RESUMEN
Thirty-five spinal fluids with leucocytosis belonging to 26 children presenting neoplasia without metastases or CNS infection, were studied. We found that 69% of the cases were receiving some kind of CNS therapy, although leucocytosis could be found at any moment of the evolution and independently of treatment. It is stressed that the criteria for meningeal infiltration in children with neoplasia must be established only if tumoral cells are found in the spinal fluid. Pleocytosis and absence of symptomatology must not be used as the main criteria.
Asunto(s)
Líquido Cefalorraquídeo/citología , Leucocitosis/líquido cefalorraquídeo , Neoplasias/líquido cefalorraquídeo , Niño , Preescolar , Femenino , Enfermedad de Hodgkin/líquido cefalorraquídeo , Humanos , Leucemia Linfoide/líquido cefalorraquídeo , Leucemia Mieloide Aguda/líquido cefalorraquídeo , Recuento de Leucocitos , Masculino , Retinoblastoma/líquido cefalorraquídeoRESUMEN
Barbiturates inhibit GLUT-1-mediated glucose transport across the blood-brain barrier, in cultured mammalian cells, and in human erythrocytes. Barbiturates also interact directly with GLUT-1. The hypotheses that this inhibition of glucose transport is (i) selective, preferring barbiturates over halogenated hydrocarbon inhalation anesthetics, and (ii) specific, favoring some GLUT-# isoforms over others were tested. Several oxy- and thio-barbiturates inhibited [3H]-2-deoxyglucose uptake by GLUT-1 expressing murine fibroblasts with IC50s of 0.2-2.9 mm. Inhibition of GLUT-1 by barbiturates correlates with their overall lipid solubility and pharmacology, and requires hydrophobic side chains on the core barbiturate structure. In contrast, several halogenated hydrocarbons and ethanol (all =10 mm) do not significantly inhibit glucose transport. The interaction of these three classes of anesthetics with purified GLUT-1 was evaluated by quenching of intrinsic protein fluorescence and displayed similar specificities and characteristics. The ability of barbiturates to inhibit other facilitative glucose transporters was determined in cell types expressing predominantly one isoform. Pentobarbital inhibits [3H]-2-deoxyglucose and [14C]-3-O-methyl-glucose uptake in cells expressing GLUT-1, GLUT-2, and GLUT-3 with IC50s of approximately 1 mm. In contrast, GLUT-4 expressed in insulin-stimulated rat adipocytes was much less sensitive than the other isoforms to inhibition by pentobarbital (IC50 of >10 mm). Thus, barbiturates selectively inhibit glucose transport by some, but not all, facilitative glucose transporter isoforms.