Jornal Vascular Brasileiro
https://www.jvascbras.org/article/doi/10.1590/1677-5449.0022
Jornal Vascular Brasileiro
Original Article

Hidrocortisona reduz as concentrações séricas dos biomarcadores inflamatórios séricos em pacientes submetidos a endarterectomia de carótida

Hydrocortisone reduces serum concentrations of inflammatory biomarkers in patients subjected to carotid endarterectomy

Sthefano Atique Gabriel; Leila Antonangelo; Vera Luiza Capelozzi; Camila Baumann Beteli; Otacílio de Camargo Júnior; José Luis Braga de Aquino; Roberto Augusto Caffaro

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Resumo

ResumoContextoA hidrocortisona pode reduzir a concentração dos biomarcadores inflamatórios séricos e teciduais.ObjetivoAnalisar a atividade inflamatória da proteína C-reativa ultrassensível (PCR-US), do fator de necrose tumoral (FNT)-alfa e do fator de crescimento do endotélio vascular (FCEV) séricos e teciduais, mediante administração intraoperatória de hidrocortisona, após endarterectomia de artéria carótida (EAC).MétodoVinte e dois pacientes foram divididos em Grupo Controle (5 assintomáticos e 6 sintomáticos) – não foi administrada hidrocortisona – e Grupo 1 (4 assintomáticos e 7 sintomáticos) – foram administrados 500 mg intravenoso de hidrocortisona. O PCR-US, o FNT-alfa e o FCEV séricos foram dosados no pré-operatório e em 1 hora, 6 horas e 24 horas após a EAC. Na placa carotídea, mensuramos os níveis de FNT-alfa e FCEV.ResultadosO grupo 1 exibiu menor concentração sérica de FNT-alfa em 1 hora (p=0,031), 6 horas (p=0,015) e 24 horas (p=0,017) após a EAC, e menor concentração de FCEV em 1 hora (p=0,006) e 6 horas (p=0,005) após a EAC, em relação ao grupo controle. Os pacientes sintomáticos do grupo 1 exibiram menor concentração de FNT-alfa em 1 hora e 6 horas após a EAC, e menor concentração de FCEV em 1 hora após a EAC, em relação ao grupo controle. Não houve diferença estatística entre as concentrações teciduais de FNT-alfa e FCEV entre o grupo controle e o grupo 1.ConclusãoA hidrocortisona reduz as concentrações séricas pós-operatórias de FNT-alfa e FCEV, em especial nos sintomáticos; porém, não reduz os níveis teciduais destes biomarcadores.

Palavras-chave

hidrocortisona, inflamação, estenose das carótidas

Abstract

AbstractBackgroundHydrocortisone may reduce serum and tissue concentrations of inflammatory biomarkers.ObjectiveTo analyze the inflammatory activity of serum and tissue high-sensitivity C-reactive protein (hsCRP), tumor necrosis factor (TNF)-α and vascular endothelial growth factor (VEGF) after intraoperative administration of hydrocortisone, after carotid endarterectomy (CEA).MethodTwenty-two patients were allocated to a Control Group (5 asymptomatic and 6 symptomatic patients) and were not administered hydrocortisone or to Group 1 (4 asymptomatic and 7 symptomatic patients) and were administered 500 mg intravenous hydrocortisone. Serum levels of hsCRP, TNF-α and VEGF were tested for the preoperative period and at 1 hour, 6 hours and 24 hours after CEA. Levels of TNF-α and VEGF were also measured in carotid plaques.ResultsGroup 1 exhibited lower concentrations of serum TNF-α at 1 hour (p=0.031), 6 hours (p=0.015) and 24 hours (p=0.017) after CEA and lower concentrations of serum VEGF at 1 hour (p=0.006) and 6 hours (p=0.005) after CEA, relative to controls. Symptomatic patients in group 1 exhibited lower concentrations than controls for serum TNF-α at 1 hour and 6 hours after CEA and lower concentrations than controls for serum VEGF at 1 hour after CEA. There were no statistical differences in tissue concentrations of TNF-α or VEGF between the control group and group 1.ConclusionHydrocortisone reduces postoperative concentrations of serum TNF-α and VEGF, especially in symptomatic patients; but does not reduce tissue levels of these biomarkers.

Keywords

hydrocortisone, inflammation, carotid stenosis

References

Teixeira BC, Lopes AL, Macedo RCO. Inflammatory markers, endothelial function and cardiovascular risk. J Vasc Bras. 2014;13(2):108-15.

Balanescu S, Calmac L, Constantinescu D, Marinescu M, Onut R, Dorobantu M. Systemic inflammation and early atheroma formation: are they related?. Maedica. 2010;5(4):292-301.

Tuttolomondo A, Di Raimondo D, Pecoraro R, Arnao V, Pinto A, Licata G. Atherosclerosis as an inflammatory disease. Curr Pharm Des. 2012;18(28):4266-88.

Moller MJ, Qin Z, Toursarkissian B. Tissue markers in human atherosclerotic carotid artery plaque. Ann Vasc Surg. 2012;26(8):1160-5.

Mauriello A, Sangiorgi GM, Virmani R. A pathobiologic link between risk factors profile and morphological markers of carotid instability. Atherosclerosis. 2010;208(2):572-80.

Wekesa AL, Cross KS, O’Donovan O. Predicting carotid artery disease and plaque instability from cell-derived microparticles. Eur J Vasc Endovasc Surg. 2014;48(5):489-95.

Hermus L, Lefrandt JD, Tio RA, Breek JC, Zeebregts CJ. Carotid plaque formation and serum biomarkers. Atherosclerosis. 2010;213(1):21-9.

Stahn C, Buttgereit F. Genomic and nongenomic effects of glucocorticoids. Nat Clin Pract Rheumatol. 2008;4(10):525-33.

Imamura K, Hayashi F, Suzumura A. [Cytokine production by peripheral blood monocytes/macrophages in the patients with multiple sclerosis and its suppression by methylprednisolone]. Rinsho Shinkeigaku. 1992;32(3):276-80.

Elenkov IJ. Neurohormonal-cytokine interactions: implications for inflammation, common human diseases and well-being. Neurochem Int. 2008;52(1-2):40-51.

Clinical alert: benefit of carotid endarterectomy for patients with high-grade stenosis of the internal carotid artery. National Institute of Neurological Disorders and Stroke Stroke and Trauma Division. North American Symptomatic Carotid Endarterectomy Trial (NASCET) investigators. Stroke. 1991;22(6):816-7.

Raja SG, Dreyfus GD. Modulation of systemic inflammatory response after cardiac surgery. Asian Cardiovasc Thorac Ann. 2005;13(4):382-95.

Rubens FD, Mesana T. The inflammatory response to cardiopulmonary bypass: a therapeutic overview. Perfusion. 2004;19(^sSuppl 1):S5-12.

Liguori GR, Kanas AF, Moreira LFP. Managing the inflammatory response after cardiopulmonary bypass: review of the studies in animal models. Rev Bras Cir Cardiovasc. 2014;29(1):93-102.

Kawamura T, Inada K, Okada H, Okada K, Wakusawa R. Methylprednisolone inhibits increase of interleukin 8 and 6 during open heart surgery. Can J Anaesth. 1995;42(5 Pt 1):399-403.

Komori K, Ishida M, Matsumoto T. Cytokine patterns and the effects of a preoperative steroid treatment in the patients with abdominal aortic aneurysms. Int Angiol. 1999;18(3):193-7.

Koutouzis M, Rallidis LS, Peros G. Serum interleukin-6 is elevated in symptomatic carotid bifurcation disease. Acta Neurol Scand. 2009;119(2):119-25.

Puz P, Lasek-Bal A, Ziaja D, Kazibutowska Z, Ziaja K. Inflammatory markers in patients with internal carotid artery stenosis. Arch Med Sci. 2013;9(2):254-60.

Alvarez Garcia B, Ruiz C, Chacon P, Sabin JA, Matas M. High-sensitivity C-reactive protein in high-grade carotid stenosis: risk marker for unstable carotid plaque. J Vasc Surg. 2003;38(5):1018-24.

Heider P, Poppert H, Wolf O. Fibrinogen and high-sensitive C-reactive protein as serologic predictors for perioperative cerebral microembolic lesions after carotid endarterectomy. J Vasc Surg. 2007;46(3):449-54.

Morrow DA, Ridker PM. C-reactive protein, inflammation, and coronary risk. Med Clin North Am. 2000;84(1):149-61, ix.

Baki ED, Sivaci RG, Kokulu S, Ela Y, Aldemir M. Effects of anesthetic choice on inflammatory response in cardiac surgery. Inflammation and Cell Signaling. 2014;1:e75.

Welsh P, Woodward M, Rumley A, Lowe G. Associations of circulating TNFalpha and IL-18 with myocardial infarction and cardiovascular risk markers: the Glasgow Myocardial Infarction Study. Cytokine. 2009;47(2):143-7.

Profumo E, Esposito C, Buttari B. Intracellular expression of cytokines in peripheral blood from patients with atherosclerosis before and after carotid endarterectomy. Atherosclerosis. 2007;191(2):340-7.

Russell DA, Abbott CR, Gough MJ. Vascular endothelial growth factor is associated with histological instability of carotid plaques. Br J Surg. 2008;95(5):576-81.

Szabó A, Laki J, Madsen HO. Early rise in serum VEGF and PDGF levels predisposes patients with a normal MBL2 genotype to restenosis after eversion endarterectomy. Stroke. 2007;38(8):2247-53.

Grufman H, Gonçalves I, Edsfeldt A. Plasma levels of high-sensitive C-reactive protein do not correlate with inflammatory activity in carotid atherosclerotic plaques. J Intern Med. 2014;275(2):127-33.

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