2f:I[703058,["/_next/static/immutable/chunks/3bhq_5eh1d760.js","/_next/static/immutable/chunks/2iy5wruuedsh6.js","/_next/static/immutable/chunks/2pfsjpn6k6zlg.js","/_next/static/immutable/chunks/26c7v3_3uwnwu.js","/_next/static/immutable/chunks/00yc7rcvua6a7.js","/_next/static/immutable/chunks/37ktb71aq3480.js","/_next/static/immutable/chunks/2d50b-7eu4558.js","/_next/static/immutable/chunks/06_yt270h41rg.js","/_next/static/immutable/chunks/2d6noqpp6ehas.js","/_next/static/immutable/chunks/1sx186c93bpzg.js","/_next/static/immutable/chunks/3dc-1n866s65i.js","/_next/static/immutable/chunks/20x2y96ldu5wx.js","/_next/static/immutable/chunks/2w1bvggzb0ga8.js","/_next/static/immutable/chunks/2051ffx3xzio9.js"],"PaperListPageClient"] 30:T6e7,We examine coverage of self-administered disease-modifying antirheumatic drugs (DMARDs) in Medicare Part D. Using 2022-2026 Part D formulary data, we assessed coverage of the following DMARD classes that treat relapsed rheumatoid arthritis (RA): tumor necrosis factor (TNF) inhibitors, T cell costimulatory modulator, interleukin-6 (IL-6) inhibitors, and JAK inhibitors. We measured (1) coverage of individual DMARDs and (2) the generosity of coverage between classes (the share of plans covering at least one drug in each class) and within classes (the share of covered drugs within each class). We included 26,915 plan-year observations, representing 217.6 million enrolled beneficiaries from 2022 to 2026. In the five-year period, coverage was relatively complete (>94%) for etanercept and adalimumab (TNF inhibitors) and upadacitinib (JAK inhibitor). However, coverage was lower for golimumab and certolizumab (TNF inhibitors), abatacept (the sole T cell costimulatory modulator), sarilumab (IL-6 inhibitor), and baricitinib (JAK inhibitor). Moreover, only 10.4% and 37.6% of stand-alone and Medicare Advantage (MA) Part D plans, respectively, covered all mechanisms of action, mostly due to low coverage of abatacept. In 2026, only 0.3% and 21.2% of stand-alone and MA Part D plans, respectively, covered abatacept. On the other hand, coverage increased for IL-6 inhibitors, likely due to the availability of biosimilar drugs for tocilizumab in 2024. The growing exclusions of self-administered DMARDs across several mechanisms of action and heterogeneity in coverage by plan type suggest potential barriers to accessing optimal RA treatments. Further monitoring of formulary adequacy and research into the clinical impacts of formulary exclusions are warranted.31:T949, Objective We examine coverage of self‐administered disease‐modifying antirheumatic drugs (DMARDs) in Medicare Part D. Methods Using 2022–2026 Part D formulary data, we assessed coverage of the following DMARD classes that treat relapsed rheumatoid arthritis (RA): tumor necrosis factor (TNF) inhibitors, T cell costimulatory modulator, interleukin‐6 (IL‐6) inhibitors, and JAK inhibitors. We measured (1) coverage of individual DMARDs and (2) the generosity of coverage between classes (the share of plans covering at least one drug in each class) and within classes (the share of covered drugs within each class). Results We included 26,915 plan‐year observations, representing 217.6 million enrolled beneficiaries from 2022 to 2026. In the five‐year period, coverage was relatively complete (>94%) for etanercept and adalimumab (TNF inhibitors) and upadacitinib (JAK inhibitor). However, coverage was lower for golimumab and certolizumab (TNF inhibitors), abatacept (the sole T cell costimulatory modulator), sarilumab (IL‐6 inhibitor), and baricitinib (JAK inhibitor). Moreover, only 10.4% and 37.6% of stand‐alone and Medicare Advantage (MA) Part D plans, respectively, covered all mechanisms of action, mostly due to low coverage of abatacept. In 2026, only 0.3% and 21.2% of stand‐alone and MA Part D plans, respectively, covered abatacept. On the other hand, coverage increased for IL‐6 inhibitors, likely due to the availability of biosimilar drugs for tocilizumab in 2024. Conclusion The growing exclusions of self‐administered DMARDs across several mechanisms of action and heterogeneity in coverage by plan type suggest potential barriers to accessing optimal RA treatments. Further monitoring of formulary adequacy and research into the clinical impacts of formulary exclusions are warranted. 32: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.33:Tf24, Importance The cardiovascular impact of biologics used in psoriasis is not fully understood. Several studies have suggested that the inhibition of the T-helper 17 cell pathway could lead to the destabilization of atherosclerotic plaques, leading to major adverse cardiovascular events (MACEs). Objective To assess whether the initiation of interleukin (IL)-17(R)A inhibitors triggers MACEs. Design, Setting, and Participants In this case–time-control study using the French National Health Insurance database, all individuals who received IL-17(R)A inhibitors (secukinumab, ixekizumab, and brodalumab) from 2016 to 2021, were included and classified according to their cardiovascular risk level. The risk period was defined as the 6 months before the MACE, and the reference period as the 6 months before the risk period. The same design for patients who received tumor necrosis factor (TNF)–α inhibitors (adalimumab or etanercept) for similar indications (psoriasis, psoriatic arthritis, ankylosing spondylitis, or juvenile arthritis), as an active comparator. The data analysis was conducted between April 2023 and August 2024. Exposure The initiation of the biologic was screened in both periods. Main Outcomes and Measures The odds ratios (ORs) for the risk of MACEs were assessed following the initiation of IL-17(R)A inhibitors and TNF-α inhibitors independently. Subsequently, the OR for the risk of MACE associated with IL-17(R)A inhibitors was estimated using TNF-α inhibitors as the comparator. Results Among the 34 241 individuals who received an IL-17(R)A inhibitor, 381 MACEs were analyzed, including 176 acute coronary syndromes and 84 ischemic strokes in the main analysis. Initiation of IL-17(R)A inhibitors was not significantly associated with MACEs (OR, 1.25 [95% CI, 0.75-2.08] vs TNF-α inhibitor initiation and MACEs: OR, 0.90 [95% CI, 0.65-1.24]). Overall, the initiation of an IL-17(R)A inhibitor was not significantly associated with MACEs in the following 6 months, using TNF-α inhibitor as a comparator (OR, 1.40 [95% CI, 0.77-2.54]), regardless of the individual cardiovascular risk ( P for homogeneity = .29). The definition of MACE was broadened in a first sensitivity analysis, and the risk period was shortened to 3 months in a second sensitivity analysis. The results did not change. Conclusions In this case–time-control study based on a national insurance database, there was no evidence of a significant association between MACEs and the initiation of IL-17(R)A inhibitors, regardless of the individual cardiovascular risk of the patient. However, a modest risk increase cannot be entirely excluded. 25:[[["$","script","0",{"type":"application/ld+json","dangerouslySetInnerHTML":{"__html":"{\"@context\":\"https://schema.org\",\"@type\":\"CollectionPage\",\"name\":\"Enbrel: brand Research & Clinical Takeaways\",\"description\":\"Explore peer-reviewed papers on Enbrel (brand). Clinician-written summaries and actionable practice insights. 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the level of evidence reflects this, not a randomized trial.","value_numeric":null},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"warning","value":"The elevated serious infection signals for apremilast and secukinumab vs. adalimumab were not consistent in sensitivity analyses — these should not be interpreted as definitive safety differences.","value_numeric":null},{"paper_doi":"10.1093/bjd/ljag174","tag_type":"warning","value":"Treatment episodes (n=46,770) far exceed patient count (n=18,976), meaning many patients switched treatments; channeling bias by disease severity or comorbidity cannot be fully excluded.","value_numeric":null}],"summaries":{"what_studied":"This large UK registry cohort (BADBIR) examined serious infection risk across systemic psoriasis treatments — including biologics (adalimumab, secukinumab, risankizumab, brodalumab, etanercept) and non-biologics (apremilast, standard treatments) — in 18,976 adult patients over 46,770 treatment episodes, using inverse probability weighting and both time-to-first-event and recurrent-event analyses.","key_result":"Overall serious infection incidence was 27.67 per 1,000 person-years; recurrent infection rate in those with prior infection was 78.70 per 1,000 person-years. The more robust recurrent-event (PWP) model showed risankizumab had lower serious infection risk vs. brodalumab (HR 0.74), etanercept (HR 0.75), and standard treatments (HR 0.80). Apparent elevated risks with apremilast (HR 1.53) and secukinumab (HR 1.34) vs. adalimumab in the time-to-first-event model were not consistent across sensitivity analyses. Serious infection-related deaths were rare (IR 1.81 per 1,000 person-years).","limitations":"- Elevated risks for apremilast and secukinumab were not replicated in sensitivity analyses, limiting confidence in those signals.\n- Observational registry design introduces potential residual confounding despite inverse probability weighting.\n- Channeling bias is possible, as sicker or higher-risk patients may have been preferentially prescribed certain agents.","practice_takeaway":"For psoriasis patients at elevated infection risk, risankizumab may offer a relative safety advantage over brodalumab, etanercept, and conventional systemic agents. The apparent higher infection risk with apremilast and secukinumab vs. adalimumab should be interpreted cautiously, as it was not robust across sensitivity analyses."}},{"doi":"10.1007/s13555-026-01761-7","pmid":"42068460","title":"A Narrative Review: Do Systemic Drugs Used in the Treatment of Psoriatic Disease Affect Alzheimer’s Disease?","journal_title":"Dermatology and Therapy","journal_issn":"2193-8210","published_at":"2026-05-02T00:00:00.000Z","url":"https://doi.org/10.1007/s13555-026-01761-7","source_score":7,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-05-10T13:20:36.620Z","updated_at":"2026-05-10T13:20:36.620Z","tags":[{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"age_group","value":"older_adult","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"brand","value":"Cosentyx","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"brand","value":"Enbrel","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"brand","value":"Humira","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"brand","value":"Otezla","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"brand","value":"Remicade","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"brand","value":"Sotyktu","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"brand","value":"Stelara","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"category","value":"Dermatology","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"condition","value":"Alzheimer's Disease","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"condition","value":"Dementia","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"condition","value":"Psoriasis","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"condition","value":"Psoriatic Arthritis","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"generic","value":"acitretin","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"generic","value":"adalimumab","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"generic","value":"apremilast","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"generic","value":"cyclosporine","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"generic","value":"deucravacitinib","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"generic","value":"etanercept","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"generic","value":"infliximab","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"generic","value":"methotrexate","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"generic","value":"roflumilast","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"generic","value":"secukinumab","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"generic","value":"tofacitinib","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"generic","value":"upadacitinib","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"generic","value":"ustekinumab","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"modality","value":"Conventional Synthetic DMARD","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"modality","value":"IL-12/23 Inhibitor","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"modality","value":"IL-17 Inhibitor","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"modality","value":"IL-23 Inhibitor","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"modality","value":"JAK Inhibitor","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"modality","value":"NSAID","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"modality","value":"PDE4 Inhibitor","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"modality","value":"Retinoid","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"modality","value":"TNF-Alpha Inhibitor","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"modality","value":"TYK2 Inhibitor","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"study_design","value":"Narrative Review","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"warning","value":"Corresponding author (Tsen-Fang Tsai) has disclosed extensive consultant relationships with manufacturers of many drugs discussed in the review.","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"warning","value":"Level of evidence assigned as 5 (narrative review/expert opinion) due to absence of PRISMA methodology, risk-of-bias tools, or meta-analytic synthesis, even though individual cited studies range from Level 1 to Level 5.","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"warning","value":"Several drug-AD associations cited are from studies in rheumatoid arthritis populations, not specifically psoriasis patients; generalizability to psoriatic disease may be limited.","value_numeric":null},{"paper_doi":"10.1007/s13555-026-01761-7","tag_type":"warning","value":"This is a narrative review without formal systematic methods; findings are hypothesis-generating and subject to selection bias in included studies.","value_numeric":null}],"summaries":{"what_studied":"This narrative review examined whether systemic drugs used for psoriatic disease (NSAIDs, methotrexate, cyclosporin, retinoids, PDE4 inhibitors, JAK inhibitors, TYK2 inhibitors, and biologics targeting TNF-α, IL-12/23, IL-17, and IL-23) influence the risk or progression of Alzheimer's disease (AD), using AD as a model for dementia. Literature from PubMed (2015–2025) was synthesized across preclinical, observational, and RCT-level evidence.","key_result":"Most preclinical and observational data suggest antipsoriatic therapies may reduce AD risk. The strongest clinical signal comes from a propensity score–matched cohort (n=1,766) showing biologic therapy for psoriasis was associated with a **53% lower risk of incident dementia** vs. conventional systemic therapy alone. In a large EHR-based study (56 million records), TNF inhibitors (etanercept, adalimumab, infliximab) were linked to markedly reduced AD odds (ORs 0.34, 0.28, and 0.52, respectively; all P<0.0001). However, several large observational studies found the psoriasis–dementia association attenuated or disappeared after adjusting for comorbidities.","limitations":"- Narrative (not systematic) review with no PRISMA flow, risk-of-bias assessment, or quantitative synthesis, limiting reproducibility.\n- Most mechanistic evidence comes from preclinical models (Level 5), with very few adequately powered RCTs in humans.\n- Residual confounding by disease severity, metabolic comorbidities, and medication use cannot be excluded in observational studies.","practice_takeaway":"For older patients with psoriasis, consider early cognitive screening, as shared inflammatory mechanisms may raise dementia risk—especially in those with metabolic comorbidities. Biologic therapy, particularly TNF inhibitors, shows the most consistent signal for possible neuroprotection, but current evidence is hypothesis-generating and should not yet change prescribing solely for dementia prevention."}},{"doi":"10.1002/art.70132","pmid":"41841636","title":"Coverage Generosity of Novel Antirheumatic Drugs in Medicare Advantage and Stand‐Alone Part D Plans","journal_title":"Arthritis & Rheumatology","journal_issn":"2326-5191","published_at":"2026-03-17T00:00:00.000Z","url":"https://doi.org/10.1002/art.70132","source_score":24,"is_retracted":false,"is_open_access":true,"raw_metadata":{"ooir":{"day":"2026-04-25","doi":"10.1002/art.70132","days":"30","issn":"2326-5191","rank":"7","field":"Clinical Medicine","score":"24","category":"Rheumatology","categories":["Rheumatology"],"_categories":["Rheumatology"]},"pubmed":{"doi":"10.1002/art.70132","title":"Coverage Generosity of Novel Antirheumatic Drugs in Medicare Advantage and Stand-Alone Part D Plans.","journal":"Arthritis & rheumatology (Hoboken, N.J.)","methods":"","results":"We included 26,915 plan-year observations, representing 217.6 million enrolled beneficiaries from 2022 to 2026. In the five-year period, coverage was relatively complete (>94%) for etanercept and adalimumab (TNF inhibitors) and upadacitinib (JAK inhibitor). However, coverage was lower for golimumab and certolizumab (TNF inhibitors), abatacept (the sole T cell costimulatory modulator), sarilumab (IL-6 inhibitor), and baricitinib (JAK inhibitor). Moreover, only 10.4% and 37.6% of stand-alone and Medicare Advantage (MA) Part D plans, respectively, covered all mechanisms of action, mostly due to low coverage of abatacept. In 2026, only 0.3% and 21.2% of stand-alone and MA Part D plans, respectively, covered abatacept. On the other hand, coverage increased for IL-6 inhibitors, likely due to the availability of biosimilar drugs for tocilizumab in 2024.","abstract":"$30","keywords":[],"pubmed_id":"41841636","conclusions":"The growing exclusions of self-administered DMARDs across several mechanisms of action and heterogeneity in coverage by plan type suggest potential barriers to accessing optimal RA treatments. Further monitoring of formulary adequacy and research into the clinical impacts of formulary exclusions are warranted.","publication_date":"2026-03-17T00:00:00"},"crossref":{"DOI":"10.1002/art.70132","URL":"https://doi.org/10.1002/art.70132","ISSN":["2326-5191","2326-5205"],"link":[{"URL":"https://acrjournals.onlinelibrary.wiley.com/doi/pdf/10.1002/art.70132","content-type":"application/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https://acrjournals.onlinelibrary.wiley.com/doi/full-xml/10.1002/art.70132","content-type":"application/xml","content-version":"vor","intended-application":"text-mining"},{"URL":"https://acrjournals.onlinelibrary.wiley.com/doi/pdf/10.1002/art.70132","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":null,"type":"journal-article","issue":null,"score":1,"title":["Coverage Generosity of Novel Antirheumatic Drugs in Medicare Advantage and Stand‐Alone Part D 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the 217.6 million figure represents cumulative enrolled beneficiaries across plan-years and should not be interpreted as unique patients.","value_numeric":null},{"paper_doi":"10.1002/art.70132","tag_type":"warning","value":"Study design is best characterized as a repeated cross-sectional analysis of administrative formulary data; no causal inference about patient outcomes is possible.","value_numeric":null},{"paper_doi":"10.1002/art.70132","tag_type":"warning","value":"The 'safety_signal' impact flag is applied here in the access/policy sense — formulary exclusions represent a barrier to care signal, not a drug safety signal in the traditional adverse-event sense.","value_numeric":null}],"summaries":{"what_studied":"Coverage generosity of self-administered DMARDs (TNF inhibitors, T cell costimulatory modulator, IL-6 inhibitors, JAK inhibitors) across Medicare Part D stand-alone and Medicare Advantage plans from 2022–2026, using 26,915 plan-year observations representing 217.6 million enrolled beneficiaries.","key_result":"Coverage exceeded 94% for etanercept, adalimumab, and upadacitinib, but was markedly lower for abatacept (only 0.3% of stand-alone and 21.2% of MA Part D plans covered it in 2026). Only 10.4% of stand-alone and 37.6% of MA plans covered all mechanisms of action. IL-6 inhibitor coverage improved after tocilizumab biosimilars launched in 2024.","limitations":"Formulary data reflect plan-level coverage but do not capture actual patient-level access, utilization, or clinical outcomes resulting from exclusions. The study period ends at 2026, so long-term trends cannot be assessed. Reasons behind specific formulary exclusion decisions (e.g., rebate negotiations) are not examined.","practice_takeaway":"Clinicians prescribing abatacept or less-covered DMARDs to Medicare patients should proactively verify formulary status, as coverage varies widely by plan type and has been declining. Awareness of biosimilar-driven coverage gains (e.g., tocilizumab biosimilars) may help identify accessible alternatives when preferred agents are excluded."}},{"doi":"10.1001/jamadermatol.2025.2972","pmid":"40900466","title":"Interleukin-17 Inhibitors and Early Major Adverse Cardiovascular Events","journal_title":"JAMA Dermatology","journal_issn":"2168-6068","published_at":"2025-09-03T00:00:00.000Z","url":"https://doi.org/10.1001/jamadermatol.2025.2972","source_score":13,"is_retracted":false,"is_open_access":false,"raw_metadata":{"ooir":{"day":"2025-11-21","doi":"10.1001/jamadermatol.2025.2972","days":"7","issn":"2168-6068","rank":"10","field":"Clinical Medicine","score":"13","category":"Dermatology","categories":["Dermatology"],"_categories":["Dermatology"]},"pubmed":{"doi":"10.1001/jamadermatol.2025.2972","title":"Interleukin-17 Inhibitors and Early Major Adverse Cardiovascular Events.","journal":"JAMA dermatology","methods":"","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.","abstract":"$32","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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Arthritis","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2025.2972","tag_type":"generic","value":"adalimumab","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2025.2972","tag_type":"generic","value":"brodalumab","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2025.2972","tag_type":"generic","value":"etanercept","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2025.2972","tag_type":"generic","value":"ixekizumab","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2025.2972","tag_type":"generic","value":"secukinumab","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2025.2972","tag_type":"modality","value":"IL-17 Inhibitor","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2025.2972","tag_type":"modality","value":"TNF-Alpha Inhibitor","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2025.2972","tag_type":"sample_size","value":"n=34,241","value_numeric":34241},{"paper_doi":"10.1001/jamadermatol.2025.2972","tag_type":"study_design","value":"Case-Time-Control Study","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2025.2972","tag_type":"warning","value":"Abstract reports odds ratios without absolute event rates by exposure group.","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2025.2972","tag_type":"warning","value":"Design labeled as case–time–control; classification may be unfamiliar to some readers.","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2025.2972","tag_type":"warning","value":"Only early (3–6 month) risk windows were evaluated; longer-term risk remains uncertain.","value_numeric":null}],"summaries":{"what_studied":"A national case–time–control study of the French health insurance database (2016–2021) assessed whether initiating IL‑17(R)A inhibitors (secukinumab, ixekizumab, brodalumab) triggers major adverse cardiovascular events (MACEs) within 6 months, using TNF‑α inhibitors (adalimumab, etanercept) as an active comparator. Among 34,241 IL‑17(R)A recipients, 381 MACEs were analyzed; risk and reference windows were the 6 months before the MACE and the preceding 6 months.","key_result":"Initiation of IL‑17(R)A inhibitors was not significantly associated with MACEs (OR 1.25, 95% CI 0.75–2.08); TNF‑α inhibitor initiation also showed no association (OR 0.90, 95% CI 0.65–1.24). Compared with TNF‑α inhibitors, IL‑17(R)A initiation had an OR of 1.40 (95% CI 0.77–2.54) over 6 months, with similar findings across cardiovascular risk strata (P for homogeneity = .29) and unchanged results in sensitivity analyses (broader MACE definition; 3‑month risk window).","limitations":"Only early risk windows (3–6 months) were evaluated, so longer‑term risk was not assessed. Precision was limited by 381 MACEs, yielding wide confidence intervals that do not exclude a modest risk increase.","practice_takeaway":"In this large real‑world analysis, starting an IL‑17(R)A inhibitor did not show a significant increase in 6‑month MACEs versus TNF‑α inhibitors, across cardiovascular risk levels. Continue standard cardiovascular risk management; a small increase in early events cannot be ruled out."}}],"initialOffset":4,"fetchConfig":{"kind":"tags","tags":[{"tag_type":"brand","value":"Enbrel"}]},"breadcrumbItems":[{"name":"Home","href":"/"},{"name":"Research Hub","href":"/hub"},{"name":"Brands","href":"/hub/tag/brand"},{"name":"Enbrel"}],"hrefConfig":{"basePath":"/hub/papers","webViewQueryParams":{"hub_ctx":"tag","hub_tag_type":"brand","hub_tag_value":"Enbrel"}}}]]

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