Background: Tildrakizumab is a humanized monoclonal antibody that binds selectively the p19 subunit of interleukin‐23. It is approved for treatment of moderate–severe chronic plaque psoriasis.Objectives: We conducted a 52‐week retrospective study to assess the effectiveness and safety of tildrakizumab in a real‐life setting.Methods: Our retrospective study included 237 consecutive adults with moderate‐to‐severe plaque psoriasis, enrolled in 10 different Italian centres, treated with tildrakizumab up to Week 52. Patient characteristics, comorbidities, previous treatments and the PASI (Psoriasis Area and Severity Index) score at each visit (baseline, Week 16, Week 28 and Week 52) were retrieved from the electronic medical records. The percentages of patients achieving 75%, 90% and 100% (PASI 75, PASI 90 and PASI 100) improvement in PASI with respect to baseline PASI were registered.Results: At Week 52, 90.91%, 73.55% and 58.68% of patients achieved a PASI reduction ≥75% (PASI 75), PASI 90 and PASI 100, respectively. An absolute PASI ≤ 2 was reached by 85.95% at Week 52. Compared with Phase 3 clinical trials, we observed similar rates of PASI 75/90 responses and higher percentages of patients achieving PASI 100. Patients who had not responded to previous biologic treatments and patients with cardio‐metabolic comorbidities were significantly more likely to achieve PASI 100 at Week 28 and PASI 90 at Week 52. The higher body mass index did not interfere with the odds of reaching PASI 75/90/100 at each time point. No significant safety findings were recorded throughout the study, and none of the patients had to interrupt the treatment because of adverse events.Conclusion: Our data suggest that the efficacy of tildrakizumab for plaque psoriasis in ‘real‐life’ clinical practice is comparable with Phase 3 clinical trials with higher percentages of patients achieving complete skin clearance (PASI 100) at Weeks 16, 28 and 52.

Atopic dermatitis and psoriasis are traditionally considered diseases that cannot coexist, since they are described as the result of the activation of opposing inflammatory pathways. However, this belief has been debunked, and numerous cases of psoriasis induced by dupilumab, a biologic treatment for atopic dermatitis, have been reported. We report three cases of dupilumab-induced psoriasis and we present a literature review including cases of “de novo” psoriasis and of the relapse of psoriasis that occurred during treatment with dupilumab. In total, 39 publications met the inclusion criteria, including 112 AD patients, 101 of whom developed “de novo” psoriasis, and 11 with a flare of pre-existent psoriasis. In the first group, patients more frequently developed plaque psoriasis on the scalp and extremities, after an average latency period from the initiation of dupilumab of 5 months. In the second group, the incidence of dupilumab-induced relapses of psoriasis was 43%, after an average of 4 months since the first administration. The most common psoriasis type was plaque psoriasis, with the involvement of the scalp and upper extremities. Dupilumab was interrupted in 38% of patients with “de novo” psoriasis and in 50% of relapsed patients, leading, in most cases, to an improvement of psoriasis. In conclusion, atopic dermatitis and psoriasis can definitely co-exist, and biologic drugs used to treat the former can promote the latter. It is thus crucial to perform a careful personal and familiar anamnesis before prescribing any biologic treatment. Moreover, a study of cytokine expression and blood proteomic markers could be considered in these patients.

Tildrakizumab is a high-affinity, humanized IgG1κ monoclonal antibody targeting the p19 subunit of IL-23, which is a key regulatory cytokine in psoriasis. Based on evidence from clinical trials, tildrakizumab is approved for the treatment of moderate-to-severe plaque psoriasis in patients eligible for systemic therapy. We report our clinical experience with 26 patients followed up to 24 weeks. No adverse event was observed and no patient discontinued tildrakizumab. Whilst no patient had a Psoriasis Area and Severity Index (PASI) score of <5 at baseline, at week 4, 8 (32%) patients had a PASI score of <3 and 6 of these had a PASI score of 0. At week 12, 19 (79%) patients had a PASI score of <5 and, among these, 18 had a PASI score of <3 of whom 16 had a PASI score of 0. At week 24, 22 (96%) patients had a PASI score of <3 and 20 (87%) had a PASI score of 0. Quality of life was improved after 4 weeks and through the whole period of observation. Our experience in the real-life setting confirms the efficacy and safety of tildrakizumab as demonstrated by clinical trials.

Drug-induced bullous pemphigoid (DBP) associated to biologics administered for psoriasis is rare. DBP has been described especially in association with anti-TNF-α drugs and anti-IL12 and 23, but never in relation to guselkumab (anti-IL23). We report the case of a 76-year-old male patient with severe psoriasis (PASI 20), presenting with generalized tense bullae and erosions after being recently switched to guselkumab therapy. Histology and direct immunofluorescence confirmed the suspect of bullous pemphigoid (BP). Guselkumab administration was interrupted, low-dose oral corticosteroid therapy was introduced and after only 1-month remission was obtained with no new lesions appearing. As outlined in the presented case, DBP's onset typically follows the introduction of a new drug in patients taking polypharmacy. In addition, DBP may spontaneously regress after discontinuation of the triggering drug and it responds very rapidly to steroid therapy. Up to date, DBP has been described after biological therapy for psoriasis in 11 patients, following administration of ustekinumab, efalizumab, etanercept, secukinumab, and adalimumab. Conversely, DBP after guselkumab therapy for psoriasis has never been reported in published studies. We highlight the need to face and document increasing, though rare, side effects of biologic therapies, as new biologic molecules are being constantly developed and administered to psoriatic patients, to promptly interrupt treatment when needed.

Background: Risankizumab is a humanized monoclonal antibody that selectively inhibits interleukin-23. It has been approved for moderate-to-severe plaque psoriasis and has shown efficacy and safety in clinical trials and real-world experiences. This study aimed to evaluate the long-term effectiveness, safety, and drug survival of risankizumab in a real-life setting. Materials and Methods: We included patients treated with risankizumab from January 2019 to February 2023. A Psoriasis Area and Severity Index score (PASI) was collected at weeks 0, 16, 28, 52, 104, and 156, when available. The occurrence of any adverse events was recorded at each visit. Results: We enrolled 1047 patients. At week 52, a ≥90% improvement in PASI was observed in 81.44% of patients, with a continuous improvement throughout the study (88.99% and 99.07% at weeks 104 and 156, respectively). After three years of treatment, all patients involving the scalp, palms/soles, and genitalia and 95% of patients with nail psoriasis achieved a complete or almost complete skin clearance. No significant safety findings were observed, and 90.73% of the patients were still on treatment after 36 months. Conclusions: This study supports the long-term effectiveness and safety of risankizumab in a real-world setting, even in patients involving difficult-to-treat areas.