Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
Más filtros










Base de datos
Intervalo de año de publicación
1.
Pediatr Pulmonol ; 51(6): 601-6, 2016 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-26663621

RESUMEN

INTRODUCTION: Meconium aspiration syndrome (MAS) is linked to inflammation, but data on the patterns of hematological indices and C-reactive protein (CRP) in MAS are lacking. The aim of the study was to evaluate CRP, white blood cell count (WBC), absolute neutrophil count (ANC), and immature-to-total neutrophil ratio (IT-ratio) in MAS and to assess their association with disease severity. METHODS: Retrospective cross-sectional study including 239 consecutively admitted neonates with MAS to a level III NICU. Neonates with early onset sepsis were excluded. Results Neonates with severe MAS (invasive mechanical ventilation for <7 days) and very severe MAS (invasive mechanical ventilation for ≥7 days or high frequency ventilation or ECMO) had higher CRP and IT-ratio compared to neonates with non-severe MAS (no invasive mechanical ventilation) during the first 2 days of life (CRP: 13.0 and 40.9 vs. 9.5 mg/L, P = 0.039 and <0.001, respectively) and neonates with very severe MAS had lower WBC and ANC. All four inflammatory indices correlated significantly with duration of invasive mechanical ventilation, duration of respiratory support and with length of hospital stay, arterial hypotension, and persistent pulmonary hypertension. Neonates with all four inflammatory indices beyond the normal range had a more than 20-fold increase in risk for very severe MAS. CONCLUSION: High CRP and IT-ratio and low WBC and ANC values were closely linked to a more severe course of MAS during the early phases of the disease. These findings reflect the role of inflammation in the pathogenesis of MAS. Pediatr Pulmonol. 2016;51:601-606. 2015 Wiley Periodicals, Inc.


Asunto(s)
Síndrome Inflamatorio de Reconstitución Inmune/diagnóstico , Síndrome de Aspiración de Meconio/inmunología , Respiración Artificial/métodos , Estudios Transversales , Femenino , Ventilación de Alta Frecuencia , Humanos , Síndrome Inflamatorio de Reconstitución Inmune/inmunología , Síndrome Inflamatorio de Reconstitución Inmune/terapia , Recién Nacido , Unidades de Cuidado Intensivo Neonatal , Tiempo de Internación , Síndrome de Aspiración de Meconio/complicaciones , Síndrome de Aspiración de Meconio/terapia , Estudios Retrospectivos , Factores de Riesgo , Índice de Severidad de la Enfermedad
2.
Med Klin (Munich) ; 100(6): 361-4, 2005 Jun 15.
Artículo en Alemán | MEDLINE | ID: mdl-15968489

RESUMEN

BACKGROUND: The Brugada syndrome is an autosomal dominant disorder characterized by life-threatening ventricular tachyarrhythmias due to cardiac conductance disturbance without structural heart disease. Mutations of the SCN5A gene cause either a reduction in cardiac Na(+) channel expression or alterations in channel-gating properties, leading to a reduction in Na(+) current amplitude. CASE REPORT: A 37-year-old patient presented after a syncopal spell preceded by dizziness. 6 years ago he had experienced similar symptoms. At that time, physical and clinical examination did not lead to a convincing diagnosis. The initial ECG showed typical signs of the Brugada syndrome with descending ST elevation in leads V(1) and V(2). The ECG changes could be observed over the next 3 days. Thereafter, ECG changes reversed to normal. Ultrasound examination did not show any signs of structural heart disease. During electrophysiological testing no sustained ventricular tachyarrhythmias were inducible. Molecular genetic analysis in this young patient revealed a mutation in the SCN5A gene. According to the patient's symptoms, an automatic cardioverter defibrillator (ICD) was implanted. CONCLUSION: A history of unexplained syncope in patients with a structurally normal heart should raise the suspicion of malignant arrythmias caused by primary arrythmogenic disorders. The diagnosis of Brugada syndrome can be concluded from typical ECG changes (i. e., incomplete right bundle branch block, ST elevation in leads V(1)-V(3)) accompanied by typical symptoms and a positive family history. To date, there is no effective therapy of the gene defect or its pathophysiological correlate available. Therefore, ICD therapy is recommended in symptomatic patients to prevent sudden cardiac death.


Asunto(s)
Síncope/etiología , Taquicardia Ventricular/complicaciones , Adulto , Aberraciones Cromosómicas , Análisis Mutacional de ADN , Muerte Súbita Cardíaca/prevención & control , Desfibriladores Implantables , Diagnóstico Diferencial , Genes Dominantes , Humanos , Masculino , Proteínas Musculares/genética , Canal de Sodio Activado por Voltaje NAV1.5 , Canales de Sodio/genética , Síncope/prevención & control , Síndrome , Taquicardia Ventricular/genética , Taquicardia Ventricular/terapia
SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA
...