Abstract
Ustekinumab is a monoclonal antibody that shows the ability to bind to subunit p40, common for interleukin 12 (IL-12) and IL-23, which prevents the activation of the JAK STAT signaling pathway. The objective of the study was to evaluate the efficacy of therapy that uses anti-IL-12/23 medicine in patients with psoriasis vulgaris, based on the disease clinical progression indices (Psoriasis Area and Severity Index (PASI), Dermatology Life Quality Index (DLQI) and Body Surface Area (BSA)) and to determine the possibilities of using changes in the expression profiles of tumor necrosis factor α (TNF-α), tumor necrosis factor receptor (TNFR1) and TNFR2 as molecular markers showing the response to ustekinumab therapy. The group under study was composed of 14 patients (10 men and 4 women, aged 49.3 ±10.2 years) with diagnosed psoriasis vulgaris, treated with ustekinumab. The group was divided into subgroups because of the selected 3 stages of therapy. The control group consisted of 20 healthy volunteers (11 men and 9 women, aged 46 ±10 years). The 120-week long observation involved a clinical assessment of the patients (PASI, BSA and DLQI), based on the following scheme: 0-4-12 weeks of the observation. The analysis of molecular changes in the TNF-α, TNFR1 and TNFR2 expression profiles was performed with the quantitative reverse-transcription polymerase chain reaction (RT-qPCR) method, using the patients' full blood. The statistical analysis was performed with STATISTICA v. 12.0 PL (StatSoft Inc., Tulsa, USA) with the level of statistical significance p < 0.05. Gradually reduced PASI, BSA and DLQI values were observed during anti-IL-12/23 therapy. An increased level of the TNF-α transcription activity was observed in the analyzed group when compared to the control. Correlations between the clinical and molecular parameters were also indicated. Ustekinumab constitutes an efficient and safe form of pharmacotherapy in psoriasis vulgaris. We did not observe any reduced efficacy of the treatment when reclassifying patients for the therapy. Tumor necrosis factor α, TNFR1 and TNFR2 may serve as supplementary markers of molecular response to the medicine.
Highlights
Material and methodsPsoriasis is a multi-factor pro-inflammatory disease, the most characteristic phenomenon of which is parakeratosis.[1–3] the disease involves the increased risk of concurrent metabolic syndrome, arterial hypertension, cardiovascular diseases, and ischemic brain stroke.[2,4–6]Development of molecular biology made it possible to observe and confirm the changes occurring in the expression of cytokines, e.g., transforming growth factor β (TGF-β), tumor necrosis factor α (TNF-α) and interleukins (IL-12, IL-23 and IL-17) in the said disease.[2,7]Biological anti-cytokine therapy is intended for those patients for whom conventional therapies proved to be insufficiently effective or in cases where contraindications for their application occurred
Reduced PASI, BSA and DLQI values were observed during anti-interleukin 12 (IL-12)/23 therapy
TNFR1 and TNFR2 may serve as supplementary markers of molecular response to the medicine
Summary
Biological anti-cytokine therapy is intended for those patients for whom conventional therapies proved to be insufficiently effective or in cases where contraindications for their application occurred. In this group of patients, psoriasis has got a severe course and a high degree of lesion advancement (Psoriasis Area and Severity Index (PASI) >10 or Body Surface Area (BSA) >10).[7–9]. Two big groups of anti-cytokine medicines are distinguished: TNF-α inhibitors (adalimumab, etanercept) and IL-12/23 inhibitor (ustekinumab),[10,11] which owe their high efficacy to their unique activity: their focus on molecular objectives.[10–12]. Ustekinumab is a monoclonal antibody that shows the ability to bind to subunit p40, common for interleukin 12 (IL-12) and IL-23, which prevents the activation of the JAK STAT signaling pathway
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