0362 Patient-reported preferences for IL-17 and IL-23 inhibitor dosing frequencies in psoriasis management

Research trends and hotspots in biologics for plaque psoriasis: A bibliometric study from 2004 to 2023

Scabies, caused by Sarcoptes scabiei, presents a significant global health challenge and is primarily transmitted through skin-to-skin contact. Despite the remarkable advances in the use of biologics to treat psoriasis, a concerning trend of increased susceptibility to infections and infestations has emerged. In this comprehensive case study, we report the complex clinical scenario of a patient with a neurological disorder and psoriasis undergoing biologic treatment who was subsequently diagnosed with crusted scabies predominantly localized to her psoriatic plaques. A 37-year-old female patient with Down syndrome undergoing risankizumab biologic therapy for psoriasis was reviewed in the biologics clinic on a routine appointment. The patient exhibited a notable escalation in her Psoriasis Area and Severity Index (PASI) score, increasing from 11.4 to 30.6, accompanied by crusted plaques resembling the distribution of her psoriasis. Dermoscopic examination revealed distinctive burrows and mites, with microscopic confirmation of three scabies mites. A scabies outbreak in the patient’s care facility prompted a comprehensive treatment regimen involving topical permethrin and oral ivermectin, resulting in nearly complete clearance. However, residual crust necessitated additional topical treatments for resolution. Crusted scabies, prevalent in individuals with immunodeficiencies and neurological disorders such as Down syndrome, is intricately linked to cognitive impairment, altering itch perception and fostering parasite proliferation despite elevated IgE and eosinophils. Notably, crusted scabies demonstrates elevated interleukin (IL)-17 levels, potentially indicating T helper (Th)17 dysregulation. Risankizumab, an IL-23 inhibitor, influences the inflammatory function of CD4+ helper T cells, particularly Th17 cells, which produce cytokines such as IL-17A and IL-17F. The pathogenesis of psoriasis involves a positive feedback loop wherein IL-17 stimulates keratinocytes to produce inflammatory mediators, exacerbating inflammation and keratinocyte proliferation. Our hypothesis suggests that risankizumab-induced downregulation of Th17, combined with the patient’s Down syndrome background, heightened the risk of scabies infestation, leading to crusted scabies development in specific areas. This comprehensive case study highlights the importance of considering crusted scabies in immunosuppressed or neurologically affected patients with refractory psoriasis, providing valuable insights into the intricate interplay between biologics, patient characteristics and cutaneous manifestations.

The current management of psoriasis does not differentiate between younger and older patients in selecting the safest and/or most effective biologic. To explore the effect of age at treatment initiation in response to biologics in patients with moderate-to-severe psoriasis in the UK and Eire. Data from patients registered in the British Association of Dermatologists Biologics and Immunomodulators Register (BADBIR) from 2007 to 2024 on a first course of tumour necrosis factor (TNF), interleukin (IL)-12/IL-23, IL-17 and IL-23 inhibitors with at least 6 months' follow-up were included. Patients aged ≥ 16 years at registration were organized into the following cohorts: 16-24 years, 25-34 years, 35-44 years, 45-54 years, 55-64 years, 65-74 years and ≥ 75 years. The 45-54 years age group was used as the reference cohort. Biologic survival was defined as the time between treatment initiation to its discontinuation associated with ineffectiveness or the occurrence of adverse events (AEs). Adjusted hazard ratios (aHR) with 95% confidence intervals (CIs) was estimated using a flexible parametric model to compare discontinuing treatment between the age groups. Each model included exposure (biologic class), effect modifier (age groups), interaction terms, baseline demographics and clinical and disease severity covariates. In total, 14 294 patients were included and organized into the following age groups: 16-24 years, n = 847 (5.9%); 25-34 years, n = 2502 (17.5%); 35-44 years, n = 3575 (25.0%); 45-54 years, n = 3863 (27.0%); 55-64 years, n = 2338 (16.4%); 65-74 years, n = 954 (6.8%); and ≥ 75 years, n = 215 (1.5%). The interaction effects model showed that individuals aged 16-24 years were more likely to discontinue TNF inhibitors (TNFi) due to ineffectiveness than those in the reference cohort (aHR 1.30, 95% CI 1.10-1.55). For survival associated with AEs, individuals aged 55-64 years were at higher risk of discontinuing TNFi and IL-12/IL-23 inhibitors [IL-12i/IL-23i; aHR 1.33 (95% CI 1.13-1.56) and aHR 1.34 (95% CI 1.03-1.75), respectively]; those aged 65-74 years were more likely to discontinue TNFi, IL-12i/IL-23i and IL-17 inhibitors [aHR 1.89 (95% CI 1.54-2.31), aHR 2.00 (95% CI 1.47-2.73) and aHR 1.69 (95% CI 1.08-2.64), respectively], whereas individuals aged ≥ 75 years were at higher risk of discontinuing the four biologic classes. Patients aged 16-24 years with psoriasis are more likely to stop TNFi due to ineffectiveness, whereas those aged ≥ 55 years are more likely to stop biologics due to AEs. These real-world findings provide important information for clinicians treating people with moderate-to-severe psoriasis across all age groups.

Background:In Cryopyrin-Associated Periodic Syndromes (CAPS), IL-1 inhibition has been proven to control disease activity and improve quality of life. With good disease management on IL-1 inhibition during reproductive age, effects...

Is There Evidence of Any Safety Differences Among DPP-4 Inhibitors in the Treatment of People with Type 2 Diabetes Mellitus and Reduced GFR Due to Chronic Kidney Disease?

Purpose: To examine proton pump inhibitor (PPI) dosing frequency and its association with PPI therapy utilization among patients with gastroesophageal reflux disease (GERD). Methods: This retrospective administrative claims data analysis included patients with ≥1 pharmacy claim for a PPI from 1/1/2006-3/31/2007; the first claim date was the index date. Patients had GERD diagnoses (ICD-9-CM 530.1, 530.10-530.12, 530.3, 530.81, 530.85, 787.1) and continuous enrollment for 12 months pre- and post-index date. Index PPI dosing frequency (quantity dispensed/days supply) was measured during post-index period. Patients were assigned to frequency categories: once daily (QD) for frequency=1.0, twice daily (BID) for frequency=2.0, >BID for frequency>2.0. Adherence was measured with medication possession ratio (MPR) and defined as MPR≥0.80. PPI change was defined as ≥1 non-index PPI fill after index date. Descriptive analysis was conducted and significance was tested with t-test and chi-square. Results: The study included 174,619 patients with GERD. The mean age of the cohort was 51.1 (±12.7) years and 54.6% were female. Most (91.4%) were on QD regimen throughout the post-index period, 8.1% were on BID and 0.5% of the patients were on >BID and excluded from analysis. Among patients whose first (index) PPI fill was QD, 1.8% increased dosing frequency during post-index and 0.5% had both an increase and decrease in frequency; all others had no change in dosing frequency. Among patients whose index PPI fill was BID, 12.3% decreased frequency, 1.0% increased frequency, and 4.3% both increased and decreased frequency during post-index. More QD PPI users (25.8%) than BID PPI (18.1%) were adherent (p<0.0001). Mean (standard deviation) MPR among patients with QD PPI and BID PPI were 0.53 (0.35) and 0.47 (0.32), respectively (p<0.0001). PPI change occurred in 26.2% of QD patients and 28.3% of BID patients (p<0.0001). Among PPI changers, 91.1% of index QD users changed to a different PPI with QD dosing, 8.3% changed to a different PPI with BID dosing and 0.6% changed to different PPI with >BID dosing. Among PPI changes, 52.2% of index BID users changed to a different PPI with QD dosing, 44.6% changed to a different PPI with BID dosing and 3.2% changed to a different PPI with >BID dosing. Conclusion: Once-daily dosing of PPI was associated with higher likelihood of adherence. More than a quarter of GERD patients changed to a different PPI during the study period and a substantial proportion of BID PPI users continued on BID dosing on a different PPI. Sponsored by Takeda Pharmaceuticals North America, Inc., Deerfield, IL, USA. Disclosure: Ronnie Fass-Consultant: Takeda, Xenoport, Vecta, Eisai, Salix; Research Suuport: Takeda, Wyeth, AstraZeneca, Sucampo; Speakers Bureau: Eisai, Takeda Reema Mody, M Charisse DeLeon-Employee: Takeda Rachel Halpern, Laura Becker-Employee: i3 Innovus, a vendor to Takeda.

Psoriasis is a chronic immune-mediated skin disease with highly variable responses to systemic therapies. Emerging evidence highlights the microbiome as a potential modulator of drug efficacy and toxicity. Gut bacteria can enzymatically metabolize drugs, such as methotrexate, altering bioavailability and therapeutic outcomes, while microbial metabolites-including short-chain fatty acids, branched-chain amino acids, and tryptophan derivatives-shape host immunity and barrier integrity, influencing drug action. Baseline microbial signatures have been linked to treatment response, potentially predicting anti-TNF or IL-17 inhibitor efficacy. Systemic therapies themselves reshape microbial communities: IL-17 blockade induces broad shifts in gut and skin microbiota, whereas cyclosporine and anti-TNF agents exert subtler effects. Small molecules such as apremilast and fumarates may reduce fungal overgrowth and influence microbial composition, whereas data on JAK/TYK2 inhibitors remain limited. Notably, current evidence exhibits a literature bias toward the gut microbiota, while the roles of the oral and skin axes remain understudied. Adjunctive microbiome-directed interventions, including probiotics and fecal microbiota transplantation, have demonstrated potential to enhance treatment outcomes by promoting anti-inflammatory taxa and restoring barrier function. Despite these promising findings, current evidence is heterogeneous, often limited by small sample sizes, short follow-up, and variable methodology. Integrating pharmacomicrobiomics data with clinical, genetic, and multi-omics profiling could enable precision medicine approaches in psoriasis, allowing therapy selection tailored to individual microbial and metabolic signatures. Future research should focus on longitudinal, multicenter studies to identify actionable microbial biomarkers, clarify mechanistic interactions between drugs, microbes, and host immunity, and evaluate microbiome-targeted adjuncts in randomized trials. Understanding the bidirectional crosstalk between systemic therapies and the microbiome may transform psoriasis management, improving efficacy, reducing adverse events, and enabling durable, personalized responses.

The pathogenesis of pain related to dyskinesia in Parkinson disease is thought to be based on hypersensitivity to pain. To relieve symptoms, it is essential to reduce dyskinesia and alleviate symptoms. Frequent small doses of levodopa, dopamine agonists, MAOB inhibitors, and amantadine are effective. If improvement is insufficient, device-aided therapy should be considered. In addition, antidepressants, weak opioid analgesics, benzodiazepines, gabapentin, botulinum toxin injections, and exercise therapy are also worth trialing.