Abstract
Psoriasis is a systemic inflammatory disease associated with an increased risk of cardiovascular and renal complications. The objective of this systematic review was to analyze the scientific evidence on the impact of systemic anti-inflammatory dermatological therapy on both outcomes from a multidisciplinary approach. The review was conducted according to PRISMA 2020, complemented by a thematic synthesis of the evidence obtained from PubMed/MEDLINE, Scopus, Web of Science, and ScienceDirect. Eighteen studies related to biological therapies, cardiovascular risk, renal function, and comprehensive management of psoriasis were included. The results show consistent evidence regarding the cardiovascular benefit of anti-TNF, anti-IL17, and anti-IL23 agents through the reduction of systemic inflammation, whereas renal evidence remains emerging. It is concluded that multidisciplinary care favors individualized therapeutic selection and may contribute to improving clinical prognosis and preventing systemic complications.
References
[2] J. M. Gelfand, A. L. Neimann, D. B. Shin, X. Wang, D. J. Margolis, and A. B. Troxel, “Risk of myocardial infarction in patients with psoriasis,” JAMA, vol. 296, no. 14, pp. 1735–1741, 2006, doi: 10.1001/jama.296.14.1735.
[3] J. Wan, S. Wang, K. Haynes, M. R. Denburg, D. B. Shin, and J. M. Gelfand, “Risk of moderate to advanced kidney disease in patients with psoriasis: Population-based cohort study,” BMJ, vol. 347, p. f5961, 2013, doi: 10.1136/bmj.f5961.
[4] A. W. Armstrong and C. Read, “Pathophysiology, clinical presentation, and treatment of psoriasis: A review,” JAMA, vol. 323, no. 19, pp. 1945–1960, 2020, doi: 10.1001/jama.2020.4006.
[5] O. Ahlehoff, L. Skov, G. Gislason et al., “Cardiovascular outcomes and systemic anti-inflammatory drugs in patients with severe psoriasis: 5-year follow-up of a Danish nationwide cohort,” J. Eur. Acad. Dermatol. Venereol., vol. 29, no. 6, pp. 1128–1134, 2015, doi: 10.1111/jdv.12768.
[6] Y. A. Elnabawi, A. K. Dey, A. Goyal et al., “Coronary artery plaque characteristics and treatment with biologic therapy in severe psoriasis: Results from a prospective observational study,” Cardiovasc. Res., vol. 115, no. 4, pp. 721–728, 2019, doi: 10.1093/cvr/cvz009.
[7] J. Takeshita, S. Grewal, S. M. Langan et al., “Psoriasis and comorbid diseases: Implications for management,” J. Am. Acad. Dermatol., vol. 80, no. 4, pp. 977–998, 2019, doi: 10.1016/j.jaad.2018.09.052.
[8] M. J. Page, J. E. McKenzie, P. M. Bossuyt et al., “The PRISMA 2020 statement: An updated guideline for reporting systematic reviews,” BMJ, vol. 372, p. n71, 2021, doi: 10.1136/bmj.n71.
[9] V. Mangkorntongsakul, J. S. Joseph, J. P. Pham, S. D. Smith, C. K. Chow, and A. D. Smith, “Biologic therapies and major cardiovascular events in psoriasis: Updated systematic review and meta-analysis,” Dermatol. Ther. (Heidelb.), vol. 15, no. 9, pp. 2455–2482, 2025, doi: 10.1007/s13555-025-01529-5.
[10] W. Chung, S. E. Lee, K. Han, and S. H. Park, “Moderate-to-severe psoriasis and the risk of chronic kidney disease in a nationwide population-based cohort study,” Br. J. Dermatol., vol. 184, no. 1, pp. 163–164, 2021, doi: 10.1111/bjd.19410.
[11] G. K. Dawwas, S. M. Smith, and M. H. Noe, “Risk of chronic kidney disease in patients with psoriasis: A population-based cohort study,” J. Am. Acad. Dermatol., vol. 86, no. 4, pp. 795–803, 2022, doi: 10.1016/j.jaad.2021.05.063.
[12] T. Alexander, K. B. Gordon, A. W. Armstrong et al., “The effect of ixekizumab on cardiometabolic and renal biomarkers in patients with moderate-to-severe psoriasis: Results from UNCOVER 1 and 2,” J. Dermatolog. Treat., vol. 34, no. 1, Art. no. 2201234, 2023, doi: 10.1080/09546634.2023.2201234.
[13] A. Silfvast-Kaiser, S. Y. Paek, and A. Menter, “Anti-IL17 therapies for psoriasis,” Expert Opin. Biol. Ther., vol. 19, no. 1, pp. 45–54, 2019.
[14] A. Ruggiero, M. Megna, G. Fabbrocini, and S. S. Ocampo-Garza, “Anti-IL23 biologic therapies in the treatment of psoriasis: Real-world experience versus clinical trials data,” Immunol. Res., vol. 71, no. 3, pp. 328–355, 2023.
[15] G. Tocci, D. Goletti, V. Marino et al., “Cardiovascular outcomes and tumour necrosis factor antagonists in chronic inflammatory rheumatic disease: A focus on rheumatoid arthritis,” Expert Opin. Drug Saf., vol. 15, Suppl. 1, pp. 55–61, 2016, doi: 10.1080/14740338.2016.1218469.
[16] M. Nurmohamed, Y. Bao, J. Signorovitch, A. Trahey, P. Mulani, and D. E. Furst, “Longer durations of antitumour necrosis factor treatment are associated with reduced risk of cardiovascular events in patients with rheumatoid arthritis,” RMD Open, vol. 1, no. 1, Art. no. e000080, 2015.
[17] J. Ma, J. Cai, H. Chen, Z. Feng, and G. Yang, “Cardiovascular adverse events associated with tumor necrosis factor-alpha inhibitors: A real-world pharmacovigilance analysis,” J. Atheroscler. Thromb., vol. 31, no. 12, pp. 1733–1747, 2024.
[18] C. Barnabe, B. J. Martin, and W. A. Ghali, “Systematic review and meta-analysis: Anti-tumor necrosis factor α therapy and cardiovascular events in rheumatoid arthritis,” Arthritis Care Res., vol. 63, no. 4, pp. 522–529, 2011.

This work is licensed under a Creative Commons Attribution 4.0 International License.
