Resumen
La psoriasis es una enfermedad inflamatoria sistémica asociada con un mayor riesgo de complicaciones cardiovasculares y renales. El objetivo de esta revisión sistemática fue analizar la evidencia científica sobre el impacto de la terapia dermatológica antiinflamatoria sistémica en ambos desenlaces desde un enfoque multidisciplinario. La revisión se realizó conforme a PRISMA 2020, complementada con una síntesis temática de la evidencia obtenida en PubMed/MEDLINE, Scopus, Web of Science y ScienceDirect. Se incluyeron dieciocho estudios relacionados con terapias biológicas, riesgo cardiovascular, función renal y manejo integral de la psoriasis. Los resultados muestran evidencia consistente sobre el beneficio cardiovascular de los agentes anti-TNF, anti-IL17 y anti-IL23 mediante la reducción de la inflamación sistémica, mientras que la evidencia renal continúa siendo emergente. Se concluye que la atención multidisciplinaria favorece una selección terapéutica individualizada y puede contribuir a mejorar el pronóstico clínico y prevenir complicaciones sistémicas.
Citas
[1] C. E. M. Griffiths, A. W. Armstrong, J. E. Gudjonsson, and J. N. W. N. Barker, “Psoriasis,” The Lancet, vol. 397, no. 10281, pp. 1301–1315, 2021, doi: 10.1016/S0140-6736(20)32549-6.
[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.
[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.
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