ABSTRACT
Resumen Introducción: entre los pacientes con infección la hiperlactatemia identifica una población de mayor gravedad. Este estudio pretende determinar en pacientes de urgencias la correlación y asociación entre los parámetros clínicos de perfusión y los valores de lactato en el momento de admisión; así como el cambio en los parámetros clínicos con la depuración del lactato. Además, determinar la asociación entre estas variables y la mortalidad intrahospitalaria. Métodos: cohorte prospectiva de pacientes que ingresaron con sospecha de infección a un hospital de tercer nivel. Se midió el lactato en la admisión a las 6 y 24 horas, concomitantemente con las variables llenado capilar, índice de choque y presión de pulso, entre otras. Se realizó correlación de Spearman entre las variables clínicas, los niveles de lactato y su depuración; así como curvas ROC para determinar la capacidad discriminativa de las variables clínicas para detectar hiperlactatemia. Se realizó un modelo de regresión logística multivariable para mortalidad. Resultados: se evaluaron 2257 pacientes, 651 correspondían a infección confirmada. No se encontró ninguna correlación de utilidad entre las variables clínicas y el lactato (r<0.25); y tampoco se detectó adecuada capacidad discriminativa para la detección de hiperlactatemia con ninguna variable clínica (AUC<0.61). En el modelo de regresión logística multivariada el valor del lactato al ingreso fue la única variable que se asoció de manera independiente con mortalidad (OR=1.4, IC95%=1.3-1.6). Conclusiones: entre los pacientes que ingresan a urgencias con infección no se encontró correlación entre las variables clínicas y el lactato; sin embargo, el lactato al ingreso es un marcador pronóstico independiente de mortalidad. (Acta Med Colomb 2017: 42: 97-105).
Abstract Introduction: among patients with infection, hyperlactatemia identifies a population of greater severity. This study aims to determine the correlation and association between clinical perfusion parameters and lactate values in emergency patients at the time of admission, as well as the change in clinical parameters with lactate clearance. In addition, to determine the association between these variables and in-hospital mortality. Methods: Prospective cohort of patients admitted with suspected infection to a third level hospital. Lactate was measured at admission, at 6 and 24 hours, concomitantly with the variables capillary filling, shock index and pulse pressure, among others. Among the clinical variables, Spearman correlation, lactate levels and their clearance, as well as ROC curves to determine the discriminative ability of clinical variables to detect hyperlactatemia were performed. A multivariate logistic regression model for mortality was carried out. Results: 2257 patients were evaluated. 651 were confirmed with infections. No utility correlation was found between clinical variables and lactate (r <0.25), and no discriminative capacity was detected for the detection of hyperlactatemia with any clinical variable (AUC <0.61). In the multivariate logistic regression model the lactate value at admission was the only variable that was independently associated with mortality (OR = 1.4, 95% CI = 1.3-1.6). Conclusions: no correlation was found between clinical variables and lactate among patients admitted to the emergency department with infection; however lactate at admission is an independent prognostic marker of mortality. (Acta Med Colomb 2017: 42: 97-105).
Subject(s)
Humans , Male , Female , Adolescent , Lactic Acid , Perfusion , Shock , Diagnosis , InfectionsABSTRACT
OBJECTIVES: To perform a complete immunological characterization of compensatory anti-inflammatory response syndrome in patients with sepsis and to explore the relationship between these changes and clinical outcomes of 28-day mortality and secondary infections. DESIGN: Prospective single-center study conducted between April 2011 and December 2012. SETTING: ICUs from Hospital Universitario San Vicente Fundación at Medellin, Colombia. PATIENTS: One hundred forty-eight patients with severe sepsis. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: At days 0, 1, 3, 5, 10, and 28, we determined the expression of HLA-DR in monocytes and the apoptosis and the proliferation index in T lymphocytes, as well as the levels of tumor necrosis factor-α, interleukin-6, interleukin-1ß, interleukin-10, and transforming growth factor-ß in both plasma and cell culture supernatants of peripheral blood mononuclear cells. The mean percentage of HLA-DR was 60.7 at enrollment and increased by 0.9% (95% CI, 0.7-1.2%) per day. The mean percentage of CD4 T cells and CD8 T cells AV+/7-AAD- at enrollment was 37.2% and 20.4%, respectively, but it diminished at a rate of -0.5% (95% CI, -0.7% to -0.3%) and -0.3% (95% CI, -0.4% to -0.2%) per day, respectively. Plasma levels of interleukin-6 and interleukin-10 were 290 and 166 pg/mL and decreased at a rate of -7.8 pg/mL (95% CI, -9.5 to -6.1 pg/mL) and -4 pg/mL (95% CI, -5.1 to -2.8 pg/mL) per day, respectively. After controlling for confounders, only sustained plasma levels of interleukin-6 increase the risk of death (hazard ratio 1.003; 95% CI, 1.001-1.006). CONCLUSIONS: We found no evidence to support a two-phase model of sepsis pathophysiology. However, immunological variables did behave in a mixed and time-dependent manner. Further studies should evaluate changes over time of interleukin-6 plasma levels as a prognostic biomarker for critically ill patients.
Subject(s)
HLA-DR Antigens/biosynthesis , Inflammation Mediators/immunology , Leukocytes, Mononuclear/immunology , Sepsis/immunology , APACHE , Aged , Apoptosis , Cell Proliferation , Comorbidity , Female , Humans , Inflammation Mediators/blood , Intensive Care Units , Longitudinal Studies , Male , Middle Aged , Organ Dysfunction Scores , Prospective Studies , Racial Groups , Sepsis/bloodABSTRACT
BACKGROUND: Evidence suggests that statins may modify the immune response against HIV. The aim was to evaluate the antiretroviral and immunomodulatory effects of lovastatin in HIV-infected patients, naïve for antiretroviral therapy. METHODS: Randomized, double-blinded, placebo-controlled, phase-II clinical trial. Primary outcomes were plasma viral load and circulating CD4+ T cell count, after 6 and 12 months of treatment; secondary outcomes were CD8+ T cell count, expression of activation markers (CD38 and HLA-DR) on T cells, and clinical outcomes. With a power of 90% to detect both a decrease of 0.3 log10 in plasma HIV-1 RNA copies and an increase of 20% in the CD4+ T cell count, we estimated a required sample size of 110 HIV-infected patients (55 per group). The results were analyzed by a model of repeated measurements using Generalized Estimating Equations. RESULTS: Patients were randomized to receive either lovastatin (n = 55) or placebo (n = 57). During the 12-month follow-up, there was no effect of lovastatin either on viral load (estimated average change = 0.157 copies/mL; CI 95% = -0.099 to 0.414), or on the CD4+ T cell count (estimated average change = -26.1 cells/µL; CI 95% = -89.8 to 37.6). Moreover, there were no significant differences in secondary outcomes. CONCLUSIONS: Daily administration of lovastatin (40 mg) for one year in HIV-infected patients, naïve for antiretroviral therapy, had no significant effect on HIV replication, the CD4+ T cell count, or the activation level of T cells. (www.clinicaltrials.gov; ID NCT00721305).
