# Exploratory Retrospective Assessment of Patients with Psoriasis Receiving Biological Therapy

**Authors:** Andrada-Luciana Lazar, Sorana D. Bolboacă, Adrian-Lucian Baican, Corina-Iulia Baican, Sorina Dănescu, Elisabeta Candrea, Diana Valentina Câmpean, Paula Iluț, Ioana Semenescu, Adela-Viviana Sitar-Tăut, Romana Vulturar, Olga Hilda Orășan, Angela Cozma

PMC · DOI: 10.3390/medicina62020257 · 2026-01-26

## TL;DR

This study examines how biological therapies affect psoriasis patients in Transylvania, finding that newer treatments like anti-IL-17 and anti-IL-23 show better outcomes than anti-TNF.

## Contribution

The study provides new insights into the effectiveness and switching patterns of biologics in a Romanian psoriasis patient population.

## Key findings

- Anti-IL-17 and anti-IL-23 therapies showed superior outcomes compared to anti-TNF at 36 weeks.
- All patients receiving anti-IL-23 achieved PASI 100 at 60 weeks.
- Anti-TNF therapy was switched more frequently due to reduced efficacy.

## Abstract

Background and Objectives: Biological therapies improve disease severity and quality of life in patients with psoriasis, but data on Romanian patients remain limited. Our study aimed to characterize patients with psoriasis from Transylvania and to evaluate the impact of biologics on disease severity, treatment switching, affected special areas response, quality of life, and laboratory biomarkers. Materials and Methods: We conducted a retrospective exploratory study at two centers in Cluj-Napoca, Romania, using routinely collected medical data. Results: One-hundred and fifteen patients (aged 2–72 years) were evaluated; 45 patients received anti-TNF, 43 received anti-IL-17, and 27 received anti-IL-23. Patients treated with anti-IL-17 or anti-IL-23 were older at diagnosis than those treated with anti-TNF (p = 0.0001). Psoriatic lesions were prevalent in the scalp (58.3%) and nails (36.5%). Methotrexate was the most common prior systemic therapy (87.8%), with no difference between the groups (p = 0.7668). Patients receiving anti-TNF therapy (46.7%) or anti-IL-17 therapy (20.9%) also most frequently received prior treatment with systemic retinoids. Cardiometabolic comorbidities, including hypertension (40.9%) and diabetes mellitus (20.9%), were prevalent. Anti-IL-17 therapies were used more frequently in patients with hypertension (46.5%), diabetes mellitus (34.9%), and psoriatic arthritis (34.9%). Baseline severity scores were comparable across the groups (p > 0.10). A therapeutic switch occurred in approximately one-quarter of the patients, most frequently in the anti-TNF group (57.8%), which also showed higher PASI and DLQI scores at switching (p < 0.0001). At 36 weeks, anti-IL-17 and anti-IL-23 therapies demonstrated superior outcomes compared to anti-TNF therapy (p = 0.045). All patients receiving anti-IL-23 therapy achieved a PASI 100 at the 60-week follow-up. Significant improvements in PASI and DLQI were observed for all biologics (p < 0.0001). Conclusions: Biological therapies were associated with significant improvements in disease severity and quality of life. Anti-TNF therapies were switched more frequently due to reduced efficacy, while clinical improvement was observed regardless of lesion localization.

## Linked entities

- **Proteins:** TNF (tumor necrosis factor), IL17A (interleukin 17A), IL37 (interleukin 37)
- **Diseases:** psoriasis (MONDO:0005083), diabetes mellitus (MONDO:0005015), psoriatic arthritis (MONDO:0011849)

## Full-text entities

- **Genes:** TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}, IL37 (interleukin 37) [NCBI Gene 27178] {aka FIL1, FIL1(ZETA), FIL1Z, IL-1F7, IL-1H, IL-1H4}, IL23A (interleukin 23 subunit alpha) [NCBI Gene 51561] {aka IL-23, IL-23A, IL23P19, P19, SGRF}
- **Diseases:** overweight (MESH:D050177), stroke (MESH:D020521), ischemic cardiomyopathy (MESH:D009202), Obesity (MESH:D009765), nausea (MESH:D009325), pruritus (MESH:D011537), Plaque-type psoriasis (MESH:D011565), Psoriatic lesions (MESH:D015535), Dermato-Venereological Disorders (MESH:C538052), skin and joint disease (MESH:D012871), dyslipidemia (MESH:D050171), Cardiometabolic disorders (MESH:D024821), inflammation (MESH:D007249), injury to (MESH:D014947), anxiety (MESH:D001007), hepatitis B and C (MESH:D006509), chronic kidney disease (MESH:D051436), abdominal pain (MESH:D015746), neoplasia (MESH:D009369), Diabetes mellitus (MESH:D003920), tuberculosis (MESH:D014376), pulmonary fibrosis (MESH:D011658), hepatic cytolysis (MESH:D056486), depression (MESH:D003866), scalp lesions (MESH:D004476), heart failure (MESH:D006333), peripheral artery disease (MESH:D058729), Infectious Diseases (MESH:D003141), PASI (MESH:D045169), erythema (MESH:D004890), multiple sclerosis (MESH:D009103), Immune dysregulation (OMIM:614878), atherosclerotic plaques (MESH:D058226), atherosclerosis (MESH:D050197), Hypertension (MESH:D006973), cytopenia (MESH:D006402), cholestasis (MESH:D002779), infection (MESH:D007239), Cardiovascular disease (MESH:D002318), myocardial infarction (MESH:D009203)
- **Chemicals:** Retinoid (MESH:D012176), Adalimumab (MESH:D000068879), MTX (MESH:D008727), Secukinumab (MESH:C555450), glycemia (MESH:D001786), Infliximab (MESH:D000069285), Ustekinumab (MESH:D000069549), Risankizumab (MESH:C000601773), lipid (MESH:D008055), Brodalumab (MESH:C571216), glucose (MESH:D005947), creatinine (MESH:D003404), sodium (MESH:D012964), cyclosporine (MESH:D016572), potassium (MESH:D011188), Guselkumab (MESH:C000588857), apremilast (MESH:C505730), GLY (-), urea (MESH:D014508), Ixekizumab (MESH:C549079)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12942126/full.md

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Source: https://tomesphere.com/paper/PMC12942126