# Sustained Efficacy and Safety of Tildrakizumab in Psoriasis Vulgaris Despite Multiple Prolonged Treatment Interruptions: A Case Report

**Authors:** Kazuki Yatsuzuka, Jun Muto, Satoshi Yoshida, Ken Shiraishi, Yasuhiro Fujisawa

PMC · DOI: 10.7759/cureus.87927 · 2025-07-14

## TL;DR

A patient with severe psoriasis remained in remission with tildrakizumab even after multiple long treatment breaks.

## Contribution

This case report demonstrates tildrakizumab's sustained efficacy despite prolonged treatment interruptions.

## Key findings

- The patient regained complete skin clearance after each treatment restart.
- No adverse events were observed during biologic treatment periods.
- Tildrakizumab may be effective for patients with unavoidable treatment gaps.

## Abstract

Psoriasis vulgaris is a persistent inflammatory skin disease that often necessitates long-term biologic therapy to maintain symptom control and prevent flares. Interruptions in biologic treatment are sometimes unavoidable due to individual health concerns or external circumstances, but the impact of repeated, extended gaps in therapy remains insufficiently understood. We describe a case involving a woman with moderate-to-severe psoriasis vulgaris who achieved sustained remission using tildrakizumab, even after multiple treatment interruptions, each lasting over a year. The patient initially received various conventional and biologic treatments before transitioning to tildrakizumab. Despite prolonged discontinuations prompted by personal concerns, she consistently regained complete skin clearance within months of restarting therapy. No therapy-related adverse events were recorded during any biologic treatment period. This case emphasizes the potential resilience of tildrakizumab efficacy in the setting of intermittent administration, suggesting its suitability for patients who may face unavoidable gaps in care. Further research is warranted to evaluate immunogenicity risks and long-term effectiveness in larger, diverse patient populations.

## Full-text entities

- **Genes:** IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}, IL23A (interleukin 23 subunit alpha) [NCBI Gene 51561] {aka IL-23, IL-23A, IL23P19, P19, SGRF}
- **Diseases:** thromboembolism (MESH:D013923), metabolic syndrome (MESH:D024821), infection (MESH:D007239), ADA (MESH:C531816), dyslipidemia (MESH:D050171), COVID-19 (MESH:D000086382), hypertension (MESH:D006973), Psoriasis (MESH:D011565), vasculitis (MESH:D014657), smoker (MESH:C000719328), Alzheimer's disease (MESH:D000544), psoriatic arthritis (MESH:D015535), cardiovascular disease (MESH:D002318), skin disease (MESH:D012871), inflammation (MESH:D007249)
- **Chemicals:** ustekinumab (MESH:D000069549), methotrexate (MESH:D008727), ADA (-), vitamin D3 (MESH:D002762), etretinate (MESH:D005050), cyclosporine (MESH:D016572), Tildrakizumab (MESH:C000598434)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12349925/full.md

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Source: https://tomesphere.com/paper/PMC12349925