Impacto do controle glicêmico no perfil de coagulação e inflamação em pacientes com choque séptico
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Data
2012-06-27
Autores
Sanches, Luciana Coelho [UNIFESP]
Orientadores
Machado, Flávia Ribeiro [UNIFESP]
Tipo
Tese de doutorado
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Objetivo: conhecer o comportamento do sistema de coagulação em pacientes sépticos que evoluem com hiperglicemia e o impacto do uso contínuo de insulina e do controle glicêmico nessas alterações. Métodos: o estudo avaliou o perfil glicêmico, de
coagulação e de inflamação de pacientes com choque séptico com menos de 48 horas de instalação da disfunção orgânica no momento da inclusão e após 24 horas. Foram coletados dados demográficos, bem como dados do perfil glicêmico dos pacientes. Dosaram-se os fatores de coagulação fator tecidual, fator VII, trombinaantitrombina, D-dímero, fibrinogênio, fragmento 1+2, tempo de trombina, proteína C,
antitrombina, plasminogênio, ativador do plasminogênio tecidual, inibidor do fator
tecidual e inibidor do ativador de plasminogênio. Para o perfil inflamatório, foram dosadas interleucinas 6, 8 e 10 e proteína C reativa. Resultados: Foram incluídos 41 pacientes, distribuídos em 20 com normoglicemia (Grupo 1) e 21 com hiperglicemia controlada (Grupo 2). A mediana de glicemia foi significativamente diferente entre os grupos no momento basal (p<0,001) mas não após 24 horas (p<0,47). O perfil de coagulação foi semelhante entre os pacientes dos Grupos 1 e 2 no momento basal, com elevação dos parâmetros de coagulação, consumo de fator VII, proteína C e
antitrombina e inibição da fibrinólise. Não houve diferença significativa após 24 horas no grupo normoglicêmico. Já os pacientes com hiperglicemia controlada apresentaram concentrações mais altas de fator VII (p=0,03), proteína C (p=0,04) e de antitrombina (p=0,04) quando comparados aos pacientes normoglicêmicos. Nesses pacientes houve aumento das concentrações de plasminogênio (p=0,03) e redução nas concentrações de inibidor do ativador de plasminogênio (p=0,01) e de ativador tecidual do plasminogênio. (p=0,03) em relação aos valores basais. Em relação ao perfil inflamatório, em ambos os grupos as concentrações de interleucina 6, 8 e 10 bem como a concentração de proteína C reativa se encontravam elevadas desde o momento basal, sem diferença entre os grupos. Após 24 horas, as
concentrações de interleucinas se encontravam significativamente mais baixos nos pacientes do Grupo 2. Não houve correlação entre as alterações no perfil de coagulação e parâmetros de gravidade ou de glicemia, exceto para as concentrações de proteína C cujo aumento associou-se a níveis basais de lactato mais baixos. Observam-se correlações fracas entre alguns parâmetros de coagulação e de inflamação, porém julgou-se haver relevantes limitações na interpretação desses
resultados. Conclusões: o padrão de coagulação em pacientes normoglicêmicos e hiperglicêmicos com choque séptico é semelhante no momento basal. Entretanto, observou-se melhora do estado de hipercoagulabilidade e das alterações da
fibrinólise após o controle da glicemia, sugerindo melhora do perfil de procoagulação. O perfil inflamatório se caracteriza por concentrações elevadas de citocinas e de PCR no momento basal com redução desses valores após 24 horas, independente do perfil glicêmico dos grupos. Não foi possível observar correlação entre a evolução dos
parâmetros de coagulação e parâmetros de gravidade dos pacientes ou modificações do perfil glicêmico, dose de insulina recebida ou insulinemia. É possível que as alterações da coagulação encontradas nos pacientes hiperglicêmicos controlados estejam correlacionadas com melhora dos parâmetros inflamatórios.
Objective: to determine the coagulation profiles in patients with septic shock with hyperglycemia and the impact of insulin and glycemic control in these parameters. Methods: this study analyzed the glycemic, coagulation and inflammatory profiles in patients with septic shock within the first 48 hours of organ dysfunction onset at baseline and after 24 hours. Demographic and glycemic data were collected and the following coagulation parameters were measured: tissue factor, factor VII, thrombinantithrombin, d-dimer, fibrinogen, fragment 1+2, thrombin time, protein C, antithrombin, plasminogen, tissue plasminogen activator, tissue factor pathway inhibitor and plasminogen activator inhibitor 1. Inflammatory profile was assessed through the measurement of interleukin 6, 8 and 10 and reactive protein C. Results: Forty-one patients were included, being 20 normoglycemic (Group 1) and 21 with controlled hyperglycemia (Group 2). The median glycemia value was significantly different between the groups at baseline (p<0,001) but not after 24 hours (p=0,47). The coagulation profile was similar between the groups at baseline, with high levels of coagulation markers, reduced levels of factor VII, protein C and antithrombin and fibrinolysis inhibition. After 24h, there was no difference in the normoglycemic group. Patients with controlled hyperglycemia presented higher concentrations of factor (p=0,03), protein C (p=0,04) and antithrombin (p=0,04) as compared with those of normoglycemic group. Group 2 patients had elevated concentration of plasminogen (p=0,03) and reduced levels of plasminogen activator inhibitor-1(p=0,01) and tissue plasminogen activator (p=0,03) as compared to the baseline levels. In the inflammatory profile, in both groups interleukin 6, 8 and 10 as well as reactive protein C levels were high at baseline, without difference between groups. After 24h, interleukin levels were significantly lower in Group 2. There was no correlation between these alterations in coagulation and severity of illness or glycemic profile, except for protein C, with higher increase after 24 hours in patients with lower baseline lactate levels. Weak correlations were found between some coagulation and inflammatory parameters. However, relevant limitations precluded interpretation of these findings. Conclusions: the coagulation profile at baseline is similar in normoglycemic and hyperglycemic patients but after glycemic control an improvement in the hypercoagulabity and impaired fibrinolysis was found. High levels of interleukins and reactive protein C are also present and improved after 24 hours, regardless the glycemic profile at baseline. We were unable to demonstrate a clear correlation between the trends in coagulation and severity of illness, glycemia or dose of insulin received. However, it is possible that these coagulation changes were related to an improvement in inflammatory profile.
Objective: to determine the coagulation profiles in patients with septic shock with hyperglycemia and the impact of insulin and glycemic control in these parameters. Methods: this study analyzed the glycemic, coagulation and inflammatory profiles in patients with septic shock within the first 48 hours of organ dysfunction onset at baseline and after 24 hours. Demographic and glycemic data were collected and the following coagulation parameters were measured: tissue factor, factor VII, thrombinantithrombin, d-dimer, fibrinogen, fragment 1+2, thrombin time, protein C, antithrombin, plasminogen, tissue plasminogen activator, tissue factor pathway inhibitor and plasminogen activator inhibitor 1. Inflammatory profile was assessed through the measurement of interleukin 6, 8 and 10 and reactive protein C. Results: Forty-one patients were included, being 20 normoglycemic (Group 1) and 21 with controlled hyperglycemia (Group 2). The median glycemia value was significantly different between the groups at baseline (p<0,001) but not after 24 hours (p=0,47). The coagulation profile was similar between the groups at baseline, with high levels of coagulation markers, reduced levels of factor VII, protein C and antithrombin and fibrinolysis inhibition. After 24h, there was no difference in the normoglycemic group. Patients with controlled hyperglycemia presented higher concentrations of factor (p=0,03), protein C (p=0,04) and antithrombin (p=0,04) as compared with those of normoglycemic group. Group 2 patients had elevated concentration of plasminogen (p=0,03) and reduced levels of plasminogen activator inhibitor-1(p=0,01) and tissue plasminogen activator (p=0,03) as compared to the baseline levels. In the inflammatory profile, in both groups interleukin 6, 8 and 10 as well as reactive protein C levels were high at baseline, without difference between groups. After 24h, interleukin levels were significantly lower in Group 2. There was no correlation between these alterations in coagulation and severity of illness or glycemic profile, except for protein C, with higher increase after 24 hours in patients with lower baseline lactate levels. Weak correlations were found between some coagulation and inflammatory parameters. However, relevant limitations precluded interpretation of these findings. Conclusions: the coagulation profile at baseline is similar in normoglycemic and hyperglycemic patients but after glycemic control an improvement in the hypercoagulabity and impaired fibrinolysis was found. High levels of interleukins and reactive protein C are also present and improved after 24 hours, regardless the glycemic profile at baseline. We were unable to demonstrate a clear correlation between the trends in coagulation and severity of illness, glycemia or dose of insulin received. However, it is possible that these coagulation changes were related to an improvement in inflammatory profile.
Descrição
Citação
SANCHES, Luciana Coelho. Impacto do controle glicêmico no perfil de coagulação e inflamação em pacientes com choque séptico. São Paulo, 2012. 97 f. Tese (Doutorado em Medicina Translacional) – Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, 2012.