Abstract
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.
Highlights
Inflammatory biomarkers, which are produced by immunocompetent cells in atheromatous plaques, can orchestrate both systemic and tissue inflammatory responses, contributing to formation of complex atherosclerotic plaques, which are responsible for manifestation of ischemic neurological events, such as transitory ischemic attacks (TIA) and cerebral vascular accidents (CVA).[1,2,3,4]
This study has demonstrated for the first time that intraoperative administration of hydrocortisone interferes in the inflammatory responses of tumor necrosis factor (TNF)-alpha and vascular endothelial growth factor (VEGF), reducing their concentrations over a period of 24 hours after endarterectomia de artéria carótida (EAC)
We observed a tendency for hydrocortisone to have an effect at the serum level, and at the tissue level, controlling inflammatory activity of TNF-alpha and of VEGF in the carotid plaque
Summary
Inflammatory biomarkers, which are produced by immunocompetent cells in atheromatous plaques, can orchestrate both systemic and tissue inflammatory responses, contributing to formation of complex atherosclerotic plaques, which are responsible for manifestation of ischemic neurological events, such as transitory ischemic attacks (TIA) and cerebral vascular accidents (CVA).[1,2,3,4]Elevated expression of inflammatory biomarkers in patients with unstable carotid plaques suggests that immunomodulatory treatments focused on the inflammatory process within the carotid plaque should be tested with a view to reducing progression of the disease and the risk of TIA and CVA.[5,6,7]Glucocorticoids have anti-inflammatory and immunosuppressive properties, reducing secretion of inflammatory biomarkers by monocytes and macrophages.[8,9] Elenkov[10] points out that glucocorticoids are immunomodulatory medications capable of modulating the systemic inflammatory response. The objective of this study was to analyze the inflammatory activity of hsCRP, of TNF-alpha and of VEGF in serum and tissue in response to intraoperative administration of hydrocortisone. Objective: To 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). 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. Conclusion: Hydrocortisone reduces postoperative concentrations of serum TNF-α and VEGF, especially in symptomatic patients; but does not reduce tissue levels of these biomarkers.
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