of IL-17(R)A inhibitors and TNF-α inhibitors independently. Subsequently, the OR for the risk of MACE associated with IL-17(R)A inhibitors was estimated using TNF-α inhibitors as the comparator. Among the 34 241 individuals who received an IL-17(R)A inhibitor, 381 MACEs were analyzed, including 176 acute coronary syndromes and 84 ischemic strokes in the main analysis. Initiation of IL-17(R)A inhibitors was not significantly associated with MACEs (OR, 1.25 [95% CI, 0.75-2.08] vs TNF-α inhibitor initiation and MACEs: OR, 0.90 [95% CI, 0.65-1.24]). Overall, the initiation of an IL-17(R)A inhibitor was not significantly associated with MACEs in the following 6 months, using TNF-α inhibitor as a comparator (OR, 1.40 [95% CI, 0.77-2.54]), regardless of the individual cardiovascular risk (P for homogeneity = .29). The definition of MACE was broadened in a first sensitivity analysis, and the risk period was shortened to 3 months in a second sensitivity analysis. The results did not change. In this case-time-control study based on a national insurance database, there was no evidence of a significant association between MACEs and the initiation of IL-17(R)A inhibitors, regardless of the individual cardiovascular risk of the patient. However, a modest risk increase cannot be entirely excluded.36:Tf24, Importance The cardiovascular impact of biologics used in psoriasis is not fully understood. Several studies have suggested that the inhibition of the T-helper 17 cell pathway could lead to the destabilization of atherosclerotic plaques, leading to major adverse cardiovascular events (MACEs). Objective To assess whether the initiation of interleukin (IL)-17(R)A inhibitors triggers MACEs. Design, Setting, and Participants In this case–time-control study using the French National Health Insurance database, all individuals who received IL-17(R)A inhibitors (secukinumab, ixekizumab, and brodalumab) from 2016 to 2021, were included and classified according to their cardiovascular risk level. The risk period was defined as the 6 months before the MACE, and the reference period as the 6 months before the risk period. The same design for patients who received tumor necrosis factor (TNF)–α inhibitors (adalimumab or etanercept) for similar indications (psoriasis, psoriatic arthritis, ankylosing spondylitis, or juvenile arthritis), as an active comparator. The data analysis was conducted between April 2023 and August 2024. Exposure The initiation of the biologic was screened in both periods. Main Outcomes and Measures The odds ratios (ORs) for the risk of MACEs were assessed following the initiation of IL-17(R)A inhibitors and TNF-α inhibitors independently. Subsequently, the OR for the risk of MACE associated with IL-17(R)A inhibitors was estimated using TNF-α inhibitors as the comparator. Results Among the 34 241 individuals who received an IL-17(R)A inhibitor, 381 MACEs were analyzed, including 176 acute coronary syndromes and 84 ischemic strokes in the main analysis. Initiation of IL-17(R)A inhibitors was not significantly associated with MACEs (OR, 1.25 [95% CI, 0.75-2.08] vs TNF-α inhibitor initiation and MACEs: OR, 0.90 [95% CI, 0.65-1.24]). Overall, the initiation of an IL-17(R)A inhibitor was not significantly associated with MACEs in the following 6 months, using TNF-α inhibitor as a comparator (OR, 1.40 [95% CI, 0.77-2.54]), regardless of the individual cardiovascular risk ( P for homogeneity = .29). The definition of MACE was broadened in a first sensitivity analysis, and the risk period was shortened to 3 months in a second sensitivity analysis. The results did not change. Conclusions In this case–time-control study based on a national insurance database, there was no evidence of a significant association between MACEs and the initiation of IL-17(R)A inhibitors, regardless of the individual cardiovascular risk of the patient. However, a modest risk increase cannot be entirely excluded. 25:[[["$","script","0",{"type":"application/ld+json","dangerouslySetInnerHTML":{"__html":"{\"@context\":\"https://schema.org\",\"@type\":\"CollectionPage\",\"name\":\"secukinumab: generic Research & Clinical Takeaways\",\"description\":\"Explore peer-reviewed papers on secukinumab (generic). Clinician-written summaries and actionable practice insights. 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no meta-analysis was conducted due to methodological heterogeneity.","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"warning","value":"Sex tag set to 'female' as the primary dataset covers maternal exposure; paternal exposure studies also exist but are a small subset (3 studies, 281 pregnancies).","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"warning","value":"The review included all indications for IL inhibitors (not psoriasis-only), so findings may not be fully generalizable to psoriasis patients specifically.","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"warning","value":"The sample size (n=5,962) reflects maternal pregnancy exposures across all included studies, not a single trial cohort; the majority originated from pharmacovigilance databases with inherent reporting bias.","value_numeric":null}],"summaries":{"what_studied":"A PRISMA-compliant systematic literature review (search date May 2026) evaluated the reproductive safety of IL-12/23, IL-17, and IL-23 inhibitors during pregnancy and with paternal exposure in patients with psoriasis, examining pregnancy and neonatal outcomes across all available study designs.","key_result":"49 publications met inclusion criteria, reporting 5,962 pregnancies with maternal exposure; ustekinumab had the most data (2,933 pregnancies), followed by secukinumab (1,877), risankizumab (589), ixekizumab (296), guselkumab (217), tildrakizumab (32), bimekizumab (11), brodalumab (6), and mirikizumab (1). Cohort-level findings were generally reassuring — no consistent signal for adverse pregnancy or neonatal outcomes — except one study reporting increased risk of small-for-gestational-age infants with ustekinumab. Paternal exposure data were very limited (3 studies, 281 pregnancies).","limitations":"- Most exposures (n=5,074) came from pharmacovigilance databases that capture only adverse events, making incidence rates incalculable and meta-analysis infeasible.\n- Critical confounders (disease activity, exposure timing, comedications) were missing or unreported in the majority of studies; only one study used confounder-adjusted analysis.\n- Data were heavily skewed toward IBD patients, limiting psoriasis-specific and IL-17-specific conclusions.","practice_takeaway":"Available data are broadly reassuring but insufficient to issue definitive safety guidance; clinicians should weigh uncontrolled disease risk against medication uncertainty on a case-by-case basis. Existing psoriasis registries (e.g., BADBIR, BioCAPTURE) should add standardized pregnancy datasets to accelerate evidence generation."}},{"doi":"10.1001/jamadermatol.2026.2633","pmid":"42555037","title":"Approved Monoclonal Antibody Therapies for Hidradenitis Suppurativa","journal_title":"JAMA Dermatology","journal_issn":"2168-6068","published_at":"2026-08-05T00:00:00.000Z","url":"https://pmc.ncbi.nlm.nih.gov/articles/PMC13445090/","source_score":4,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-08-12T13:26:05.687Z","updated_at":"2026-08-12T13:26:05.687Z","tags":[{"paper_doi":"10.1001/jamadermatol.2026.2633","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2633","tag_type":"brand","value":"Bimzelx","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2633","tag_type":"brand","value":"Cosentyx","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2633","tag_type":"brand","value":"Humira","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2633","tag_type":"category","value":"Dermatology","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2633","tag_type":"condition","value":"Hidradenitis Suppurativa","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2633","tag_type":"generic","value":"adalimumab","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2633","tag_type":"generic","value":"bimekizumab","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2633","tag_type":"generic","value":"secukinumab","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2633","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2633","tag_type":"level_of_evidence","value":"4","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2633","tag_type":"modality","value":"IL-17A/F Inhibitor","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2633","tag_type":"modality","value":"Monoclonal Antibody","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2633","tag_type":"modality","value":"TNF-alpha Inhibitor","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2633","tag_type":"sample_size","value":"n=6","value_numeric":6},{"paper_doi":"10.1001/jamadermatol.2026.2633","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2633","tag_type":"study_design","value":"Economic Evaluation","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2633","tag_type":"warning","value":"Bimekizumab brand name 'Bimzelx' assumed based on known regulatory approval; not explicitly stated in the source text.","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2633","tag_type":"warning","value":"Full text was inaccessible; summary is based solely on the abstract and results excerpt. Methodological nuances (e.g., discounting, time horizon, sensitivity analyses beyond severity adjustment) could not be verified.","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2633","tag_type":"warning","value":"Level of evidence assigned as 4 (economic/decision analysis); no direct clinical trial was conducted in this study.","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2633","tag_type":"warning","value":"Sample size tag reflects 6 Phase 3 trials used for efficacy data synthesis, not a patient-level N — no total patient count was reported in the available abstract.","value_numeric":null}],"summaries":{"what_studied":"This economic evaluation compared the cost-efficiency of three approved monoclonal antibody therapies for moderate-to-severe hidradenitis suppurativa (HS) — adalimumab, secukinumab, and bimekizumab — across five countries (US, Canada, France, Germany, Australia) using Phase 3 trial efficacy data and publicly available drug pricing as of January 31, 2026.","key_result":"Adalimumab 40 mg weekly was on the efficiency frontier in all five countries for both HiSCR-50 and HiSCR-75 outcomes. Secukinumab 300 mg every 4 weeks reached the frontier only when US wholesale acquisition costs were used. Annual costs ranged from $11,345 (adalimumab in Australia) to $411,990 (bimekizumab in the US).","limitations":"- Only publicly available list prices were used; negotiated or rebated prices, which vary widely, were not included.\n- Efficacy data were drawn from separate Phase 3 trials without head-to-head comparisons, limiting direct cross-drug efficacy inference.\n- Full-text access was unavailable; some methodological details may be incomplete.","practice_takeaway":"Adalimumab remains the most cost-efficient approved biologic for HS across major health systems, with costs up to 36-fold lower than bimekizumab in the US. Clinicians and payers advocating for value-based formulary decisions should weigh these large pricing differentials alongside efficacy data."}},{"doi":"10.1038/s41584-026-01413-2","pmid":"42463536","title":"Secukinumab shows diverging efficacy in PMR and GCA","journal_title":"Nature Reviews Rheumatology","journal_issn":"1759-4790","published_at":"2026-07-16T00:00:00.000Z","url":"https://doi.org/10.1038/s41584-026-01413-2","source_score":6,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-18T13:39:48.448Z","updated_at":"2026-07-18T13:39:48.448Z","tags":[{"paper_doi":"10.1038/s41584-026-01413-2","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01413-2","tag_type":"brand","value":"Cosentyx","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01413-2","tag_type":"category","value":"Rheumatology","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01413-2","tag_type":"condition","value":"Giant Cell Arteritis","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01413-2","tag_type":"condition","value":"Polymyalgia Rheumatica","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01413-2","tag_type":"generic","value":"secukinumab","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01413-2","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01413-2","tag_type":"level_of_evidence","value":"2","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01413-2","tag_type":"modality","value":"IL-17A Inhibitor","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01413-2","tag_type":"study_design","value":"Research Highlight (Phase III Trial Summary)","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01413-2","tag_type":"warning","value":"Level of evidence is assigned based on the underlying referenced phase III trials, not the research highlight format itself.","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01413-2","tag_type":"warning","value":"The brand name 'Cosentyx' is the known proprietary name for secukinumab but is not explicitly mentioned in the source text.","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01413-2","tag_type":"warning","value":"The 'practice_changing' impact flag is applied cautiously based on the diverging efficacy signal across two phase III trials; full data review is needed to confirm clinical impact.","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01413-2","tag_type":"warning","value":"This is a publisher preview/research highlight only — the full article is behind a paywall and no primary trial data or patient numbers are accessible from the provided text.","value_numeric":null}],"summaries":{"what_studied":"A research highlight summarizing two phase III trials evaluating secukinumab (an IL-17A inhibitor) in polymyalgia rheumatica (PMR) and giant cell arteritis (GCA), both conditions currently managed with glucocorticoids.","key_result":"Secukinumab showed diverging efficacy between PMR and GCA across the two trials; however, specific outcome data and numbers are not available in this publisher preview.","limitations":"This is a brief research highlight with no access to full trial data — specific efficacy figures, sample sizes, and safety profiles are not reported in the available text.","practice_takeaway":"IL-17A inhibition with secukinumab may offer a steroid-sparing option in PMR and/or GCA, but clinicians should await full trial data before changing practice, as efficacy appears to differ between the two conditions."}},{"doi":"10.1136/rmdopen-2025-006577","pmid":"42457215","title":"Psoriatic arthritis and obesity: a review of clinical burden and considerations for comprehensive care","journal_title":"RMD Open","journal_issn":"2056-5933","published_at":"2026-07-15T00:00:00.000Z","url":"https://doi.org/10.1136/rmdopen-2025-006577","source_score":11,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-20T13:36:05.406Z","updated_at":"2026-07-20T13:36:05.406Z","tags":[{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"brand","value":"Cosentyx","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"brand","value":"Mounjaro","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"brand","value":"Ozempic","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"brand","value":"Taltz","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"brand","value":"Wegovy","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"brand","value":"Zepbound","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"category","value":"Rheumatology","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"condition","value":"Metabolic Syndrome","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"condition","value":"Obesity","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"condition","value":"Psoriasis","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"condition","value":"Psoriatic Arthritis","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"generic","value":"bimekizumab","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"generic","value":"ixekizumab","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"generic","value":"methotrexate","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"generic","value":"secukinumab","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"generic","value":"semaglutide","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"generic","value":"tirzepatide","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"generic","value":"tofacitinib","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"generic","value":"upadacitinib","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"generic","value":"ustekinumab","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"modality","value":"GIP/GLP-1 Receptor Agonist","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"modality","value":"GLP-1 Receptor Agonist","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"modality","value":"IL-17 Inhibitor","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"modality","value":"IL-23 Inhibitor","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"modality","value":"JAK Inhibitor","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"modality","value":"TNF Inhibitor","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"sample_size","value":"n=49","value_numeric":49},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"study_design","value":"Narrative Review","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"warning","value":"Sample size tag reflects the number of included studies in the narrative review, not a patient-level N.","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"warning","value":"The 'practice_changing' impact flag reflects the TOGETHER-PsA combination therapy signal and the emerging incretin data; clinicians should note that PsA-specific regulatory approvals for GLP-1/GIP RAs are not yet established.","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"warning","value":"The TOGETHER-PsA trial (n=271) results cited are from a 2026 publication; full peer-reviewed data should be independently verified as the review appears to have had early access.","value_numeric":null},{"paper_doi":"10.1136/rmdopen-2025-006577","tag_type":"warning","value":"This review was funded by Eli Lilly and Company, and three co-authors are Lilly employees; tirzepatide (a Lilly product) is featured prominently including data from the TOGETHER-PsA trial authored by overlapping investigators.","value_numeric":null}],"summaries":{"what_studied":"This narrative review examined the interplay between psoriatic arthritis (PsA) and obesity, covering shared inflammatory pathways, impact on disease severity and treatment response, weight-management strategies (lifestyle, bariatric surgery, pharmacological), and the potential role of incretin-based therapies (GLP-1 RAs, dual GIP/GLP-1 RAs). Literature search covered PubMed, Embase, and Scopus up to October 2025; 49 studies were included.","key_result":"Obesity (BMI ≥30) worsens PsA severity, reduces biologic response, and raises cardiovascular risk. Key data points: each 1-unit BMI rise in psoriasis patients increases PsA risk by 5.3%; modest weight loss (5–10% body weight) improves disease activity; in one trial, ACR20 response was 71% vs 30% (p=0.008) in patients who lost ≥18.6% weight. The TOGETHER-PsA trial (n=271) found ixekizumab plus tirzepatide achieved ACR50 and ≥10% weight loss at week 36 in 31.7% vs 0.8% with ixekizumab alone (p<0.001), with higher ACR50 rates (33.5% vs 20.4%; p=0.02).","limitations":"- Non-systematic search introduces selection bias despite efforts to prioritize higher-quality evidence.\n- Three authors are Eli Lilly employees and the study was funded by Eli Lilly, raising potential conflict of interest given tirzepatide (Mounjaro/Zepbound) is a Lilly product prominently featured.\n- PsA-specific outcome data for incretin-based therapies remain limited; most cardiovascular and weight-loss data derive from diabetes or general obesity populations.","practice_takeaway":"Treat obesity as a core comorbidity in PsA—screen BMI routinely, integrate weight-management counseling into every rheumatology visit, and consider GLP-1 RA or GIP/GLP-1 RA co-therapy for patients with PsA and obesity who have inadequate response to biologics alone. Multidisciplinary coordination with endocrinology, dietetics, and primary care is recommended by EULAR, GRAPPA, and ACR/NPF guidelines."}},{"doi":"10.1186/s12879-026-13782-w","pmid":"42286536","title":"Adverse events associated with candida infections in secukinumab treatment","journal_title":"BMC Infectious Diseases","journal_issn":"1471-2334","published_at":"2026-06-12T00:00:00.000Z","url":"https://doi.org/10.1186/s12879-026-13782-w","source_score":7,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-16T13:54:37.668Z","updated_at":"2026-06-16T13:54:37.668Z","tags":[{"paper_doi":"10.1186/s12879-026-13782-w","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1186/s12879-026-13782-w","tag_type":"brand","value":"Cosentyx","value_numeric":null},{"paper_doi":"10.1186/s12879-026-13782-w","tag_type":"category","value":"Infectious Diseases","value_numeric":null},{"paper_doi":"10.1186/s12879-026-13782-w","tag_type":"condition","value":"Candidiasis","value_numeric":null},{"paper_doi":"10.1186/s12879-026-13782-w","tag_type":"condition","value":"Opportunistic Infection","value_numeric":null},{"paper_doi":"10.1186/s12879-026-13782-w","tag_type":"condition","value":"Psoriasis","value_numeric":null},{"paper_doi":"10.1186/s12879-026-13782-w","tag_type":"generic","value":"secukinumab","value_numeric":null},{"paper_doi":"10.1186/s12879-026-13782-w","tag_type":"impact_flag","value":"safety_signal","value_numeric":null},{"paper_doi":"10.1186/s12879-026-13782-w","tag_type":"level_of_evidence","value":"4","value_numeric":null},{"paper_doi":"10.1186/s12879-026-13782-w","tag_type":"modality","value":"IL-17A Inhibitor","value_numeric":null},{"paper_doi":"10.1186/s12879-026-13782-w","tag_type":"sample_size","value":"n=1075","value_numeric":1075},{"paper_doi":"10.1186/s12879-026-13782-w","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1186/s12879-026-13782-w","tag_type":"study_design","value":"Pharmacovigilance / Disproportionality Analysis","value_numeric":null},{"paper_doi":"10.1186/s12879-026-13782-w","tag_type":"warning","value":"Brand name 'Cosentyx' was not explicitly stated in the abstract but is the established proprietary name for secukinumab; tagged accordingly.","value_numeric":null},{"paper_doi":"10.1186/s12879-026-13782-w","tag_type":"warning","value":"FAERS-based disproportionality analyses cannot establish causation or true incidence rates; clinical application of ROR signals should be interpreted with caution.","value_numeric":null},{"paper_doi":"10.1186/s12879-026-13782-w","tag_type":"warning","value":"The sample size of n=1,075 refers to Candida adverse event reports, not unique patients; total secukinumab reports in FAERS were not specified, limiting context for the 0.8% figure.","value_numeric":null}],"summaries":{"what_studied":"A retrospective FAERS pharmacovigilance analysis (Q1 2004–Q1 2025) evaluated the clinical profile, severity, onset timing, and risk factors of Candida infections reported in association with secukinumab (an IL-17A inhibitor) across all approved indications.","key_result":"1,075 Candida adverse events were identified (0.8% of all secukinumab reports); all 8 analyzed MedDRA preferred terms showed significant disproportionality, with genital candidiasis carrying the strongest signal (ROR 19.85; 95% CI 12.91–30.53). Over half of events were serious, signals were strongest in females and adults aged 18–64, and median onset was 2–3 months with a Weibull β <1 (early-failure pattern).","limitations":"- FAERS data are subject to under-reporting, duplicate entries, and lack of denominator data, limiting incidence estimation.\n- Causality cannot be established; confounders such as concomitant medications and underlying disease severity are not fully captured.\n- Disproportionality signals reflect reporting patterns, not true relative risk.","practice_takeaway":"Monitor patients starting secukinumab closely for Candida infections during the first 2–3 months, with heightened vigilance in females and adults aged 18–64. Serious outcomes were common, so prompt evaluation and treatment of any candidiasis symptoms are warranted."}},{"doi":"10.1007/s13555-026-01797-9","pmid":"42262460","title":"Real-World Long-Term Effectiveness and Safety of Secukinumab in Psoriasis: Up to 7 Years of Evidence from the Italian Landscape Psoriasis (IL PSO) Multicenter Retrospective Study","journal_title":"Dermatology and Therapy","journal_issn":"2193-8210","published_at":"2026-06-09T00:00:00.000Z","url":"https://doi.org/10.1007/s13555-026-01797-9","source_score":7,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-17T13:29:45.016Z","updated_at":"2026-06-17T13:29:45.016Z","tags":[{"paper_doi":"10.1007/s13555-026-01797-9","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01797-9","tag_type":"brand","value":"Cosentyx","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01797-9","tag_type":"category","value":"Dermatology","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01797-9","tag_type":"condition","value":"Plaque Psoriasis","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01797-9","tag_type":"condition","value":"Psoriatic Arthritis","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01797-9","tag_type":"generic","value":"secukinumab","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01797-9","tag_type":"impact_flag","value":"confirms_prior","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01797-9","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01797-9","tag_type":"modality","value":"IL-17A Inhibitor","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01797-9","tag_type":"sample_size","value":"n=769","value_numeric":769},{"paper_doi":"10.1007/s13555-026-01797-9","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01797-9","tag_type":"study_design","value":"Multicenter Retrospective Cohort Study","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01797-9","tag_type":"warning","value":"Several authors disclosed financial relationships with Novartis (secukinumab's manufacturer) and other biologic makers; no external funding was reported, but conflicts of interest are extensive.","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01797-9","tag_type":"warning","value":"Survivor bias is a major confounder: the study enrolled only patients who completed ≥4 years of continuous secukinumab, systematically excluding non-responders and those with early AEs, which substantially inflates the reported long-term effectiveness figures.","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01797-9","tag_type":"warning","value":"The cohort shrinks markedly at later time points (n=231 at year 6, n=101 at year 7), limiting the generalizability of the longest follow-up data.","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01797-9","tag_type":"warning","value":"The higher PASI 100 rates in PsA patients is an exploratory finding from univariate subgroup analysis without multiplicity correction — caution is warranted in clinical interpretation.","value_numeric":null}],"summaries":{"what_studied":"This multicenter retrospective study evaluated the real-world long-term effectiveness and safety of secukinumab (300 mg SC every 4 weeks) in 769 adults with moderate-to-severe plaque psoriasis treated continuously for at least 4 years across 15 Italian dermatology units (2017–2025), with follow-up up to 7 years.","key_result":"PASI 90 rose from 36.0% at week 16 to 90.0% at year 6; PASI 100 rose from 27.4% at week 16 to 80.2% at year 7. Absolute PASI ≤2 reached 95.0% at year 7. Patients with concomitant PsA had significantly higher PASI 100 rates at years 5 (77.9% vs. 69.8%) and 6 (85.7% vs. 71.4%; p ≤ 0.05). Serious AEs led to permanent discontinuation in only 5 patients (3 de novo malignancies, 1 pulmonary embolism, 1 eosinophilic pneumonia).","limitations":"- **Survivor bias**: only patients on continuous treatment ≥4 years were included; early discontinuers (for inefficacy, AEs, or preference) are excluded, inflating long-term response rates.\n- **Retrospective, as-observed analysis**: missing data could not be recovered, and progressively smaller cohorts at later time points (n=769 at year 4 down to n=101 at year 7) limit interpretation.\n- **No formal drug survival analysis or multivariate adjustment**: confounders cannot be excluded, and subgroup findings should be considered exploratory.","practice_takeaway":"In patients who tolerate and respond to secukinumab, skin clearance rates continue to improve over years — not plateau — suggesting strong long-term durability for those who stay on therapy. Cardiometabolic comorbidities and difficult-to-treat areas did not significantly reduce response rates, supporting secukinumab as a durable option regardless of these factors."}},{"doi":"10.2340/actadv.v106.adv-2026-0461","pmid":"42257527","title":"Prior Specific Biologic Use as a Potential Risk Factor for Administration-related Reactions to Ixekizumab after Excipient Modification: A Single-centre Retrospective Study","journal_title":"Acta Dermato-Venereologica","journal_issn":"1651-2057","published_at":"2026-06-08T00:00:00.000Z","url":"https://doi.org/10.2340/actadv.v106.adv-2026-0461","source_score":1,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-10T14:24:43.016Z","updated_at":"2026-06-10T14:24:43.016Z","tags":[{"paper_doi":"10.2340/actadv.v106.adv-2026-0461","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0461","tag_type":"brand","value":"Taltz","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0461","tag_type":"category","value":"Dermatology","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0461","tag_type":"condition","value":"Erythrodermic Psoriasis","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0461","tag_type":"condition","value":"Generalized Pustular Psoriasis","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0461","tag_type":"condition","value":"Plaque Psoriasis","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0461","tag_type":"condition","value":"Psoriatic Arthritis","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0461","tag_type":"generic","value":"ixekizumab","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0461","tag_type":"generic","value":"secukinumab","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0461","tag_type":"impact_flag","value":"safety_signal","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0461","tag_type":"level_of_evidence","value":"4","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0461","tag_type":"modality","value":"IL-17A Inhibitor","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0461","tag_type":"sample_size","value":"n=23","value_numeric":23},{"paper_doi":"10.2340/actadv.v106.adv-2026-0461","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0461","tag_type":"study_design","value":"Retrospective Cohort Study","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0461","tag_type":"warning","value":"All authors have disclosed financial relationships with multiple pharmaceutical companies, including Eli Lilly (ixekizumab manufacturer), which may introduce bias.","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0461","tag_type":"warning","value":"ARR definition relied on clinical records from a single centre, with potential for ascertainment variability.","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0461","tag_type":"warning","value":"Very small sample size (n=23) produces highly imprecise odds ratios (e.g., 95% CI 1.41–192.00); findings should be considered hypothesis-generating only.","value_numeric":null}],"summaries":{"what_studied":"This single-centre retrospective study examined risk factors for administration-related reactions (ARRs) to the modified (citrate-free) ixekizumab formulation in 23 psoriasis patients treated between January 2023 and December 2025.","key_result":"7 of 23 patients (30.4%) developed ARRs; 6 of those 7 had switched from secukinumab. Multivariate logistic regression showed prior secukinumab use was significantly associated with ARRs (OR 16.40, 95% CI 1.41–192.00, p=0.03). All ARRs were grade 1; 4 women discontinued ixekizumab due to intolerable reactions.","limitations":"Very small sample size (n=23) from a single centre limits generalisability; wide confidence intervals reflect imprecision; no mechanistic data to confirm causal pathway between prior secukinumab use and ARRs.","practice_takeaway":"When switching psoriasis patients from secukinumab to ixekizumab, counsel them about a higher likelihood of injection-site reactions, even with the newer citrate-free formulation. Monitor closely after the first dose and have a contingency plan if reactions are intolerable."}},{"doi":"10.1093/bjd/ljag174","pmid":"42082393","title":"Serious infection risk with systemic treatments for psoriasis: A cohort study from the British Association of Dermatologists Biologic Interventions Register (BADBIR)","journal_title":"British Journal of Dermatology","journal_issn":"0007-0963","published_at":"2026-05-05T00:00:00.000Z","url":"https://doi.org/10.1093/bjd/ljag174","source_score":7,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-05-09T13:22:33.628Z","updated_at":"2026-05-09T13:22:33.628Z","tags":[{"paper_doi":"10.1093/bjd/ljag174","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"brand","value":"Cosentyx","value_numeric":null},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"brand","value":"Enbrel","value_numeric":null},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"brand","value":"Humira","value_numeric":null},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"brand","value":"Otezla","value_numeric":null},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"brand","value":"Siliq","value_numeric":null},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"brand","value":"Skyrizi","value_numeric":null},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"category","value":"Dermatology","value_numeric":null},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"condition","value":"Psoriasis","value_numeric":null},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"condition","value":"Serious Infection","value_numeric":null},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"generic","value":"adalimumab","value_numeric":null},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"generic","value":"apremilast","value_numeric":null},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"generic","value":"brodalumab","value_numeric":null},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"generic","value":"etanercept","value_numeric":null},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"generic","value":"risankizumab","value_numeric":null},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"generic","value":"secukinumab","value_numeric":null},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"impact_flag","value":"safety_signal","value_numeric":null},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"modality","value":"IL-17 Inhibitor","value_numeric":null},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"modality","value":"IL-23 Inhibitor","value_numeric":null},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"modality","value":"PDE4 Inhibitor","value_numeric":null},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"modality","value":"TNF Inhibitor","value_numeric":null},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"sample_size","value":"n=18976","value_numeric":18976},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"study_design","value":"Prospective Cohort Study","value_numeric":null},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"warning","value":"Study design is labeled as a registry cohort (observational); the level of evidence reflects this, not a randomized trial.","value_numeric":null},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"warning","value":"The elevated serious infection signals for apremilast and secukinumab vs. adalimumab were not consistent in sensitivity analyses — these should not be interpreted as definitive safety differences.","value_numeric":null},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"warning","value":"Treatment episodes (n=46,770) far exceed patient count (n=18,976), meaning many patients switched treatments; channeling bias by disease severity or comorbidity cannot be fully excluded.","value_numeric":null}],"summaries":{"what_studied":"This large UK registry cohort (BADBIR) examined serious infection risk across systemic psoriasis treatments — including biologics (adalimumab, secukinumab, risankizumab, brodalumab, etanercept) and non-biologics (apremilast, standard treatments) — in 18,976 adult patients over 46,770 treatment episodes, using inverse probability weighting and both time-to-first-event and recurrent-event analyses.","key_result":"Overall serious infection incidence was 27.67 per 1,000 person-years; recurrent infection rate in those with prior infection was 78.70 per 1,000 person-years. The more robust recurrent-event (PWP) model showed risankizumab had lower serious infection risk vs. brodalumab (HR 0.74), etanercept (HR 0.75), and standard treatments (HR 0.80). Apparent elevated risks with apremilast (HR 1.53) and secukinumab (HR 1.34) vs. adalimumab in the time-to-first-event model were not consistent across sensitivity analyses. Serious infection-related deaths were rare (IR 1.81 per 1,000 person-years).","limitations":"- Elevated risks for apremilast and secukinumab were not replicated in sensitivity analyses, limiting confidence in those signals.\n- Observational registry design introduces potential residual confounding despite inverse probability weighting.\n- Channeling bias is possible, as sicker or higher-risk patients may have been preferentially prescribed certain agents.","practice_takeaway":"For psoriasis patients at elevated infection risk, risankizumab may offer a relative safety advantage over brodalumab, etanercept, and conventional systemic agents. The apparent higher infection risk with apremilast and secukinumab vs. adalimumab should be interpreted cautiously, as it was not robust across sensitivity analyses."}},{"doi":"10.1007/s13555-026-01761-7","pmid":"42068460","title":"A Narrative Review: Do Systemic Drugs Used in the Treatment of Psoriatic Disease Affect Alzheimer’s Disease?","journal_title":"Dermatology and Therapy","journal_issn":"2193-8210","published_at":"2026-05-02T00:00:00.000Z","url":"https://doi.org/10.1007/s13555-026-01761-7","source_score":7,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-05-10T13:20:36.620Z","updated_at":"2026-05-10T13:20:36.620Z","tags":[{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"age_group","value":"older_adult","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"brand","value":"Cosentyx","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"brand","value":"Enbrel","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"brand","value":"Humira","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"brand","value":"Otezla","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"brand","value":"Remicade","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"brand","value":"Sotyktu","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"brand","value":"Stelara","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"category","value":"Dermatology","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"condition","value":"Alzheimer's Disease","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"condition","value":"Dementia","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"condition","value":"Psoriasis","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"condition","value":"Psoriatic Arthritis","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"generic","value":"acitretin","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"generic","value":"adalimumab","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"generic","value":"apremilast","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"generic","value":"cyclosporine","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"generic","value":"deucravacitinib","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"generic","value":"etanercept","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"generic","value":"infliximab","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"generic","value":"methotrexate","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"generic","value":"roflumilast","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"generic","value":"secukinumab","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"generic","value":"tofacitinib","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"generic","value":"upadacitinib","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"generic","value":"ustekinumab","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"modality","value":"Conventional Synthetic DMARD","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"modality","value":"IL-12/23 Inhibitor","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"modality","value":"IL-17 Inhibitor","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"modality","value":"IL-23 Inhibitor","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"modality","value":"JAK Inhibitor","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"modality","value":"NSAID","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"modality","value":"PDE4 Inhibitor","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"modality","value":"Retinoid","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"modality","value":"TNF-Alpha Inhibitor","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"modality","value":"TYK2 Inhibitor","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"study_design","value":"Narrative Review","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"warning","value":"Corresponding author (Tsen-Fang Tsai) has disclosed extensive consultant relationships with manufacturers of many drugs discussed in the review.","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"warning","value":"Level of evidence assigned as 5 (narrative review/expert opinion) due to absence of PRISMA methodology, risk-of-bias tools, or meta-analytic synthesis, even though individual cited studies range from Level 1 to Level 5.","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"warning","value":"Several drug-AD associations cited are from studies in rheumatoid arthritis populations, not specifically psoriasis patients; generalizability to psoriatic disease may be limited.","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"warning","value":"This is a narrative review without formal systematic methods; findings are hypothesis-generating and subject to selection bias in included studies.","value_numeric":null}],"summaries":{"what_studied":"This narrative review examined whether systemic drugs used for psoriatic disease (NSAIDs, methotrexate, cyclosporin, retinoids, PDE4 inhibitors, JAK inhibitors, TYK2 inhibitors, and biologics targeting TNF-α, IL-12/23, IL-17, and IL-23) influence the risk or progression of Alzheimer's disease (AD), using AD as a model for dementia. Literature from PubMed (2015–2025) was synthesized across preclinical, observational, and RCT-level evidence.","key_result":"Most preclinical and observational data suggest antipsoriatic therapies may reduce AD risk. The strongest clinical signal comes from a propensity score–matched cohort (n=1,766) showing biologic therapy for psoriasis was associated with a **53% lower risk of incident dementia** vs. conventional systemic therapy alone. In a large EHR-based study (56 million records), TNF inhibitors (etanercept, adalimumab, infliximab) were linked to markedly reduced AD odds (ORs 0.34, 0.28, and 0.52, respectively; all P<0.0001). However, several large observational studies found the psoriasis–dementia association attenuated or disappeared after adjusting for comorbidities.","limitations":"- Narrative (not systematic) review with no PRISMA flow, risk-of-bias assessment, or quantitative synthesis, limiting reproducibility.\n- Most mechanistic evidence comes from preclinical models (Level 5), with very few adequately powered RCTs in humans.\n- Residual confounding by disease severity, metabolic comorbidities, and medication use cannot be excluded in observational studies.","practice_takeaway":"For older patients with psoriasis, consider early cognitive screening, as shared inflammatory mechanisms may raise dementia risk—especially in those with metabolic comorbidities. Biologic therapy, particularly TNF inhibitors, shows the most consistent signal for possible neuroprotection, but current evidence is hypothesis-generating and should not yet change prescribing solely for dementia prevention."}},{"doi":"10.1002/art.70051","pmid":"41524618","title":"In synergy with interferon‐gamma, interleukin‐17 activates vascular stromal cells towards a pro‐inflammatory profile in giant cell arteritis","journal_title":"Arthritis & Rheumatology","journal_issn":"2326-5191","published_at":"2026-01-12T00:00:00.000Z","url":"https://doi.org/10.1002/art.70051","source_score":12,"is_retracted":false,"is_open_access":false,"raw_metadata":{"ooir":{"day":"2026-01-16","doi":"10.1002/art.70051","days":"7","issn":"2326-5191","rank":"3","field":"Clinical Medicine","score":"12","category":"Rheumatology","categories":["Rheumatology"],"_categories":["Rheumatology"]},"pubmed":{"doi":"10.1002/art.70051","title":"In synergy with interferon-gamma, interleukin-17 activates vascular stromal cells towards a pro-inflammatory profile in giant cell arteritis.","journal":"Arthritis & rheumatology (Hoboken, N.J.)","methods":"","results":"Transcriptomic analysis showed that secukinumab treatment of positive TABs reduced expression of genes linked to vascular inflammation, notably IL6. RT-qPCR analysis confirmed that secukinumab decreased mRNA encoding IL-6, CCL20, and GM-CSF in positive-TABs, while IL-17 upregulated them in negative-TABs. No changes were observed regarding the expression of genes related to vascular remodeling. IL-17 receptor chains were expressed on MFs, and their expression was enhanced by IFN-γ. RT-qPCR and Luminex® analyses confirmed IL-17-driven upregulation of IL-6, CCL20, CCL2, GM-CSF, and VEGF in MFs, which was reversed by secukinumab. Addition of IFN-γ to the culture increased the expression level of IL-17 receptor chains, resulting in a synergistic effect. Additionally, IL-17 pre-treated MFs promoted Th17 polarization.","abstract":"$30","keywords":[],"pubmed_id":"41524618","conclusions":"","publication_date":"2026-01-12T00:00:00"},"crossref":{"DOI":"10.1002/art.70051","URL":"https://doi.org/10.1002/art.70051","ISSN":["2326-5191","2326-5205"],"link":[{"URL":"https://acrjournals.onlinelibrary.wiley.com/doi/pdf/10.1002/art.70051","content-type":"application/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https://acrjournals.onlinelibrary.wiley.com/doi/pdf/10.1002/art.70051","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":null,"type":"journal-article","issue":null,"score":1,"title":["In synergy with interferon‐gamma, interleukin‐17 activates vascular stromal cells towards a pro‐inflammatory profile in giant cell arteritis"],"author":[{"given":"Hélène","family":"Greigert","sequence":"first","affiliation":[{"name":"Department of Internal Medicine and Clinical Immunology, Referral Center for Rare Systemic Autoimmune and Autoinflammatory Diseases (MAIS), Dijon University Hospital Université EPE Bourgogne Europe Dijon France"},{"name":"Department of Vascular Medicine, Dijon University Hospital Université EPE Bourgogne Europe Dijon France"},{"name":"Université Marie et Louis Pasteur, EFS, INSERM UMR1098 RIGHT Besançon F‐25000 France"}]},{"given":"André","family":"Ramon","sequence":"additional","affiliation":[{"name":"Université Marie et Louis Pasteur, EFS, INSERM UMR1098 RIGHT Besançon F‐25000 France"},{"name":"Department of Rheumatology, Dijon University Hospital Université EPE Bourgogne Europe Dijon France"}]},{"given":"Claudie","family":"Cladiere","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine and Clinical Immunology, Referral Center for Rare Systemic Autoimmune and Autoinflammatory Diseases (MAIS), Dijon University Hospital Université EPE Bourgogne Europe Dijon France"},{"name":"Université Marie et Louis Pasteur, EFS, INSERM UMR1098 RIGHT Besançon F‐25000 France"}]},{"given":"Baptiste","family":"Lamarthée","sequence":"additional","affiliation":[{"name":"Université Marie et Louis Pasteur, EFS, INSERM UMR1098 RIGHT Besançon F‐25000 France"}]},{"given":"Corentin","family":"Richard","sequence":"additional","affiliation":[{"name":"Unit of Molecular Biology, Department of Biology and Pathology of Tumors, Georges‐François Leclerc Cancer Center, UNICANCER, Dijon, France ; 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Bioexperienced: 2-year risk was 0.39 (0.36-0.43) for ustekinumab and lower for bimekizumab 0.27 (0.20-0.34), guselkumab 0.29 (0.22-0.36), and risankizumab 0.25 (0.15-0.36).","limitations":"Bionaive analyses included only adalimumab, secukinumab, and ustekinumab, limiting class-wide comparisons. Some bioexperienced drugs had small sample sizes (e.g., risankizumab n=78), and follow-up windows differed (5-year bionaive vs 2-year bioexperienced), complicating cross-cohort comparisons.","practice_takeaway":"In routine practice, ustekinumab showed better 5-year persistence than adalimumab and secukinumab in bionaive patients; among bioexperienced patients, bimekizumab, guselkumab, and risankizumab had lower 2-year discontinuation risks than ustekinumab. 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(secukinumab, ixekizumab, brodalumab) triggers major adverse cardiovascular events (MACEs) within 6 months, using TNF‑α inhibitors (adalimumab, etanercept) as an active comparator. Among 34,241 IL‑17(R)A recipients, 381 MACEs were analyzed; risk and reference windows were the 6 months before the MACE and the preceding 6 months.","key_result":"Initiation of IL‑17(R)A inhibitors was not significantly associated with MACEs (OR 1.25, 95% CI 0.75–2.08); TNF‑α inhibitor initiation also showed no association (OR 0.90, 95% CI 0.65–1.24). Compared with TNF‑α inhibitors, IL‑17(R)A initiation had an OR of 1.40 (95% CI 0.77–2.54) over 6 months, with similar findings across cardiovascular risk strata (P for homogeneity = .29) and unchanged results in sensitivity analyses (broader MACE definition; 3‑month risk window).","limitations":"Only early risk windows (3–6 months) were evaluated, so longer‑term risk was not assessed. Precision was limited by 381 MACEs, yielding wide confidence intervals that do not exclude a modest risk increase.","practice_takeaway":"In this large real‑world analysis, starting an IL‑17(R)A inhibitor did not show a significant increase in 6‑month MACEs versus TNF‑α inhibitors, across cardiovascular risk levels. Continue standard cardiovascular risk management; a small increase in early events cannot be ruled out."}}],"initialOffset":13,"fetchConfig":{"kind":"tags","tags":[{"tag_type":"generic","value":"secukinumab"}]},"breadcrumbItems":[{"name":"Home","href":"/"},{"name":"Research Hub","href":"/hub"},{"name":"Generics","href":"/hub/tag/generic"},{"name":"secukinumab"}],"hrefConfig":{"basePath":"/hub/papers","webViewQueryParams":{"hub_ctx":"tag","hub_tag_type":"generic","hub_tag_value":"secukinumab"}}}]]

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