RESUMEN
Recommendations for vitamin K supplementation were recently changed to 3 x 1 mg orally in healthy term neonates and 0.2 mg parenterally in prematures and high-risk neonates. Prothrombin times (PT) at reduced vitamin K doses (120 patients, 170 samples) during the first 6 weeks of life were below 40% in 6 patients only; all low PTs were unrelated to vitamin K. In the remaining patients, median PT was 100%; 79% of patients had values above 70%. PT was related to birthweight, gestational age and age. There was no decrease over the observation period. Following reduced oral and parenteral vitamin K regimens PTs were well within published reference values for neonates given larger amounts of vitamin K.
Asunto(s)
Hemostáticos/administración & dosificación , Recien Nacido Prematuro/sangre , Tiempo de Protrombina , Vitamina K/administración & dosificación , Administración Oral , Factores de Edad , Peso al Nacer , Edad Gestacional , Humanos , Recién Nacido , Inyecciones Intramusculares , Estudios Prospectivos , Valores de ReferenciaAsunto(s)
Cefotaxima/uso terapéutico , Ceftriaxona/uso terapéutico , Histerectomía , Infección de la Herida Quirúrgica/prevención & control , Bacterias/efectos de los fármacos , Cefotaxima/farmacología , Ceftriaxona/farmacología , Ensayos Clínicos como Asunto , Femenino , Humanos , Pruebas de Sensibilidad Microbiana , Distribución Aleatoria , VaginaRESUMEN
Cultured fibroblasts from mucolipidosis II (ML-II) patients demonstrated an elevated cystine content which increased with time in culture compared to fibroblasts from cystinotic patients or normal controls under the same conditions. In both cystinotic and ML-II cells the increased levels of cystine could be derived either from endogenous proteolysis or from in vitro supplementation of the cultured cells with cysteine-glutathione mixed disulfide. Cystine was depleted from both cell types by cysteamine. When cysteamine was replaced with complete medium, the cystine reaccumulated in both cystinotic and ML-II cells within 24 h, although a lag of 4 h was seen with ML-II cells. The intracellular location of the increased cystine in cultured fibroblasts was examined utilizing free-flow electrophoresis and found to be in the purified population of secondary lysosomes of both cystinotic and ML-II cells. White blood cell and hepatic cystine, which was greatly increased in cystinotic patients, was not elevated in ML-II patients. Compared to normal control fibroblasts the efflux of cystine from isolated granular fractions was virtually absent in cystinotic fibroblasts and considerably reduced in ML-II fibroblasts. The examination of such similarities and differences in cystine accumulation and transport in tissues from cystinotic and ML-II patients has provided some insight into the defects in these diseases.