RESUMO
OBJECTIVE: To evaluate if type 2 diabetes mellitus (DM) constitutes a prognostic factor for death and severe disability in patients with aneurysm clipping after subarachnoid hemorrhage (ASH), in an Intensive Care Unit (ICU). MATERIAL AND METHODS: This is a cohort study in patients who were admitted to the ICU between December-2009 and June-2010; 20 with DM (exposed group) and 40 without DM (non-exposed group). Mortality was quantified during ICU stay. At ICU discharge, severe disability was measured through the Glasgow Outcome Scale (category 2); and Glasgow Coma Scale was used to estimate the difference in consciousness level between ICU arrival and discharge. Descriptive statistics and Kaplan Meier survival curves were performed. RESULTS: Mean age was similar between groups (55.8 +/- 11 and 55.6 +/- 15 years, respectively, p = 0.40). A vegetative state was present in one patient without DM. The Glasgow Coma Scale score at ICU entry was 14.1 +/- 1.4 and at discharge, 12.0 +/- 3.6 in the exposed group (p = 0.01); and 13.9 +/- 2.0 us. 13.5 +/- 2.6, in the non-exposed group, respectively (p = 0.45). There were 3 deaths in patients with DM and 5, in patients without DM (p > 0.05); survival time was 12 (95%CI 7, 16) and 10 days (95%CI 7, 13), respectively. Mean glucose remained higher in patients who died at the ICU (p < 0.001). Hydrocephaly was present in 6 exposed patients and 2, non-exposed (p = 0.007). Additionally, 7 and 5 with and without DM, respectively registered a positive blood culture (p = 0.04). CONCLUSIONS: DM was not associated with higher mortality in ICU patients, but hyperglycemia was; thus, it is essential that the intensive care provider watches closely the glycemic control.
Assuntos
Diabetes Mellitus Tipo 2/complicações , Mortalidade Hospitalar , Aneurisma Intracraniano/cirurgia , Hemorragia Subaracnóidea/cirurgia , Idoso , Bacteriemia/complicações , Bacteriemia/epidemiologia , Glicemia/análise , Dano Encefálico Crônico/sangue , Dano Encefálico Crônico/epidemiologia , Dano Encefálico Crônico/etiologia , Estudos de Coortes , Diabetes Mellitus Tipo 2/sangue , Feminino , Escala de Coma de Glasgow , Humanos , Hidrocefalia/sangue , Hidrocefalia/epidemiologia , Hidrocefalia/etiologia , Hiperglicemia/epidemiologia , Hiperglicemia/etiologia , Unidades de Terapia Intensiva/estatística & dados numéricos , Aneurisma Intracraniano/sangue , Aneurisma Intracraniano/complicações , Estimativa de Kaplan-Meier , Tempo de Internação/estatística & dados numéricos , Masculino , Pessoa de Meia-Idade , Estado Vegetativo Persistente/sangue , Estado Vegetativo Persistente/epidemiologia , Estado Vegetativo Persistente/etiologia , Complicações Pós-Operatórias/sangue , Complicações Pós-Operatórias/epidemiologia , Complicações Pós-Operatórias/etiologia , Prognóstico , Estudos Retrospectivos , Hemorragia Subaracnóidea/sangue , Hemorragia Subaracnóidea/complicaçõesRESUMO
OBJECTIVE: To evaluate the hypothesis that elevated levels of inflammation-related proteins in early postnatal blood predict impaired mental and motor development in extremely preterm infants. STUDY DESIGN: We measured concentrations of 25 inflammation-related proteins in blood collected on postnatal days 1, 7, and 14 from 939 infants born before 28 weeks gestation. An elevated level was defined as a concentration in the highest quartile for gestational age and day of blood collection. We identified impaired development at age 24 months using the Bayley Scales of Infant Development, Second Edition. The primary outcomes were scores on the Mental Scale or the Motor Scale of <55 (more than 3 SDs below the mean). RESULTS: For 17 of the 25 inflammation-related proteins, 1 or more statistically significant associations (P<.01) was found between an elevated blood level of the protein and a developmental impairment. Elevations on multiple days were more often associated with developmental impairment than were elevations present for only 1 day. The highest number of predictive elevations was found in day-14 blood. CONCLUSION: In extremely preterm infants, elevated levels of inflammation-related proteins in blood collected on postnatal days 7 and 14, especially when sustained, are associated with impaired mental and motor development at age 2 years.
Assuntos
Proteínas Sanguíneas/análise , Dano Encefálico Crônico/sangue , Deficiências do Desenvolvimento/etiologia , Idade Gestacional , Doenças do Prematuro/sangue , Dano Encefálico Crônico/complicações , Desenvolvimento Infantil , Pré-Escolar , Deficiências do Desenvolvimento/diagnóstico , Humanos , Recém-Nascido , Recém-Nascido Prematuro , Inflamação , Fatores de RiscoRESUMO
OBJECTIVE: Studies have shown signs of brain damage caused by different mechanisms in cocaine users. The serum neuron specific enolase and S100B protein are considered specific biochemical markers of neuronal and glial cell injury. This study aimed at comparing blood levels of S100B and NSE in chronic cocaine users and in volunteers who did not use cocaine or other illicit drugs. METHOD: Twenty subjects dependent on cocaine but not on alcohol or marijuana, and 20 non-substance using controls were recruited. Subjects were selected by consecutive and non-probabilistic sampling. Neuron specific enolase and S100B levels were determined by luminescence assay. RESULTS: Cocaine users had significantly higher scores than controls in all psychiatric dimensions of the SCL-90 and had cognitive deficits in the subtest cubes of WAIS and the word span. Mean serum S100B level was 0.09 +/- 0.04 microg/l among cocaine users and 0.08 +/- 0.04 microg/l among controls. Mean serum neuron specific enolase level was 9.7 +/- 3.5 ng/l among cocaine users and 8.3 +/- 2.6 ng/l among controls. CONCLUSIONS: In this first study using these specific brain damage markers in cocaine users, serum levels of S100B and neuron specific enolase were not statistically different between cocaine dependent subjects and controls.
Assuntos
Dano Encefálico Crônico/sangue , Transtornos Relacionados ao Uso de Cocaína/sangue , Transtornos Cognitivos/etiologia , Transtornos Mentais/etiologia , Fatores de Crescimento Neural/sangue , Fosfopiruvato Hidratase/sangue , Proteínas S100/sangue , Adulto , Biomarcadores/sangue , Dano Encefálico Crônico/induzido quimicamente , Estudos de Casos e Controles , Doença Crônica , Transtornos Relacionados ao Uso de Cocaína/complicações , Transtornos Relacionados ao Uso de Cocaína/enzimologia , Transtornos Cognitivos/diagnóstico , Estudos Transversais , Feminino , Humanos , Escala de Gravidade do Ferimento , Masculino , Transtornos Mentais/diagnóstico , Pessoa de Meia-Idade , Subunidade beta da Proteína Ligante de Cálcio S100RESUMO
OBJECTIVE: Studies have shown signs of brain damage caused by different mechanisms in cocaine users. The serum neuron specific enolase and S100B protein are considered specific biochemical markers of neuronal and glial cell injury. This study aimed at comparing blood levels of S100B and NSE in chronic cocaine users and in volunteers who did not use cocaine or other illicit drugs. METHOD: Twenty subjects dependent on cocaine but not on alcohol or marijuana, and 20 non-substance using controls were recruited. Subjects were selected by consecutive and non-probabilistic sampling. Neuron specific enolase and S100B levels were determined by luminescence assay. RESULTS: Cocaine users had significantly higher scores than controls in all psychiatric dimensions of the SCL-90 and had cognitive deficits in the subtest cubes of WAIS and the word span. Mean serum S100B level was 0.09 ± 0.04 µg/l among cocaine users and 0.08 ± 0.04 µg/l among controls. Mean serum neuron specific enolase level was 9.7 ± 3.5 ng/l among cocaine users and 8.3 ± 2.6 ng/l among controls. CONCLUSIONS: In this first study using these specific brain damage markers in cocaine users, serum levels of S100B and neuron specific enolase were not statistically different between cocaine dependent subjects and controls.
OBJETIVO: Estudos têm demonstrado sinais de lesão cerebral causadas por diferentes mecanismos em usuários de cocaína. A enolase sérica neurônio-específica e a proteína S100B são consideradas marcadores bioquímicos específicos de lesão neuronal e glial. Este estudo objetivou comparar os níveis sangüíneos de S100B e enolase sérica neurônio-específica em usuários crônicos de cocaína e em voluntários que não usam cocaína ou outras drogas ilícitas. MÉTODO: Vinte sujeitos dependentes de cocaína, mas não dependentes de álcool, maconha ou outra droga, e 20 sujeitos controles não usuários de drogas foram recrutados. Os sujeitos foram selecionados por amostragem consecutiva e não-probabilística e os níveis de enolase neurônio-específica e S100B foram determinados por ensaio de luminescência. RESULTADOS: Os usuários de cocaína tiveram escores significativamente maior que os controles em todas as dimensões psiquiátricas do SCL-90 e apresentaram prejuízos cognitivos no subteste cubos do WAIS e no span de palavras. Os níveis de S100B foram em média 0,09 ± 0,04 µg/l nos usuários de cocaína e 0,08 ± 0,04 µg/l nos controles. Os níveis de enolase neurônio-específica foram em média 9,7 ± 3,5 ng/l nos usuários e 8,3 ± 2,6 ng/l nos controles. CONCLUSÃO: Neste primeiro estudo utilizando esses marcadores específicos de lesão cerebral em usuários de cocaína, os níveis séricos de S100B e enolase específica do neurônio não foram significativamente diferentes entre dependentes de cocaína e controles.
Assuntos
Adulto , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Dano Encefálico Crônico/sangue , Transtornos Relacionados ao Uso de Cocaína/sangue , Transtornos Cognitivos/etiologia , Transtornos Mentais/etiologia , Fatores de Crescimento Neural/sangue , Fosfopiruvato Hidratase/sangue , /sangue , Biomarcadores/sangue , Dano Encefálico Crônico/induzido quimicamente , Estudos de Casos e Controles , Doença Crônica , Transtornos Relacionados ao Uso de Cocaína/complicações , Transtornos Relacionados ao Uso de Cocaína/enzimologia , Transtornos Cognitivos/diagnóstico , Estudos Transversais , Escala de Gravidade do Ferimento , Transtornos Mentais/diagnósticoRESUMO
BACKGROUND AND PURPOSE: Obstructive sleep apnea syndrome (OSAS) is a chronic disease ranging from innocuous to life-threatening and causes brain alterations manifested by neuropsychiatric symptoms. Neuron-specific enolase (NSE) and the astrocytic protein S100B are established sensitive peripheral biochemical markers of brain injury. In the present work we measured the serum levels of S100B and NSE in order to evaluate the deleterious effects of OSAS to the brain. PATIENTS AND METHODS: We studied 29 male patients with OSAS and 17 male asymptomatic control subjects with an apnea-hypopnea index (AHI) less than five events per hour. Patients and control subjects were evaluated by full-night polysomnography (PSG) and by Mini International Neuropsychiatric Interview (MINI) for the presence of neuropsychiatric symptoms. In the morning following the PSG, blood was collected and serum levels of S100B and NSE were measured using standard techniques. RESULTS: The AHI in the OSAS group was (mean+/-SD) 27+/-25 AH/h, ranging from 5 to 99 AH/h. S100B was higher in OSAS (0.15+/-0.09 microg/l) than in the control group (0.08+/-0.06 microg/l; P<0.01). Serum NSE was similar in both groups (17.5+/-12.2 vs. 15.8+/-6.8ng/ml). CONCLUSIONS: We report elevated serum S100B levels in OSAS patients in this study.
Assuntos
Dano Encefálico Crônico/sangue , Fatores de Crescimento Neural/sangue , Fosfopiruvato Hidratase/sangue , Proteínas S100/sangue , Apneia Obstrutiva do Sono/sangue , Adulto , Biomarcadores/sangue , Humanos , Hipóxia Encefálica/sangue , Masculino , Pessoa de Meia-Idade , Polissonografia , Subunidade beta da Proteína Ligante de Cálcio S100RESUMO
For an assessment of whether cord plasma arginine vasopressin, erythropoietin, and hypoxanthine concentrations are predictors of perinatal brain damage, these concentrations were measured in 62 infants born after preeclampsia of pregnancy, 31 acutely asphyxiated infants, and 38 control infants. Follow-up at 2 years included neurologic examination and the determination of a Bayley mental score. Clear abnormality (death, cerebral palsy, or developmental delay) was found in four infants in the preeclampsia group and five in the asphyxia group; slight abnormality was found in 12 and 6 infants, respectively; and no abnormality was found in the remainder. Neither arginine vasopressin values nor hypoxanthine values predicted adverse outcome in either study group. A high erythropoietin level was found in infants born after preeclampsia regardless of outcome: normal outcome (geometric mean (GM), 102; 95% confidence interval [CI], 69 to 153 mU/ml), slightly abnormal outcome (GM, 100; 95% CI, 37 to 270 mU/ml) or clearly abnormal outcome (GM, 84; 95% CI, 19 to 378 mU/ml). However, asphyxiated infants with clearly abnormal outcome had higher erythropoietin values (GM, 67; 95% CI, 33 to 137 mU/ml; p less than 0.05) than the normal infants (GM, 37; 95% CI, 23 to 59 mU/ml). We conclude that a high erythropoietin level after normal pregnancy, but not after preeclampsia, indicates an increased risk for cerebral palsy or death.