Lucia Medjedovic
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Lucia Medjedovic has a total of 6 co-authors. Here are the top co-authors by number of shared publications:
- Admir Vižlin
Department of Dermatology and Venereology, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, 413 45 Gothenburg, Sweden
1 shared publication - Amra Osmancevic
Department of Dermatology and Venereology, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, 413 45 Gothenburg, Sweden
1 shared publication - Anna-Maj Albertsson
Department of Clinical Immunology and Transfusion Medicine, Sahlgrenska University Hospital, Region Västra Götaland, 413 45 Gothenburg, Sweden
1 shared publication - Martin Gillstedt
Department of Dermatology and Venereology, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, 413 45 Gothenburg, Sweden
1 shared publication - Sukanya Raghavan
Department of Clinical Immunology and Transfusion Medicine, Sahlgrenska University Hospital, Region Västra Götaland, 413 45 Gothenburg, Sweden
1 shared publication - Ylva Andersch Björkman
Department of Dermatology and Venereology, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, 413 45 Gothenburg, Sweden
1 shared publication
Latest Publications
- Open Access
- 1 January 2026
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 27 (1) , 458
Impact of Brodalumab on Serum Levels of IL-6, IL-17A, IFN-α, IFN-γ, and TNF-α in Patients with Psoriasis Who Failed Treatment with TNF-α Inhibitors
Psoriasis is a chronic, immune-mediated inflammatory skin disorder that significantly impacts patients’ quality of life. While TNF-α inhibitors are frequently used to treat moderate-to-severe cases, not all patients respond adequately. Brodalumab, a monoclonal antibody targeting the IL-17 receptor A, has emerged as an alternative for individuals unresponsive to prior therapies. This prospective study investigated the effects of brodalumab on serum cytokine levels—specifically IL-6, IL-17A, IFN-α, IFN-γ, and TNF-α—and their correlation with disease severity as assessed by Psoriasis Area and Severity Index (PASI). Eighteen patients with moderate-to-severe psoriasis who were unresponsive to TNF-α inhibitors received brodalumab for 12 weeks. Cytokine concentrations were measured at baseline and week 12 using an automated immunoassay (ELLA), and clinical outcomes were evaluated using PASI. The results showed a significant increase in IL-17A levels, while changes in IL-6, IFN-α, IFN-γ, and TNF-α did not reach statistical significance. No significant correlations were found between changes in cytokine levels and PASI improvement. However, the small number of available serum samples at week 12 (n = 11) limited the statistical power to detect treatment-related changes in cytokine levels. These findings suggest that while brodalumab influences specific immune markers, the clinical response may not be directly reflected by serum cytokine levels. This highlights the multifactorial nature of psoriasis pathogenesis and underscores the need for further studies to clarify the role of cytokine biomarkers in treatment response.
- 1 January 2026
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 27 (1) , 458
Open AccessImpact of Brodalumab on Serum Levels of IL-6, IL-17A, IFN-α, IFN-γ, and TNF-α in Patients with Psoriasis Who Failed Treatment with TNF-α Inhibitors
Psoriasis is a chronic, immune-mediated inflammatory skin disorder that significantly impacts patients’ quality of life. While TNF-α inhibitors are frequently used to treat moderate-to-severe cases, not all patients respond adequately. Brodalumab, a monoclonal antibody targeting the IL-17 receptor A, has emerged as an alternative for individuals unresponsive to prior therapies. This prospective study investigated the effects of brodalumab on serum cytokine levels—specifically IL-6, IL-17A, IFN-α, IFN-γ, and TNF-α—and their correlation with disease severity as assessed by Psoriasis Area and Severity Index (PASI). Eighteen patients with moderate-to-severe psoriasis who were unresponsive to TNF-α inhibitors received brodalumab for 12 weeks. Cytokine concentrations were measured at baseline and week 12 using an automated immunoassay (ELLA), and clinical outcomes were evaluated using PASI. The results showed a significant increase in IL-17A levels, while changes in IL-6, IFN-α, IFN-γ, and TNF-α did not reach statistical significance. No significant correlations were found between changes in cytokine levels and PASI improvement. However, the small number of available serum samples at week 12 (n = 11) limited the statistical power to detect treatment-related changes in cytokine levels. These findings suggest that while brodalumab influences specific immune markers, the clinical response may not be directly reflected by serum cytokine levels. This highlights the multifactorial nature of psoriasis pathogenesis and underscores the need for further studies to clarify the role of cytokine biomarkers in treatment response.