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1.
Rom J Intern Med ; 61(2): 112-115, 2023 Jun 01.
Article in English | MEDLINE | ID: mdl-36803989

ABSTRACT

INTRODUCTION: The sepsis syndrome is potentially affecting several organs and systems irrespectively of the primary source of the infection. Alterations of the brain function in sepsis patients may result either from a primary central nervous system (CNS) infection or could be part of the sepsis-associated encephalopathy (SAE), a common complication of sepsis, characterized by a diffuse dysfunction of the brain due to an infection elsewhere in the body without overt CNS infection. Aim of the study was to evaluate the usefulness of electroencephalography and the biomarker neutrophil gelatinase-associated lipocalin (NGAL) when measured in the cerebrospinal fluid (CSF) in the management of these patients. METHODS: Patients presenting at the emergency department with altered mental status and signs of infection were included in this study. Among initial assessment and treatment of the patients based on the international guidelines for treating sepsis, NGAL was measured in the cerebrospinal fluid (CSF) using ELISA technique. Electroencephalography was performed when possible within 24 hours after admission and EEG abnormalities were recorded. RESULTS: 32 of 64 patients included in this study were diagnosed with central nervous system (CNS) infection. CSF NGAL was significantly higher in patients with CNS infection compared to patients without CNS infection (18.1 [5.1-71.1] vs 3.6 [1.2-11.6]; p<0.001). There was a trend for higher CSF NGAL in patients with EEG abnormalities, which did not reach statistical significance (p=0.106). CSF NGAL levels were similar between survivors and non-survivors (medians: 7.04 vs 11.79). CONCLUSION: In patients presenting at the emergency department with altered mental status and signs of infection, CSF NGAL was significantly higher in patients with CSF infection. Its role in this acute setting should be evaluated further. CSF NGAL could be suggestive of EEG abnormalities.


Subject(s)
Consciousness Disorders , Lipocalin-2 , Sepsis , Humans , Biomarkers , Electroencephalography , Lipocalin-2/cerebrospinal fluid , Sepsis/complications , Sepsis/diagnosis , Consciousness Disorders/etiology
2.
J Infect ; 55(4): 340-6, 2007 Oct.
Article in English | MEDLINE | ID: mdl-17631968

ABSTRACT

OBJECTIVES: To investigate whether stress hyperglycemia affects the production of the main pro- and anti-inflammatory cytokines and the 28-day hospital mortality in patients with severe sepsis. METHODS: The study included 62 patients with severe sepsis, divided in three groups according to their glycemic profile within 24h after admission: patients with stress hyperglycemia (group SH, n=16), diabetes mellitus type II (group DM, n=27), and normal glucose levels (group NG, n=19). The serum levels of the cytokines TNF-alpha, IL-6, IL-10 and TGFbeta-1 were measured within 24h after admission. RESULTS: A higher percentage of septic patients with stress hyperglycemia died compared to diabetic patients (43.7 vs. 14.8%) and group NG (43.7 vs. 5.2%). Group SH had higher SOFA score and levels of IL-6 and IL-10 than group DM and group NG. It also had higher levels of TNF-alpha than group DM but not group NG. There was no difference in the levels of TGFbeta-1 among the three groups. Non-survivors had higher levels of IL-10, no difference was detected for IL-6, TNF-alpha, IL-10/TNF-alpha ratio and TGFbeta-1. Interleukin-10 values, mean fasting glucose values and age were found as prognostic factors associated with outcome. CONCLUSIONS: Stress hyperglycemia is associated with increased cytokine production and an adverse clinical outcome in patients with severe sepsis.


Subject(s)
Cytokines/biosynthesis , Hyperglycemia/immunology , Hyperglycemia/mortality , Sepsis/immunology , Aged , Aged, 80 and over , Cytokines/blood , Female , Hospital Mortality , Humans , Hyperglycemia/etiology , Interleukin-10/biosynthesis , Interleukin-10/blood , Interleukin-6/biosynthesis , Interleukin-6/blood , Male , Middle Aged , Sepsis/complications , Transforming Growth Factor beta1/biosynthesis , Transforming Growth Factor beta1/blood , Tumor Necrosis Factor-alpha/biosynthesis , Tumor Necrosis Factor-alpha/blood
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