RESUMEN
OBJECTIVE: To assess whether an oxygen saturation (Spo2) target of 85%-89% compared with 91%-95% reduced the incidence of the composite outcome of death or major disability at 2 years of age in infants born at <28 weeks' gestation. STUDY DESIGN: A total 340 infants were randomized to a lower or higher target from <24 hours of age until 36 weeks' gestational age. Blinding was achieved by targeting a displayed Spo2 of 88%-92% using a saturation monitor offset by ±3% within the range 85%-95%. True saturations were displayed outside this range. Follow-up at 2 years' corrected age was by pediatric examination and formal neurodevelopmental assessment. Major disability was gross motor disability, cognitive or language delay, severe hearing loss, or blindness. RESULTS: The primary outcome was known for 335 infants with 33 using surrogate language information. Targeting a lower compared with a higher Spo2 target range had no significant effect on the rate of death or major disability at 2 years' corrected age (65/167 [38.9%] vs 76/168 [45.2%]; relative risk 1.15, 95% CI 0.90-1.47) or any secondary outcomes. Death occurred in 25 (14.7%) and 27 (15.9%) of those randomized to the lower and higher target, respectively, and blindness in 0% and 0.7%. CONCLUSIONS: Although there was no benefit or harm from targeting a lower compared with a higher saturation in this trial, further information will become available from the prospectively planned meta-analysis of this and 4 other trials comprising a total of nearly 5000 infants.
Asunto(s)
Enfermedades del Prematuro/metabolismo , Recien Nacido Prematuro , Recién Nacido de muy Bajo Peso/metabolismo , Terapia por Inhalación de Oxígeno/métodos , Oxígeno/sangre , Australia , Preescolar , Evaluación de la Discapacidad , Método Doble Ciego , Femenino , Edad Gestacional , Humanos , Lactante , Recién Nacido , Enfermedades del Prematuro/mortalidad , Enfermedades del Prematuro/terapia , Masculino , Evaluación de Resultado en la Atención de Salud , Medición de RiesgoRESUMEN
The first reported case of clinically significant congenital Factor VII deficiency in association with the 13q deletion syndrome is presented. It illustrates the importance of knowledge of the specific genes involved in gross deletion syndromes and adds to the current clinical experience of this rare disease.