2f:I[703058,["/_next/static/immutable/chunks/3bhq_5eh1d760.js","/_next/static/immutable/chunks/1855-ogyi8eh4.js","/_next/static/immutable/chunks/2pfsjpn6k6zlg.js","/_next/static/immutable/chunks/26c7v3_3uwnwu.js","/_next/static/immutable/chunks/25a3ozcrvi1ff.js","/_next/static/immutable/chunks/2r4wx50nvjh_4.js","/_next/static/immutable/chunks/23fsw06hsi5b1.js","/_next/static/immutable/chunks/06_yt270h41rg.js","/_next/static/immutable/chunks/3ezsiz-7shkna.js","/_next/static/immutable/chunks/20x2y96ldu5wx.js","/_next/static/immutable/chunks/2lxntcm3pd1_h.js","/_next/static/immutable/chunks/00dgco8irq3jw.js","/_next/static/immutable/chunks/00nwe-kq0rboc.js","/_next/static/immutable/chunks/2051ffx3xzio9.js"],"PaperListPageClient"] 30:T9de,Psoriasis and depression frequently coexist, creating a complex, bidirectional relationship that complicates treatment. This study, integrating clinical assessments with transcriptomic and metabolomic analyses, hypothesizes that TYK2 (tyrosine kinase 2) inhibitors possess a dual therapeutic potential to simultaneously address both dermatological manifestations of psoriasis and the frequently accompanied depressive symptoms. In a cohort of 298 psoriasis patients evaluated using the Hospital Anxiety and Depression Scale (HADS), participants were categorized into a TYK2 inhibitor group, a Janus kinase (JAK) inhibitor group, and a non-JAK pool (comprising interleukin [IL]-23 biologics, IL-17 biologics, and other treatments) to avoid overlapping JAK pathway inhibition. Statistical analysis was conducted using generalized linear models (GENMOD), with adjustments for the following covariates: age, sex, Psoriasis Area and Severity Index (PASI), body surface area (BSA), prior systemic or biologic therapy within 12 months, disease duration, and phototherapy history. For HADS-D scores, the TYK2 inhibitor group showed significantly lower values compared with the non-JAK pool (β = 1.23, 95% confidence interval [CI]: 0.37-2.10). However, no significant differences were observed when compared with the IL-23 biologics group (β = 0.67, 95% CI: -0.76-2.10) or the JAK inhibitor group (β = 0.84, 95% CI: -1.54-3.21). Transcriptomic analysis of peripheral blood revealed significant downregulation of genes related to the IL-6 receptor, long-term depression pathways, and Th17 cell differentiation, while pathways associated with neuronal activity were upregulated. Metabolomic profiling highlighted a decrease in kynurenic acid, which is known for its pro-inflammatory and depressive effects, and an increase in 1H-indole-3-propanoic acid, an anti-inflammatory metabolite with neuroprotective properties. It is important to note that these findings are based on exploratory omics analyses, for which false discovery rate (FDR) control was applied. These findings provide a hypothesis that TYK2 inhibitors disrupt the persistent "peripheral inflammation-central depression" cycle by targeting the IL-23/Th17 axis and modulating the IL-6/tryptophan metabolic hub. This innovative, multi-targeted approach represents a possibility for treating psoriasis with comorbid depression, offering not only clinical improvements in both skin and mood symptoms but also enhanced patient adherence to treatment regimens.31:Td92,ABSTRACT Background Psoriasis and depression frequently coexist, creating a complex, bidirectional relationship that complicates treatment. This study, integrating clinical assessments with transcriptomic and metabolomic analyses, hypothesizes that TYK2 (tyrosine kinase 2) inhibitors possess a dual therapeutic potential to simultaneously address both dermatological manifestations of psoriasis and the frequently accompanied depressive symptoms. Methods In a cohort of 298 psoriasis patients evaluated using the Hospital Anxiety and Depression Scale (HADS), participants were categorized into a TYK2 inhibitor group, a Janus kinase (JAK) inhibitor group, and a non‐JAK pool (comprising interleukin [IL]‐23 biologics, IL‐17 biologics, and other treatments) to avoid overlapping JAK pathway inhibition. Statistical analysis was conducted using generalized linear models (GENMOD), with adjustments for the following covariates: age, sex, Psoriasis Area and Severity Index (PASI), body surface area (BSA), prior systemic or biologic therapy within 12 months, disease duration, and phototherapy history. Results For HADS‐D scores, the TYK2 inhibitor group showed significantly lower values compared with the non‐JAK pool ( β = 1.23, 95% confidence interval [CI]: 0.37–2.10). However, no significant differences were observed when compared with the IL‐23 biologics group ( β = 0.67, 95% CI: −0.76–2.10) or the JAK inhibitor group ( β = 0.84, 95% CI: −1.54–3.21). Transcriptomic analysis of peripheral blood revealed significant downregulation of genes related to the IL‐6 receptor, long‐term depression pathways, and Th17 cell differentiation, while pathways associated with neuronal activity were upregulated. Metabolomic profiling highlighted a decrease in kynurenic acid, which is known for its pro‐inflammatory and depressive effects, and an increase in 1H‐indole‐3‐propanoic acid, an anti‐inflammatory metabolite with neuroprotective properties. It is important to note that these findings are based on exploratory omics analyses, for which false discovery rate (FDR) control was applied. Conclusions These findings provide a hypothesis that TYK2 inhibitors disrupt the persistent “peripheral inflammation–central depression” cycle by targeting the IL‐23/Th17 axis and modulating the IL‐6/tryptophan metabolic hub. This innovative, multi‐targeted approach represents a possibility for treating psoriasis with comorbid depression, offering not only clinical improvements in both skin and mood symptoms but also enhanced patient adherence to treatment regimens. 32: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.33: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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34:T710,Many biologic therapies are available for moderate-to-severe plaque psoriasis. A systematic literature review and network meta-analysis (NMA) was conducted to compare the efficacy of the interleukin (IL)-23 inhibitor, tildrakizumab, with other biologics at up to 28 weeks of treatment. The literature search was conducted on January 22, 2024, searching MEDLINE, Embase, and CENTRAL for randomized controlled trials (RCTs) investigating the comparative efficacy and safety of biologics in adult Asian patients with moderate-to-severe plaque psoriasis. NMAs were conducted for ≥ 75%, ≥ 90%, and 100% reduction in Psoriasis Area and Severity Index score (PASI 75, 90, and 100) and achieving a Physician Global Assessment (PGA) score of 0 or 1 after the induction period (12 and 16 weeks) and mid-term (28 weeks) follow-up. NMAs were conducted using the Bayesian framework outlined in the National Institute of Clinical Excellence guidelines. Nineteen RCTs conducted in China, Japan, Korea, and Taiwan with 11 different biologics were included. At Week 12, tildrakizumab had lower efficacy compared to other biologics. Between Weeks 12 and 28, the proportion of patients achieving PASI 75/90/100 with tildrakizumab increased from 60.77% to 81.84%, from 38.54% to 71.23%, and from 6.97% to 22.64%, respectively. At Week 28, tildrakizumab efficacy was comparable to other biologic therapies studied here, including tumor necrosis factor-alpha (TNFα), IL-17, IL-12/IL-23, and other IL-23 inhibitors. The efficacy of tildrakizumab improved over time, which underscores the importance of evaluating the sustained efficacy of tildrakizumab over the long term. Combined with low dosing frequency, tildrakizumab offers an effective treatment option for patients with moderate-to-severe plaque psoriasis.35:T760,ABSTRACTMany biologic therapies are available for moderate‐to‐severe plaque psoriasis. A systematic literature review and network meta‐analysis (NMA) was conducted to compare the efficacy of the interleukin (IL)‐23 inhibitor, tildrakizumab, with other biologics at up to 28 weeks of treatment. The literature search was conducted on January 22, 2024, searching MEDLINE, Embase, and CENTRAL for randomized controlled trials (RCTs) investigating the comparative efficacy and safety of biologics in adult Asian patients with moderate‐to‐severe plaque psoriasis. NMAs were conducted for ≥ 75%, ≥ 90%, and 100% reduction in Psoriasis Area and Severity Index score (PASI 75, 90, and 100) and achieving a Physician Global Assessment (PGA) score of 0 or 1 after the induction period (12 and 16 weeks) and mid‐term (28 weeks) follow‐up. NMAs were conducted using the Bayesian framework outlined in the National Institute of Clinical Excellence guidelines. Nineteen RCTs conducted in China, Japan, Korea, and Taiwan with 11 different biologics were included. At Week 12, tildrakizumab had lower efficacy compared to other biologics. Between Weeks 12 and 28, the proportion of patients achieving PASI 75/90/100 with tildrakizumab increased from 60.77% to 81.84%, from 38.54% to 71.23%, and from 6.97% to 22.64%, respectively. At Week 28, tildrakizumab efficacy was comparable to other biologic therapies studied here, including tumor necrosis factor‐alpha (TNFα), IL‐17, IL‐12/IL‐23, and other IL‐23 inhibitors. The efficacy of tildrakizumab improved over time, which underscores the importance of evaluating the sustained efficacy of tildrakizumab over the long term. Combined with low dosing frequency, tildrakizumab offers an effective treatment option for patients with moderate‐to‐severe plaque psoriasis.36: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.37: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. 38:T461,Among 82 399 individuals identified with PsA, 542 individuals (median [IQR] age, 52.5 [44.0-59.0] years; 341 female individuals [62.9%]) were receiving combination targeted therapy for 3 consecutive months and 200 (median [IQR] age, 55.0 [45.0-61.0] years; 114 female individuals [57.0%]) were receiving combination therapy for 6 consecutive months. The 2 most common combinations used were a tumor necrosis factor inhibitor with apremilast (34%-37%) and an interleukin 17 inhibitor with apremilast (27%-29%). The serious infection incidence rate among patients receiving combination targeted therapy ranged from 7.38 to 15.00 events per 1000 patients; the opportunistic infection incidence rate ranged from 0 to 1.85 events per 1000 patients. Patients receiving combination targeted therapy did not have a significantly increased risk of serious infection (propensity score-matched 3-month and 6-month RRs, 0.53 [95% CI, 0.17-1.63] and 1.50 [95% CI, 0.34-6.65], respectively) or opportunistic infection (adjusted 3-month and 6-month RRs, 1.00 [95% CI, 0.09-11.02] and not applicable, respectively) across all analyses.39:Tb5e,Achieving good disease control in psoriatic arthritis (PsA) remains a major challenge. Combining multiple systemic immunomodulatory therapies has been shown to be beneficial in other immune-mediated diseases with reasonable safety profiles, but data on the current use and safety of combination targeted therapy among individuals with PsA are limited. To evaluate the use and safety of combination targeted therapies among adults with PsA. Data from the IBM MarketScan Commercial Claims Database from January 2015 to December 2024 were used to describe use patterns and perform safety analyses. Data were analyzed from April 2024 to June 2025. A validated claims algorithm was used to identify adults with PsA, who were separated into a standard therapy control cohort that was matched 2:1 with the combination targeted therapy cohort. Descriptive analysis of the use of combination targeted therapies. The safety analysis included a comparison of frequencies of International Statistical Classification of Diseases and Related Health Problems, Tenth Revision (ICD-10) codes for serious or opportunistic infections requiring an inpatient level of care. Relative risks (RRs) were calculated before and after propensity score matching. Among 82 399 individuals identified with PsA, 542 individuals (median [IQR] age, 52.5 [44.0-59.0] years; 341 female individuals [62.9%]) were receiving combination targeted therapy for 3 consecutive months and 200 (median [IQR] age, 55.0 [45.0-61.0] years; 114 female individuals [57.0%]) were receiving combination therapy for 6 consecutive months. The 2 most common combinations used were a tumor necrosis factor inhibitor with apremilast (34%-37%) and an interleukin 17 inhibitor with apremilast (27%-29%). The serious infection incidence rate among patients receiving combination targeted therapy ranged from 7.38 to 15.00 events per 1000 patients; the opportunistic infection incidence rate ranged from 0 to 1.85 events per 1000 patients. Patients receiving combination targeted therapy did not have a significantly increased risk of serious infection (propensity score-matched 3-month and 6-month RRs, 0.53 [95% CI, 0.17-1.63] and 1.50 [95% CI, 0.34-6.65], respectively) or opportunistic infection (adjusted 3-month and 6-month RRs, 1.00 [95% CI, 0.09-11.02] and not applicable, respectively) across all analyses. The results of this cohort study suggest that among commercially insured adults with PsA, around 1% of individuals were receiving combination targeted therapy. The most common combinations used different biologics with apremilast. This study found no significant difference between the incidence of serious bacterial and opportunistic infections requiring hospitalization compared with standard therapy, suggesting that combination targeted therapy may not be associated with significantly increased infection risk, but further larger studies are needed.3a:Tffb, Importance Achieving good disease control in psoriatic arthritis (PsA) remains a major challenge. Combining multiple systemic immunomodulatory therapies has been shown to be beneficial in other immune-mediated diseases with reasonable safety profiles, but data on the current use and safety of combination targeted therapy among individuals with PsA are limited. Objective To evaluate the use and safety of combination targeted therapies among adults with PsA. Design, Setting, and Participants Data from the IBM MarketScan Commercial Claims Database from January 2015 to December 2024 were used to describe use patterns and perform safety analyses. Data were analyzed from April 2024 to June 2025. A validated claims algorithm was used to identify adults with PsA, who were separated into a standard therapy control cohort that was matched 2:1 with the combination targeted therapy cohort. Main Outcomes and Measures Descriptive analysis of the use of combination targeted therapies. The safety analysis included a comparison of frequencies of International Statistical Classification of Diseases and Related Health Problems, Tenth Revision (ICD-10) codes for serious or opportunistic infections requiring an inpatient level of care. Relative risks (RRs) were calculated before and after propensity score matching. Results Among 82 399 individuals identified with PsA, 542 individuals (median [IQR] age, 52.5 [44.0-59.0] years; 341 female individuals [62.9%]) were receiving combination targeted therapy for 3 consecutive months and 200 (median [IQR] age, 55.0 [45.0-61.0] years; 114 female individuals [57.0%]) were receiving combination therapy for 6 consecutive months. The 2 most common combinations used were a tumor necrosis factor inhibitor with apremilast (34%-37%) and an interleukin 17 inhibitor with apremilast (27%-29%). The serious infection incidence rate among patients receiving combination targeted therapy ranged from 7.38 to 15.00 events per 1000 patients; the opportunistic infection incidence rate ranged from 0 to 1.85 events per 1000 patients. Patients receiving combination targeted therapy did not have a significantly increased risk of serious infection (propensity score–matched 3-month and 6-month RRs, 0.53 [95% CI, 0.17-1.63] and 1.50 [95% CI, 0.34-6.65], respectively) or opportunistic infection (adjusted 3-month and 6-month RRs, 1.00 [95% CI, 0.09-11.02] and not applicable, respectively) across all analyses. Conclusions and Relevance The results of this cohort study suggest that among commercially insured adults with PsA, around 1% of individuals were receiving combination targeted therapy. The most common combinations used different biologics with apremilast. This study found no significant difference between the incidence of serious bacterial and opportunistic infections requiring hospitalization compared with standard therapy, suggesting that combination targeted therapy may not be associated with significantly increased infection risk, but further larger studies are needed. 3b:Tbcc,Patients with psoriasis may require a switch to another therapy due to high treatment costs, primary effectiveness failure, biologic fatigue, or adverse effects associated with the initial biologic treatment; however, the availability of evidence for the effectiveness and safety of interclass biologic switching for the treatment of psoriasis is unknown. To investigate the effectiveness and safety of psoriasis treatment after the failure of initial biologic therapy, particularly when patients switch to a second biologic. PubMed, Embase, and the Cochrane Library were searched from inception through January 25, 2025. The study included randomized clinical trials (RCTs) of patients with plaque psoriasis aged 18 years or older involving crossover or switching from 1 biologic agent to another initial biologic within the same or different drug class. Two researchers independently screened the records and abstracted data using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses reporting guideline. Data were pooled using random-effects models. The prespecified primary end point was psoriasis area and severity index (PASI) 90. Secondary end points included clinician- and patient-reported outcomes (PROMs) and safety. Clinical effectiveness was evaluated based on the PASI responses (PASI 75, 90, and 100) and the Investigator's and Physician's Global Assessments scores of 0 or 1 and body surface area of 1% or less. PROMs included the dermatology life quality index and psoriasis symptoms and signs diary. Safety concerns included adverse events (AEs), serious AEs, severe AEs, treatment-related AEs, and specific AEs. Twenty-four RCTs involving 12 661 patients with psoriasis and 8 switching categories were analyzed. Significant differences observed in PASI 90 between week 4 and week 0 (odds ratio [OR], 6.53; 95% CI, 2.58-16.51). Substantial disparities were noted across various PASI response metrics, specifically PASI 90 (OR, 28.61; 95% CI, 12.89-63.47), PASI 75 (OR, 11.11; 95% CI, 5.95-20.75), and PASI 100 (OR, 18.76; 95% CI, 8.37-42.01). No difference exists in safety outcomes between the end point and week 0, including in serious AEs (OR, 1.63; 95% CI, 0.72-3.69), severe AEs (OR, 1.40; 95% CI, 0.61-3.26), and treatment-related AEs (OR, 1.79; 95% CI, 0.41-7.88). The highest risk of infection was associated with switching from anti-TNF-α agents to anti-interleukin (IL)-23p19, anti-IL-17A, or anti-IL-12/23p40 agents, with infection rates of 0.62%, 0.54% and 0.39%, respectively. This systematic review and meta-analysis found that interclass biologic switching was effective in a significant number of patients. With the introduction of biologics with diverse mechanisms of action, these options may become viable and potentially superior. However, further confirmatory data from larger patient cohorts and longer follow-up periods are required to obtain more conclusive results. Our results highlight the importance of vigilance for infections when switching biologics.3c:Tef0,ImportancePatients with psoriasis may require a switch to another therapy due to high treatment costs, primary effectiveness failure, biologic fatigue, or adverse effects associated with the initial biologic treatment; however, the availability of evidence for the effectiveness and safety of interclass biologic switching for the treatment of psoriasis is unknown.ObjectiveTo investigate the effectiveness and safety of psoriasis treatment after the failure of initial biologic therapy, particularly when patients switch to a second biologic.Data SourcesPubMed, Embase, and the Cochrane Library were searched from inception through January 25, 2025.Study SelectionThe study included randomized clinical trials (RCTs) of patients with plaque psoriasis aged 18 years or older involving crossover or switching from 1 biologic agent to another initial biologic within the same or different drug class.Data Extraction and SynthesisTwo researchers independently screened the records and abstracted data using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses reporting guideline. Data were pooled using random-effects models.Main Outcomes and MeasuresThe prespecified primary end point was psoriasis area and severity index (PASI) 90. Secondary end points included clinician- and patient-reported outcomes (PROMs) and safety. Clinical effectiveness was evaluated based on the PASI responses (PASI 75, 90, and 100) and the Investigator’s and Physician’s Global Assessments scores of 0 or 1 and body surface area of 1% or less. PROMs included the dermatology life quality index and psoriasis symptoms and signs diary. Safety concerns included adverse events (AEs), serious AEs, severe AEs, treatment-related AEs, and specific AEs.ResultsTwenty-four RCTs involving 12 661 patients with psoriasis and 8 switching categories were analyzed. Significant differences observed in PASI 90 between week 4 and week 0 (odds ratio [OR], 6.53; 95% CI, 2.58-16.51). Substantial disparities were noted across various PASI response metrics, specifically PASI 90 (OR, 28.61; 95% CI, 12.89-63.47), PASI 75 (OR, 11.11; 95% CI, 5.95-20.75), and PASI 100 (OR, 18.76; 95% CI, 8.37-42.01). No difference exists in safety outcomes between the end point and week 0, including in serious AEs (OR, 1.63; 95% CI, 0.72-3.69), severe AEs (OR, 1.40; 95% CI, 0.61-3.26), and treatment-related AEs (OR, 1.79; 95% CI, 0.41-7.88). The highest risk of infection was associated with switching from anti−TNF-α agents to anti−interleukin (IL)-23p19, anti−IL-17A, or anti−IL-12/23p40 agents, with infection rates of 0.62%, 0.54% and 0.39%, respectively.Conclusions and RelevanceThis systematic review and meta-analysis found that interclass biologic switching was effective in a significant number of patients. With the introduction of biologics with diverse mechanisms of action, these options may become viable and potentially superior. However, further confirmatory data from larger patient cohorts and longer follow-up periods are required to obtain more conclusive results. Our results highlight the importance of vigilance for infections when switching biologics.25:[[["$","script","0",{"type":"application/ld+json","dangerouslySetInnerHTML":{"__html":"{\"@context\":\"https://schema.org\",\"@type\":\"CollectionPage\",\"name\":\"IL-17 Inhibitor: modality Research & Clinical Takeaways\",\"description\":\"Explore peer-reviewed papers on IL-17 Inhibitor (modality). Clinician-written summaries and actionable practice insights. 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Nonrandomized studies showed a pooled IBD incidence of 3.90% (95% CI, 2.30%–6.50%), though crude incidence was 1.49% (7/469 patients). Across all study types, 17 new-onset and 4 IBD flare events were reported.","limitations":"- RCT follow-up was limited to 16 weeks, too short to capture delayed IBD onset.\n- Very low event rates reduced statistical power to detect a true difference.\n- Inconsistent IBD reporting across studies made pooled interpretation difficult.","practice_takeaway":"IL-17 inhibitors do not appear to significantly raise IBD risk in HS patients over the short term, but clinicians should screen for IBD history before starting therapy and monitor for GI symptoms, given the baseline elevated IBD risk in HS populations and limited long-term data."}},{"doi":"10.2340/actadv.v106.adv-2026-0797","pmid":"42708646","title":"Current Evidence on IL-17 and IL-(12)/23 Inhibitor Safety during Pregnancy in Psoriasis: A Call for Harmonized Data Collection","journal_title":"Acta Dermato-Venereologica","journal_issn":"1651-2057","published_at":"2026-09-08T00:00:00.000Z","url":"https://doi.org/10.2340/actadv.v106.adv-2026-0797","source_score":1,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-09-12T06:20:17.230Z","updated_at":"2026-09-12T06:20:17.230Z","tags":[{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"brand","value":"Bimzelx","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"brand","value":"Cosentyx","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"brand","value":"Siliq","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"brand","value":"Skyrizi","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"brand","value":"Stelara","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"brand","value":"Taltz","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"brand","value":"Tremfya","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"category","value":"Dermatology","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"condition","value":"Psoriasis","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"generic","value":"bimekizumab","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"generic","value":"brodalumab","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"generic","value":"guselkumab","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"generic","value":"ixekizumab","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"generic","value":"mirikizumab","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"generic","value":"risankizumab","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"generic","value":"secukinumab","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"generic","value":"tildrakizumab","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"generic","value":"ustekinumab","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"modality","value":"IL-12/23 Inhibitor","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"modality","value":"IL-17 Inhibitor","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"modality","value":"IL-23 Inhibitor","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"sample_size","value":"n=5962","value_numeric":5962},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"sex","value":"female","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"study_design","value":"Systematic Review","value_numeric":null},{"paper_doi":"10.2340/actadv.v106.adv-2026-0797","tag_type":"warning","value":"Level of evidence assigned as 3 (systematic review of heterogeneous, mostly observational studies); 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":"10.1002/art.70297","pmid":"42605840","title":"Risk of Cancer according to Duration of Targeted Therapy Exposure in Spondyloarthritis: A Nationwide Cohort Study from the French Health Insurance Database","journal_title":"Arthritis & Rheumatology","journal_issn":"2326-5191","published_at":"2026-08-17T00:00:00.000Z","url":"https://doi.org/10.1002/art.70297","source_score":3,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-08-22T06:53:21.288Z","updated_at":"2026-08-22T06:53:21.288Z","tags":[{"paper_doi":"10.1002/art.70297","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1002/art.70297","tag_type":"category","value":"Rheumatology","value_numeric":null},{"paper_doi":"10.1002/art.70297","tag_type":"condition","value":"Axial Spondyloarthritis","value_numeric":null},{"paper_doi":"10.1002/art.70297","tag_type":"condition","value":"Cancer","value_numeric":null},{"paper_doi":"10.1002/art.70297","tag_type":"condition","value":"Psoriatic Arthritis","value_numeric":null},{"paper_doi":"10.1002/art.70297","tag_type":"condition","value":"Spondyloarthritis","value_numeric":null},{"paper_doi":"10.1002/art.70297","tag_type":"impact_flag","value":"confirms_prior","value_numeric":null},{"paper_doi":"10.1002/art.70297","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1002/art.70297","tag_type":"modality","value":"IL-12/23 Inhibitor","value_numeric":null},{"paper_doi":"10.1002/art.70297","tag_type":"modality","value":"IL-17 Inhibitor","value_numeric":null},{"paper_doi":"10.1002/art.70297","tag_type":"modality","value":"IL-23 Inhibitor","value_numeric":null},{"paper_doi":"10.1002/art.70297","tag_type":"modality","value":"JAK Inhibitor","value_numeric":null},{"paper_doi":"10.1002/art.70297","tag_type":"modality","value":"TNF Inhibitor","value_numeric":null},{"paper_doi":"10.1002/art.70297","tag_type":"sample_size","value":"n=56591","value_numeric":56591},{"paper_doi":"10.1002/art.70297","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1002/art.70297","tag_type":"study_design","value":"Nationwide Cohort Study","value_numeric":null},{"paper_doi":"10.1002/art.70297","tag_type":"warning","value":"Causal inference relies on inverse probability weighting from claims data; unmeasured confounders (e.g., disease severity, concomitant medications) may not be fully accounted for.","value_numeric":null},{"paper_doi":"10.1002/art.70297","tag_type":"warning","value":"The protective signal for hematological malignancies (wHR 0.65) is based on only 116 events, so this estimate should be interpreted cautiously — wide confidence intervals reflect limited precision.","value_numeric":null},{"paper_doi":"10.1002/art.70297","tag_type":"warning","value":"The study pools multiple SpA subtypes and multiple drug classes (TNFi, IL-17i, IL-12/23i, IL-23i, JAKi) into a single exposure variable; drug-class-specific or subtype-specific cancer risks may differ and are not fully delineated in the abstract.","value_numeric":null}],"summaries":{"what_studied":"This nationwide French cohort study examined whether duration of targeted therapy exposure (TNFi, IL-17i, IL-12/23i, IL-23i, JAKi) affects cancer risk in 56,591 adults with spondyloarthritis (including psoriatic arthritis and axial SpA), followed for a median of 5.0 years (2014–2024).","key_result":"Exposure >6 months/year vs. ≤6 months/year was associated with a **lower** overall cancer risk (wHR 0.86, 95% CI 0.75–0.99), driven primarily by hematological malignancies (wHR 0.65, 95% CI 0.42–0.99); no significant reduction was seen for solid cancers (wHR 0.92, 95% CI 0.79–1.07). Of 1,224 total cancers, 1,029 were solid and 116 hematological. Cumulative multi-year exposure was not associated with cancer risk.","limitations":"- **Observational design**: residual confounding cannot be excluded despite inverse probability weighting.\n- **Database-based exposure**: therapy adherence is inferred from insurance claims, not directly measured.\n- **Heterogeneous SpA subtypes**: pooling psoriatic arthritis, axial SpA, and other subtypes may obscure subgroup-specific risks.","practice_takeaway":"Clinicians can reassure patients with SpA that prolonged targeted therapy use is not associated with increased cancer risk — and may even lower hematological malignancy risk. Cumulative years of exposure should not, on its own, prompt treatment discontinuation over cancer concerns."}},{"doi":"10.3899/jrheum.2025-1171","pmid":"42542376","title":"Who Achieves Minimal and Very Low Disease Activity in Psoriatic Arthritis? An Analysis of the CorEvitas Psoriatic Arthritis/Spondyloarthritis Registry","journal_title":"The Journal of Rheumatology","journal_issn":"0315-162X","published_at":"2026-08-01T00:00:00.000Z","url":"https://doi.org/10.3899/jrheum.2025-1171","source_score":2,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-08-11T13:26:24.973Z","updated_at":"2026-08-11T13:26:24.973Z","tags":[{"paper_doi":"10.3899/jrheum.2025-1171","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.3899/jrheum.2025-1171","tag_type":"category","value":"Rheumatology","value_numeric":null},{"paper_doi":"10.3899/jrheum.2025-1171","tag_type":"condition","value":"Psoriatic Arthritis","value_numeric":null},{"paper_doi":"10.3899/jrheum.2025-1171","tag_type":"impact_flag","value":"confirms_prior","value_numeric":null},{"paper_doi":"10.3899/jrheum.2025-1171","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.3899/jrheum.2025-1171","tag_type":"modality","value":"Biologic DMARD","value_numeric":null},{"paper_doi":"10.3899/jrheum.2025-1171","tag_type":"modality","value":"IL-17 Inhibitor","value_numeric":null},{"paper_doi":"10.3899/jrheum.2025-1171","tag_type":"modality","value":"IL-23 Inhibitor","value_numeric":null},{"paper_doi":"10.3899/jrheum.2025-1171","tag_type":"modality","value":"JAK Inhibitor","value_numeric":null},{"paper_doi":"10.3899/jrheum.2025-1171","tag_type":"modality","value":"PDE4 Inhibitor","value_numeric":null},{"paper_doi":"10.3899/jrheum.2025-1171","tag_type":"modality","value":"Targeted Synthetic DMARD","value_numeric":null},{"paper_doi":"10.3899/jrheum.2025-1171","tag_type":"modality","value":"TNF Inhibitor","value_numeric":null},{"paper_doi":"10.3899/jrheum.2025-1171","tag_type":"sample_size","value":"n=2491","value_numeric":2491},{"paper_doi":"10.3899/jrheum.2025-1171","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.3899/jrheum.2025-1171","tag_type":"study_design","value":"Prospective Observational Registry Study","value_numeric":null},{"paper_doi":"10.3899/jrheum.2025-1171","tag_type":"warning","value":"Analyses were conducted at the b/tsDMARD initiation level, not patient level, so some patients contributed multiple observations; standard errors may be under- or overestimated.","value_numeric":null},{"paper_doi":"10.3899/jrheum.2025-1171","tag_type":"warning","value":"Study was funded by UCB; two authors are UCB employees, which may introduce publication bias.","value_numeric":null},{"paper_doi":"10.3899/jrheum.2025-1171","tag_type":"warning","value":"The two cohorts (MDA: n=2,093; VLDA: n=2,491) are non-mutually exclusive and overlap; the larger VLDA cohort includes patients who were in MDA but not VLDA at baseline. The sample_size tag reflects the larger VLDA cohort.","value_numeric":null}],"summaries":{"what_studied":"This real-world registry study (CorEvitas PsA/SpA Registry, March 2013–September 2023) examined rates of minimal disease activity (MDA) and very low disease activity (VLDA) achievement in adults with PsA starting a b/tsDMARD, assessed at a follow-up visit ~6 months post-initiation (n=2,093 for MDA cohort; n=2,491 for VLDA cohort).","key_result":"Only 17.68% (370/2,093) achieved MDA and 7.51% (187/2,491) achieved VLDA at ~6 months. Pain was the most commonly unmet criterion: 95.41% of MDA non-achievers and 87.02% of VLDA non-achievers failed this threshold. Female sex, higher baseline fatigue/pain, and prior b/tsDMARD use were linked to lower MDA/VLDA likelihood; b/tsDMARD monotherapy (RR 1.36 [95% CI 1.07–1.73]) and higher EQ-5D-3L scores were linked to higher MDA likelihood. Notably, 23.10% of MDA non-achievers and 10.24% of VLDA non-achievers missed the target by just 1 criterion.","limitations":"- Registry-based design introduces selection bias and confounding by indication (e.g., sicker patients less likely to receive b/tsDMARDs).\n- Patients who discontinued their b/tsDMARD before follow-up were classified as non-achievers, potentially underestimating true MDA/VLDA rates.\n- Analyses at the b/tsDMARD initiation level (not patient level) may introduce within-patient correlation, affecting precision of confidence intervals.","practice_takeaway":"Most PsA patients on b/tsDMARDs do not reach MDA or VLDA at 6 months, with pain and patient-reported function as the biggest barriers—clinicians should address residual pain and PROs explicitly, not just joint counts. Nearly a quarter of MDA non-achievers missed the target by just one criterion, signaling that targeted pain management could meaningfully improve treat-to-target outcomes."}},{"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":"10.1016/j.ard.2026.06.017","pmid":"42431784","title":"Cancer risk of Janus kinase inhibitors and other advanced therapies in immune-mediated inflammatory diseases: a systematic review and Bayesian network meta-analysis of RCTs","journal_title":"Annals of the Rheumatic Diseases","journal_issn":"0003-4967","published_at":"2026-07-10T00:00:00.000Z","url":"https://doi.org/10.1016/j.ard.2026.06.017","source_score":7,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-23T13:33:19.238Z","updated_at":"2026-07-23T13:33:19.238Z","tags":[{"paper_doi":"10.1016/j.ard.2026.06.017","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.017","tag_type":"category","value":"Rheumatology","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.017","tag_type":"condition","value":"Inflammatory Bowel Disease","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.017","tag_type":"condition","value":"Psoriasis","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.017","tag_type":"condition","value":"Psoriatic Arthritis","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.017","tag_type":"condition","value":"Rheumatoid Arthritis","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.017","tag_type":"generic","value":"tofacitinib","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.017","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.017","tag_type":"level_of_evidence","value":"1","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.017","tag_type":"modality","value":"CD20 Inhibitor","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.017","tag_type":"modality","value":"CTLA-4 Inhibitor","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.017","tag_type":"modality","value":"IL-12/23 Inhibitor","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.017","tag_type":"modality","value":"IL-17 Inhibitor","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.017","tag_type":"modality","value":"IL-23 Inhibitor","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.017","tag_type":"modality","value":"IL-6 Inhibitor","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.017","tag_type":"modality","value":"JAK Inhibitor","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.017","tag_type":"modality","value":"TNF Inhibitor","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.017","tag_type":"sample_size","value":"n=164824","value_numeric":164824},{"paper_doi":"10.1016/j.ard.2026.06.017","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.017","tag_type":"study_design","value":"Systematic Review and Network Meta-Analysis","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.017","tag_type":"warning","value":"Class-level pooling of JAK inhibitors may mask agent-specific or dose-specific differences; individual drug comparisons are not reported.","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.017","tag_type":"warning","value":"Long-term extension studies are included alongside RCTs, which may introduce exposure-time bias favoring detection of malignancy in longer studies.","value_numeric":null},{"paper_doi":"10.1016/j.ard.2026.06.017","tag_type":"warning","value":"The absolute risk calculations depend on assumed baseline cancer incidence rates for 'standard-risk' vs 'higher-risk' populations, which are not fully specified in the abstract—clinicians should interpret absolute numbers cautiously without the full paper.","value_numeric":null}],"summaries":{"what_studied":"This systematic review and Bayesian network meta-analysis evaluated relative and absolute cancer risk of JAK inhibitors (JAKis) vs other advanced therapies (TNFi, IL-6, IL-17, IL-23, IL-12/23, CTLA-4, CD20 inhibitors) across immune-mediated inflammatory diseases (RA, PsO/PsA, IBD) using 305 RCTs and long-term extension studies (164,824 participants; 264,100 person-years exposure) published up to February 2026.","key_result":"JAKis were associated with higher malignancy risk than TNFi (RR 1.60; 95% CrI 1.27–2.02) and standard care (RR 1.85; 95% CrI 1.38–2.47) across all three disease areas. Absolute excess risk vs TNFi was negligible in standard-risk patients (~1 extra cancer per 27,000 person-years) but clinically meaningful in high-risk patients (~1 extra cancer per 147 person-years). IL-6, IL-17, IL-23, IL-12/23, CTLA-4, and CD20 inhibitors showed cancer risks broadly comparable to TNFi.","limitations":"- Relies on RCT and long-term extension data, which may underrepresent older or higher-risk patients seen in routine care.\n- Class-level pooling may obscure differences between individual JAKi agents or doses.\n- Malignancy outcomes (including non-melanoma skin cancer) vary in ascertainment and reporting across trials.","practice_takeaway":"Clinicians should apply risk-stratified decision-making when prescribing JAKis across all IMIDs—not just RA—particularly in patients with prior malignancy or other cancer risk factors. For standard-risk patients the absolute excess risk vs TNFi is very small, but it becomes meaningful in higher-risk populations (~1 extra cancer per 147 person-years)."}},{"doi":"10.1038/s41584-026-01404-3","pmid":"42414762","title":"Going beyond cycling versus swapping for treatment sequencing in psoriatic arthritis","journal_title":"Nature Reviews Rheumatology","journal_issn":"1759-4790","published_at":"2026-07-07T00:00:00.000Z","url":"https://doi.org/10.1038/s41584-026-01404-3","source_score":8,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-13T17:42:38.735Z","updated_at":"2026-07-13T17:42:38.735Z","tags":[{"paper_doi":"10.1038/s41584-026-01404-3","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01404-3","tag_type":"category","value":"Rheumatology","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01404-3","tag_type":"condition","value":"Psoriatic Arthritis","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01404-3","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01404-3","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01404-3","tag_type":"modality","value":"Biologic Therapy","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01404-3","tag_type":"modality","value":"IL-17 Inhibitor","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01404-3","tag_type":"modality","value":"IL-23 Inhibitor","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01404-3","tag_type":"modality","value":"JAK Inhibitor","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01404-3","tag_type":"modality","value":"TNF Inhibitor","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01404-3","tag_type":"study_design","value":"Narrative Review","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01404-3","tag_type":"warning","value":"Full paper text was not provided — summary is based solely on the title, journal, and DOI metadata. Key results, specific recommendations, and cited evidence could not be verified from the source text. Treat all extracted content as provisional.","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01404-3","tag_type":"warning","value":"Impact flag 'practice_changing' applied cautiously given the paper's framing around updating a clinical decision framework, but cannot be confirmed without full text.","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01404-3","tag_type":"warning","value":"No sample size tag applied as this appears to be a review article with no primary patient cohort.","value_numeric":null},{"paper_doi":"10.1038/s41584-026-01404-3","tag_type":"warning","value":"Study design tagged as 'Narrative Review' based on journal type and title framing; this could not be confirmed without access to the full text.","value_numeric":null}],"summaries":{"what_studied":"This paper evaluates treatment sequencing strategies in psoriatic arthritis (PsA), moving beyond the traditional binary framework of cycling (switching within the same drug class) versus swapping (switching to a different class) after treatment failure.","key_result":"The paper argues that a more nuanced, individualized approach to sequencing — considering mechanism of action, domain-specific disease activity, prior treatment history, and patient factors — may better guide clinical decisions than the cycling/swapping dichotomy alone.","limitations":"As a review published in a high-impact journal, the conclusions may reflect expert opinion and narrative synthesis rather than head-to-head trial data on sequencing strategies; specific quantitative outcomes from randomized sequencing trials are not reported.","practice_takeaway":"When a PsA patient fails a biologic or targeted therapy, clinicians should consider disease domain profile, mechanism of action, and reason for failure rather than defaulting to a simple cycle-or-swap rule. Personalized sequencing may improve long-term outcomes."}},{"doi":"10.1126/sciimmunol.adq6406","pmid":"42284373","title":"The tissue-specific regulation of immunobiology by IL-17 signaling","journal_title":"Science Immunology","journal_issn":"2470-9468","published_at":"2026-06-12T00:00:00.000Z","url":"https://doi.org/10.1126/sciimmunol.adq6406","source_score":51,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-16T13:54:34.783Z","updated_at":"2026-06-16T13:54:34.783Z","tags":[{"paper_doi":"10.1126/sciimmunol.adq6406","tag_type":"category","value":"Immunology","value_numeric":null},{"paper_doi":"10.1126/sciimmunol.adq6406","tag_type":"condition","value":"Autoimmune Disease","value_numeric":null},{"paper_doi":"10.1126/sciimmunol.adq6406","tag_type":"condition","value":"Cancer","value_numeric":null},{"paper_doi":"10.1126/sciimmunol.adq6406","tag_type":"condition","value":"Inflammatory Disease","value_numeric":null},{"paper_doi":"10.1126/sciimmunol.adq6406","tag_type":"impact_flag","value":"confirms_prior","value_numeric":null},{"paper_doi":"10.1126/sciimmunol.adq6406","tag_type":"level_of_evidence","value":"7","value_numeric":null},{"paper_doi":"10.1126/sciimmunol.adq6406","tag_type":"modality","value":"IL-17 Inhibitor","value_numeric":null},{"paper_doi":"10.1126/sciimmunol.adq6406","tag_type":"study_design","value":"Narrative Review","value_numeric":null},{"paper_doi":"10.1126/sciimmunol.adq6406","tag_type":"warning","value":"No sample size is applicable — this is a review article with no primary patient cohort.","value_numeric":null},{"paper_doi":"10.1126/sciimmunol.adq6406","tag_type":"warning","value":"Sex and age group tags were omitted as the review does not focus on a specific population.","value_numeric":null},{"paper_doi":"10.1126/sciimmunol.adq6406","tag_type":"warning","value":"Specific branded or generic IL-17 inhibitors are not named in the abstract; modality tag is based on the review's stated therapeutic focus.","value_numeric":null}],"summaries":{"what_studied":"This review examines how IL-17 family cytokines and their receptor (IL-17R) complexes regulate tissue immunity, covering cell- and tissue-specific signaling pathways, transcriptional and posttranscriptional mechanisms, and emerging roles in immunometabolism, neuroimmune interactions, and cancer.","key_result":"The review synthesizes recent advances showing that IL-17 drives functional diversity across tissues through intersecting signaling cascades, and highlights the latest targeted therapeutic approaches aimed at modulating IL-17 activity.","limitations":"As a review article, no original experimental data are presented; conclusions depend on the scope and quality of cited primary studies. Emerging topics (immunometabolism, neuroimmune interactions, cancer) are discussed but may reflect early-stage evidence.","practice_takeaway":"Clinicians managing IL-17-driven diseases (e.g., psoriasis, ankylosing spondylitis, IBD) should be aware that tissue context shapes IL-17 responses and that targeted IL-17R pathway therapies are an active area of development. Awareness of tissue-specific effects may help predict which patients benefit most from IL-17 blockade."}},{"doi":"10.1002/art.70221","pmid":"42112876","title":"T cells, the Next Big Target in Axial Spondyloarthritis?","journal_title":"Arthritis & Rheumatology","journal_issn":"2326-5191","published_at":"2026-05-25T00:00:00.000Z","url":"https://doi.org/10.1002/art.70221","source_score":4,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-16T13:54:25.645Z","updated_at":"2026-06-16T13:54:25.645Z","tags":[{"paper_doi":"10.1002/art.70221","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1002/art.70221","tag_type":"category","value":"Rheumatology","value_numeric":null},{"paper_doi":"10.1002/art.70221","tag_type":"condition","value":"Axial Spondyloarthritis","value_numeric":null},{"paper_doi":"10.1002/art.70221","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1002/art.70221","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1002/art.70221","tag_type":"modality","value":"Anti-TRBV9 Antibody","value_numeric":null},{"paper_doi":"10.1002/art.70221","tag_type":"modality","value":"IL-17 Inhibitor","value_numeric":null},{"paper_doi":"10.1002/art.70221","tag_type":"modality","value":"IL-23 Inhibitor","value_numeric":null},{"paper_doi":"10.1002/art.70221","tag_type":"modality","value":"JAK Inhibitor","value_numeric":null},{"paper_doi":"10.1002/art.70221","tag_type":"modality","value":"TNF Inhibitor","value_numeric":null},{"paper_doi":"10.1002/art.70221","tag_type":"study_design","value":"Narrative Review","value_numeric":null},{"paper_doi":"10.1002/art.70221","tag_type":"warning","value":"No sample size tag applied — this is a review article with no primary patient cohort.","value_numeric":null},{"paper_doi":"10.1002/art.70221","tag_type":"warning","value":"Study design is a narrative (not systematic) review; conclusions on therapeutic targeting are expert synthesis, not meta-analytic findings.","value_numeric":null},{"paper_doi":"10.1002/art.70221","tag_type":"warning","value":"The anti-TRBV9 antibody therapy mentioned is described as 'emerging' with no clinical trial results reported in this paper; its efficacy and safety profile in axSpA are not yet established.","value_numeric":null}],"summaries":{"what_studied":"This narrative review synthesizes current knowledge on diverse T cell subsets in axial spondyloarthritis (axSpA) — including CD8+ T cells, CD4+ Th17, Tregs, tissue-resident memory T cells, γδ T cells, MAITs, and iNKT cells — their pathogenic mechanisms, and emerging therapeutic strategies targeting these cells.","key_result":"Multiple T cell subsets drive axSpA inflammation primarily through IL-17 production via IL-23 signaling; direct targeting strategies (e.g., anti-TRBV9 antibody therapy, JAK inhibition) and indirect approaches (IL-17 and TNF inhibition) are discussed as potential avenues, with T cell complexity offering explanations for why some cytokine inhibitors fail.","limitations":"This is a narrative review without systematic search criteria or meta-analytic data, so conclusions on therapeutic efficacy are not based on pooled quantitative evidence. No original clinical trial data are presented.","practice_takeaway":"For patients with axSpA who respond poorly to current cytokine inhibitors, the evidence reviewed here suggests that T cell subset heterogeneity — particularly innate-like T cells and tissue-resident memory T cells — may explain treatment gaps, supporting interest in JAK inhibitors and emerging anti-TRBV9 approaches. Clinicians should watch for trials targeting these pathways as next-generation options."}},{"doi":"10.1001/jamadermatol.2026.1694","pmid":"42139041","title":"Targeting Cardiometabolic Disease to Improve Psoriasis—A New Treatment Paradigm Emerges","journal_title":"JAMA Dermatology","journal_issn":"2168-6068","published_at":"2026-05-15T00:00:00.000Z","url":"https://doi.org/10.1001/jamadermatol.2026.1694","source_score":14,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-05-18T13:25:20.020Z","updated_at":"2026-05-18T13:25:20.020Z","tags":[{"paper_doi":"10.1001/jamadermatol.2026.1694","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1694","tag_type":"brand","value":"Mounjaro","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1694","tag_type":"brand","value":"Taltz","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1694","tag_type":"category","value":"Dermatology","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1694","tag_type":"condition","value":"Cardiometabolic Disease","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1694","tag_type":"condition","value":"Obesity","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1694","tag_type":"condition","value":"Psoriasis","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1694","tag_type":"condition","value":"Psoriatic Arthritis","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1694","tag_type":"generic","value":"ixekizumab","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1694","tag_type":"generic","value":"tirzepatide","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1694","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1694","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1694","tag_type":"modality","value":"GLP-1/GIP Receptor Agonist","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1694","tag_type":"modality","value":"IL-17 Inhibitor","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1694","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1694","tag_type":"study_design","value":"Editorial / Commentary on Randomized Controlled Trial","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1694","tag_type":"warning","value":"Brand name 'Mounjaro' listed for tirzepatide reflects its obesity/diabetes indication branding; the editorial does not specify a brand name.","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1694","tag_type":"warning","value":"No sample size for the TOGETHER-PsO trial is reported in this editorial; the sample_size tag has been omitted accordingly.","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1694","tag_type":"warning","value":"Several authors report financial relationships with manufacturers of relevant drugs (Novo Nordisk, Lilly, AbbVie, Johnson & Johnson, Pfizer, others), which should be considered when interpreting the editorial framing.","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.1694","tag_type":"warning","value":"This is an editorial commentary, not the primary trial report — specific trial data (e.g., PASI 100 rates, metabolic outcomes) are cited from the TOGETHER-PsO trial paper (Lebwohl et al., JAMA Dermatol 2026) and cannot be fully verified from this text alone.","value_numeric":null}],"summaries":{"what_studied":"This editorial discusses the TOGETHER-PsO phase 3b trial, which added tirzepatide (GLP-1/GIP agonist) to ixekizumab (IL-17 biologic) vs. ixekizumab alone in adults with moderate-to-severe psoriasis and overweight/obesity over 36 weeks, and argues for a new cardiometabolic treatment paradigm in psoriasis.","key_result":"At week 36, 40.6% of patients on ixekizumab + tirzepatide achieved PASI 100 vs. 29.0% on ixekizumab alone (P = .04); 27.1% vs. 5.8% met the composite primary endpoint of PASI 100 plus ≥10% weight loss (P < .001). The combination also reduced triglycerides by ~30 mg/dL and systolic blood pressure by ~10 mm Hg.","limitations":"- Trial was open-label with no placebo control, making skin benefit estimates imprecise and potentially biased.\n- Skin improvement was a secondary endpoint, limiting the strength of that inference.\n- It is unclear whether benefit came from tirzepatide's direct anti-inflammatory effects, weight loss, or improved ixekizumab pharmacokinetics.","practice_takeaway":"Dermatologists treating moderate-to-severe psoriasis in patients with overweight or obesity should screen routinely for cardiometabolic risk factors (BP, HbA1c, lipids, BMI) and consider collaborative care with cardiologists or obesity specialists. Adding tirzepatide to IL-17 biologic therapy may improve both skin clearance and cardiovascular risk factors simultaneously."}},{"doi":"10.1111/jdv.70503","pmid":"42132049","title":"Treatment‐associated phenotype switching between psoriasis and atopic dermatitis","journal_title":"Journal of the European Academy of Dermatology and Venereology","journal_issn":"0926-9959","published_at":"2026-05-14T00:00:00.000Z","url":"https://doi.org/10.1111/jdv.70503","source_score":8,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-05-22T13:22:25.132Z","updated_at":"2026-05-22T13:22:25.132Z","tags":[{"paper_doi":"10.1111/jdv.70503","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1111/jdv.70503","tag_type":"brand","value":"Dupixent","value_numeric":null},{"paper_doi":"10.1111/jdv.70503","tag_type":"category","value":"Dermatology","value_numeric":null},{"paper_doi":"10.1111/jdv.70503","tag_type":"condition","value":"Atopic Dermatitis","value_numeric":null},{"paper_doi":"10.1111/jdv.70503","tag_type":"condition","value":"Psoriasis","value_numeric":null},{"paper_doi":"10.1111/jdv.70503","tag_type":"generic","value":"dupilumab","value_numeric":null},{"paper_doi":"10.1111/jdv.70503","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1111/jdv.70503","tag_type":"level_of_evidence","value":"4","value_numeric":null},{"paper_doi":"10.1111/jdv.70503","tag_type":"modality","value":"Biologic Therapy","value_numeric":null},{"paper_doi":"10.1111/jdv.70503","tag_type":"modality","value":"IL-17 Inhibitor","value_numeric":null},{"paper_doi":"10.1111/jdv.70503","tag_type":"modality","value":"IL-23 Inhibitor","value_numeric":null},{"paper_doi":"10.1111/jdv.70503","tag_type":"modality","value":"JAK Inhibitor","value_numeric":null},{"paper_doi":"10.1111/jdv.70503","tag_type":"sample_size","value":"n=148","value_numeric":148},{"paper_doi":"10.1111/jdv.70503","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1111/jdv.70503","tag_type":"study_design","value":"Retrospective Observational Study","value_numeric":null},{"paper_doi":"10.1111/jdv.70503","tag_type":"warning","value":"Age group tagged as 'adult' based on the finding that PsO→eczematous patients were described as older with cardiometabolic comorbidities; pediatric patients are not explicitly excluded but not described.","value_numeric":null},{"paper_doi":"10.1111/jdv.70503","tag_type":"warning","value":"'Impact_flag' set to practice_changing given the bidirectional management implications, though the evidence level is observational (Level 4).","value_numeric":null},{"paper_doi":"10.1111/jdv.70503","tag_type":"warning","value":"The study is descriptive with no control group or standardized severity scoring, so effect sizes and clinical improvement rates should be interpreted cautiously.","value_numeric":null}],"summaries":{"what_studied":"A retrospective, multicentre, multinational observational study across 17 dermatology centres in 6 countries evaluated treatment-associated phenotype switching ('flip-flop') between psoriasis and atopic dermatitis (AD) in 148 patients receiving systemic or biologic therapy, focusing on clinical features, implicated therapies, management, and outcomes.","key_result":"101 patients (68.2%) switched from psoriasis to eczematous phenotype (mainly under IL-17/IL-23 inhibitors) and 47 (31.8%) switched from AD to psoriasiform disease (exclusively under type 2–targeting biologics, predominantly dupilumab); all required treatment modification, and JAK inhibitors were the most frequently used rescue strategy with marked clinical improvement observed in both directions.","limitations":"Retrospective design with descriptive analysis limits causal inference; no standardized outcome scores or control group reported; selection bias is possible given referral-centre recruitment across heterogeneous international sites.","practice_takeaway":"Clinicians should recognize phenotype switching as a reproducible, bidirectional phenomenon when patients on IL-17/IL-23 inhibitors or dupilumab develop features of the opposite inflammatory skin disease. JAK inhibitors appear to be an effective management option in both switch directions and should be considered when treatment modification is needed."}},{"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":"10.1001/jamadermatol.2026.0200","pmid":"41879788","title":"Systemic Pharmacological Treatments for Chronic Plaque Psoriasis","journal_title":"JAMA Dermatology","journal_issn":"2168-6068","published_at":"2026-03-25T00:00:00.000Z","url":"https://doi.org/10.1001/jamadermatol.2026.0200","source_score":29,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-05-24T13:22:59.803Z","updated_at":"2026-05-24T13:22:59.803Z","tags":[{"paper_doi":"10.1001/jamadermatol.2026.0200","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.0200","tag_type":"category","value":"Dermatology","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.0200","tag_type":"condition","value":"Chronic Plaque Psoriasis","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.0200","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.0200","tag_type":"level_of_evidence","value":"1","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.0200","tag_type":"modality","value":"IL-17 Inhibitor","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.0200","tag_type":"modality","value":"IL-23 Inhibitor","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.0200","tag_type":"modality","value":"Oral Small Molecule","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.0200","tag_type":"study_design","value":"Network Meta-Analysis","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.0200","tag_type":"warning","value":"No absolute PASI 90 response rates or sample sizes are provided in the abstract; numeric tags could not be populated.","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.0200","tag_type":"warning","value":"Publication date (2026-03-25) is in the future relative to most training data; findings should be verified against the full text.","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.0200","tag_type":"warning","value":"Sex distribution of study populations is not reported in the abstract.","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.0200","tag_type":"warning","value":"The abstract does not specify the study design explicitly; 'Network Meta-Analysis' is inferred from the comparative framing and JAMA Dermatology publication context — clinicians should verify this upon full-text review.","value_numeric":null}],"summaries":{"what_studied":"A comparative analysis of systemic pharmacological treatments for moderate-to-severe chronic plaque psoriasis in adults, evaluating likelihood of achieving PASI 90 response and rates of serious adverse events across biologic and oral agents.","key_result":"IL-17 and IL-23 inhibitors demonstrated the highest short-term probability of achieving PASI 90. Serious adverse events were uncommon across all therapies and were similar in frequency to placebo in the short term.","limitations":"Only short-term efficacy and safety outcomes are reported; long-term comparative data are not addressed. The abstract does not provide absolute response rates or head-to-head trial counts, limiting precision of estimates.","practice_takeaway":"For patients with moderate-to-severe plaque psoriasis, IL-17 and IL-23 inhibitors are the most effective systemic options for achieving near-complete skin clearance (PASI 90). Oral agents remain a meaningful alternative for patients who prefer non-injectable routes, though with more modest efficacy."}},{"doi":"10.1111/ijd.70230","pmid":"41524454","title":"TYK2 and IL‐23 Pathway Therapies in Psoriasis: Associations With IL‐6, Tryptophan Metabolism, and Depressive Symptoms","journal_title":"International Journal of Dermatology","journal_issn":"0011-9059","published_at":"2026-01-12T00:00:00.000Z","url":"https://doi.org/10.1111/ijd.70230","source_score":15,"is_retracted":false,"is_open_access":false,"raw_metadata":{"ooir":{"day":"2026-01-17","doi":"10.1111/ijd.70230","days":"7","issn":"0011-9059","rank":"4","field":"Clinical Medicine","score":"15","category":"Dermatology","categories":["Dermatology"],"_categories":["Dermatology"]},"pubmed":{"doi":"10.1111/ijd.70230","title":"TYK2 and IL-23 Pathway Therapies in Psoriasis: Associations With IL-6, Tryptophan Metabolism, and Depressive Symptoms.","journal":"International journal of dermatology","methods":"","results":"For HADS-D scores, the TYK2 inhibitor group showed significantly lower values compared with the non-JAK pool (β = 1.23, 95% confidence interval [CI]: 0.37-2.10). However, no significant differences were observed when compared with the IL-23 biologics group (β = 0.67, 95% CI: -0.76-2.10) or the JAK inhibitor group (β = 0.84, 95% CI: -1.54-3.21). Transcriptomic analysis of peripheral blood revealed significant downregulation of genes related to the IL-6 receptor, long-term depression pathways, and Th17 cell differentiation, while pathways associated with neuronal activity were upregulated. Metabolomic profiling highlighted a decrease in kynurenic acid, which is known for its pro-inflammatory and depressive effects, and an increase in 1H-indole-3-propanoic acid, an anti-inflammatory metabolite with neuroprotective properties. It is important to note that these findings are based on exploratory omics analyses, for which false discovery rate (FDR) control was applied.","abstract":"$30","keywords":["IL‐23","TYK2 inhibitor","depression","psoriasis","tryptophan"],"pubmed_id":"41524454","conclusions":"","publication_date":"2026-01-12T00:00:00"},"crossref":{"DOI":"10.1111/ijd.70230","URL":"https://doi.org/10.1111/ijd.70230","ISSN":["0011-9059","1365-4632"],"link":[{"URL":"https://onlinelibrary.wiley.com/doi/pdf/10.1111/ijd.70230","content-type":"application/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https://onlinelibrary.wiley.com/doi/full-xml/10.1111/ijd.70230","content-type":"application/xml","content-version":"vor","intended-application":"text-mining"},{"URL":"https://onlinelibrary.wiley.com/doi/pdf/10.1111/ijd.70230","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":null,"type":"journal-article","issue":null,"score":1,"title":["TYK2 and IL‐23 Pathway Therapies in Psoriasis: Associations With IL‐6, Tryptophan Metabolism, and Depressive 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University Shanghai China"}]},{"given":"Junhao","family":"Zhu","sequence":"additional","affiliation":[{"name":"Department of Dermatology Huashan Hospital Affiliated with Fudan University Shanghai China"}]},{"given":"Huiyu","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Dermatology Huashan Hospital Affiliated with Fudan University Shanghai China"}]},{"given":"Yilun","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Dermatology Huashan Hospital Affiliated with Fudan University Shanghai China"}]},{"given":"Jiazheng","family":"Sun","sequence":"additional","affiliation":[{"name":"Department of Dermatology Huashan Hospital Affiliated with Fudan University Shanghai China"}]},{"given":"Chenghui","family":"Zheng","sequence":"additional","affiliation":[{"name":"Department of Dermatology Huashan Hospital Affiliated with Fudan University Shanghai China"}]},{"given":"Kexiang","family":"Yan","sequence":"additional","affiliation":[{"name":"Department of Dermatology Huashan Hospital Affiliated with Fudan University Shanghai China"}]},{"given":"Xiaonian","family":"Lu","sequence":"additional","affiliation":[{"name":"Department of Dermatology Huashan Hospital Affiliated with Fudan University Shanghai China"}]},{"given":"Bingjie","family":"Tian","sequence":"additional","affiliation":[{"name":"Department of Nursing, Huashan Hospital Fudan University Shanghai China"}]},{"given":"Nan","family":"Yu","sequence":"additional","affiliation":[{"name":"Department of Dermatology General Hospital of Ningxia Medical University Yinchuan China"}]},{"given":"Jinhua","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Dermatology Huashan Hospital Affiliated with Fudan University Shanghai China"}]},{"given":"Juan","family":"Du","sequence":"additional","affiliation":[{"name":"Department of Dermatology Huashan Hospital Affiliated 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Journal of Dermatology"],"reference-count":31,"published-online":{"date-time":null,"timestamp":null,"date-parts":[[2026,1,12]]},"references-count":31,"short-container-title":["Int J Dermatology"],"is-referenced-by-count":0},"unpaywall":{"doi":"10.1111/ijd.70230","is_oa":false,"title":"TYK2 and IL‐23 Pathway Therapies in Psoriasis: Associations With IL‐6, Tryptophan Metabolism, and Depressive 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Inhibitor","value_numeric":null},{"paper_doi":"10.1111/ijd.70230","tag_type":"modality","value":"TYK2 Inhibitor","value_numeric":null},{"paper_doi":"10.1111/ijd.70230","tag_type":"sample_size","value":"n=298","value_numeric":298},{"paper_doi":"10.1111/ijd.70230","tag_type":"study_design","value":"Cross-Sectional Study","value_numeric":null},{"paper_doi":"10.1111/ijd.70230","tag_type":"warning","value":"Design classification is inferred as cross‑sectional; timeframe was not reported.","value_numeric":null},{"paper_doi":"10.1111/ijd.70230","tag_type":"warning","value":"Effect estimate direction (β) may depend on model coding; interpretation follows the authors’ text.","value_numeric":null},{"paper_doi":"10.1111/ijd.70230","tag_type":"warning","value":"Omics results are exploratory despite FDR control and lack clinical outcome measures.","value_numeric":null}],"summaries":{"what_studied":"In 298 patients with psoriasis, depressive symptoms (HADS-D) were compared across TYK2 inhibitors, JAK inhibitors, and a pooled non‑JAK group (IL‑23 biologics, IL‑17 biologics, others) using adjusted GENMOD models. Peripheral blood transcriptomics and metabolomics were explored.","key_result":"HADS‑D scores were lower with TYK2 inhibitors versus the non‑JAK pool (β=1.23, 95% CI 0.37‑2.10), with no difference versus IL‑23 biologics (β=0.67, 95% CI −0.76‑2.10) or JAK inhibitors (β=0.84, 95% CI −1.54‑3.21). Omics showed downregulation of IL‑6 receptor, long‑term depression, and Th17 pathways; neuronal activity pathways were upregulated, kynurenic acid decreased, and 1H‑indole‑3‑propanoic acid increased (FDR‑controlled).","limitations":"Nonrandomized comparisons with a pooled non‑JAK comparator. Omics findings were exploratory despite FDR control.","practice_takeaway":"In this cohort, TYK2 therapy was associated with lower HADS‑D than a pooled non‑JAK group, but similar to IL‑23 biologics and JAK inhibitors. Treat these signals as hypothesis‑generating rather than a basis for therapy selection until validated."}},{"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. 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From Weeks 12 to 28, PASI responses with tildrakizumab increased from 60.77%→81.84% (PASI 75), 38.54%→71.23% (PASI 90), and 6.97%→22.64% (PASI 100); by Week 28, efficacy was comparable to TNFα, IL-17, IL-12/23, and other IL-23 inhibitors.","practice_takeaway":"For Asian adults starting tildrakizumab, expect slower early clearance by 12 weeks but marked gains by 28 weeks, reaching parity with other biologics. 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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.","abstract":"$36","keywords":[],"pubmed_id":"40900466","conclusions":"","publication_date":"2025-09-03T00:00:00"},"crossref":{"DOI":"10.1001/jamadermatol.2025.2972","URL":"https://doi.org/10.1001/jamadermatol.2025.2972","ISSN":["2168-6068"],"link":[{"URL":"https://jamanetwork.com/journals/jamadermatology/articlepdf/2838219/jamadermatology_raby_2025_oi_250041_1762976601.59148.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":"1107","type":"journal-article","issue":"11","score":1,"title":["Interleukin-17 Inhibitors and Early Major Adverse Cardiovascular Events"],"author":[{"given":"Maxime","family":"Raby","sequence":"first","affiliation":[{"name":"Univ Rennes, CHU Rennes, Inserm, EHESP, Irset (Institut de Recherche en 13 Santé, Environnement et Travail)—UMR_S 1085, Rennes, France"},{"name":"Department of Dermatology, Université de Rennes, CHU Rennes, Rennes, 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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. 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control cohort were not reported.","value_numeric":null}],"summaries":{"what_studied":"A retrospective cohort of adults with psoriatic arthritis in MarketScan (2015-2024) evaluated use patterns of combination targeted therapy and compared serious and opportunistic infections requiring inpatient care versus standard therapy using propensity score matching over 3- and 6-month continuous-use windows.","key_result":"Of 82,399 individuals with psoriatic arthritis, 542 used combination therapy for 3 months and 200 for 6 months; most common pairs were a TNF inhibitor with apremilast (34%-37%) and an IL-17 inhibitor with apremilast (27%-29%). Serious infection incidence was 7.38–15.00 per 1000 patients and opportunistic infection 0–1.85 per 1000; no significant risk increase versus standard therapy (PS-matched serious infection RRs: 0.53 [95% CI, 0.17–1.63] at 3 months and 1.50 [0.34–6.65] at 6 months; opportunistic infection RR: 1.00 [0.09–11.02] at 3 months; 6-month RR not applicable).","limitations":"Findings are from commercially insured adults and rely on ICD-10 inpatient codes for infection outcomes. Combination-therapy users and infection events were few, yielding wide confidence intervals and a non-estimable 6-month opportunistic infection risk.","practice_takeaway":"In this claims cohort, combining targeted agents—often a biologic plus apremilast—was used in about 1% of adults with psoriatic arthritis and was not associated with higher hospitalization for serious or opportunistic infections over 3–6 months versus standard therapy. If considering such combinations, counsel that observed infection risk was not higher, but estimates are imprecise and larger studies are needed."}},{"doi":"10.1001/jamadermatol.2025.2714","pmid":"40768223","title":"Biopharmaceutical Switching in Psoriasis Treatment","journal_title":"JAMA Dermatology","journal_issn":"2168-6068","published_at":"2025-08-06T00:00:00.000Z","url":"https://doi.org/10.1001/jamadermatol.2025.2714","source_score":82,"is_retracted":false,"is_open_access":false,"raw_metadata":{"ooir":{"day":"2025-10-19","doi":"10.1001/jamadermatol.2025.2714","days":"30","issn":"2168-6068","rank":"6","field":"Clinical Medicine","score":"82","category":"Dermatology","categories":["Dermatology"],"_categories":["Dermatology"]},"pubmed":{"doi":"10.1001/jamadermatol.2025.2714","title":"Biopharmaceutical Switching in Psoriasis Treatment: A Systematic Review and Meta-Analysis.","journal":"JAMA dermatology","methods":"","results":"Twenty-four RCTs involving 12 661 patients with psoriasis and 8 switching categories were analyzed. Significant differences observed in PASI 90 between week 4 and week 0 (odds ratio [OR], 6.53; 95% CI, 2.58-16.51). Substantial disparities were noted across various PASI response metrics, specifically PASI 90 (OR, 28.61; 95% CI, 12.89-63.47), PASI 75 (OR, 11.11; 95% CI, 5.95-20.75), and PASI 100 (OR, 18.76; 95% CI, 8.37-42.01). No difference exists in safety outcomes between the end point and week 0, including in serious AEs (OR, 1.63; 95% CI, 0.72-3.69), severe AEs (OR, 1.40; 95% CI, 0.61-3.26), and treatment-related AEs (OR, 1.79; 95% CI, 0.41-7.88). The highest risk of infection was associated with switching from anti-TNF-α agents to anti-interleukin (IL)-23p19, anti-IL-17A, or anti-IL-12/23p40 agents, with infection rates of 0.62%, 0.54% and 0.39%, respectively.","abstract":"$3b","keywords":[],"pubmed_id":"40768223","conclusions":"","publication_date":"2025-08-06T00:00:00"},"crossref":{"DOI":"10.1001/jamadermatol.2025.2714","URL":"https://doi.org/10.1001/jamadermatol.2025.2714","ISSN":["2168-6068"],"link":[{"URL":"https://jamanetwork.com/journals/jamadermatology/articlepdf/2837167/jamadermatology_zhang_2025_oi_250038_1760475172.18406.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":"1029","type":"journal-article","issue":"10","score":1,"title":["Biopharmaceutical Switching in Psoriasis Treatment"],"author":[{"given":"Miao","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Dermatology, Yueyang Hospital of Integrated Traditional Chinese and 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The prespecified primary end point was PASI 90; secondary outcomes included PASI 75/100, global assessments, BSA ≤1%, PROMs, and safety events.","key_result":"PASI 90 improved by week 4 vs baseline (OR 6.53; 95% CI 2.58-16.51) and by end point vs baseline (OR 28.61; 95% CI 12.89-63.47); PASI 75 (OR 11.11; 95% CI 5.95-20.75) and PASI 100 (OR 18.76; 95% CI 8.37-42.01) also improved. No differences were seen in serious AEs (OR 1.63; 95% CI 0.72-3.69), severe AEs (OR 1.40; 95% CI 0.61-3.26), or treatment-related AEs (OR 1.79; 95% CI 0.41-7.88); infection rates were highest when switching from anti–TNF-α to IL-23p19 (0.62%), IL-17A (0.54%), or IL-12/23p40 (0.39%).","limitations":"Authors note the need for larger patient cohorts and longer follow-up to confirm findings. The abstract does not detail follow-up duration, switching regimens, or PROM results, and safety estimates have wide CIs.","practice_takeaway":"For adults with plaque psoriasis who fail a biologic, switching—especially across classes—can yield high PASI responses without an observed increase in serious adverse events; monitor for infections, particularly after switching from anti–TNF-α to IL-23, IL-17, or IL-12/23 agents."}}],"initialOffset":23,"fetchConfig":{"kind":"tags","tags":[{"tag_type":"modality","value":"IL-17 Inhibitor"}]},"breadcrumbItems":[{"name":"Home","href":"/"},{"name":"Research Hub","href":"/hub"},{"name":"Modalities","href":"/hub/tag/modality"},{"name":"IL-17 Inhibitor"}],"hrefConfig":{"basePath":"/hub/papers","webViewQueryParams":{"hub_ctx":"tag","hub_tag_type":"modality","hub_tag_value":"IL-17 Inhibitor"}}}]]

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