RESUMEN
One representative case of burns caused by the negligent use of bioethanol, which was treated at our burns centre is used to illustrate the severity and depth of the burn injuries as well as the complexity of the further long-term course of treatment including complex secondary-reconstructive techniques.
Asunto(s)
Quemaduras/etiología , Quemaduras/cirugía , Etanol , Procedimientos de Cirugía Plástica/métodos , Piel/lesiones , Colgajos Quirúrgicos , Accidentes Domésticos , Adulto , Quemaduras/diagnóstico , Terapia Combinada/métodos , Procedimientos Quirúrgicos Dermatologicos/métodos , Femenino , Humanos , Mala Praxis , Prevención Secundaria/métodos , Piel Artificial , Resultado del TratamientoRESUMEN
This study investigated plasma protein binding by the novel oral hypoglycemic agent, repaglinide, and assessed the influence of other protein-bound drugs upon this process. Varying concentrations of [3H]-repaglinide (0.01 to 100 micrograms/ml) were incubated in solutions of plasma proteins (human serum albumin, HSA; alpha 1-acid glycoprotein, AAGP), or human plasma in the absence or presence of several test drugs. Protein binding was assessed using an ultrafiltration technique. At all concentrations tested, the mean binding of repaglinide in plasma was 98.5%, binding to HSA averaged 98.6%, and the binding to AAGP was saturable and remained below 50%. Warfarin 10 micrograms/ml, furosemide 0.2 microgram/ml, and tolbutamide 100 micrograms/ml, significantly reduced in vitro binding of repaglinide at 1 and 100 micrograms/ml versus control (p < 0.05), producing an 18-36% increase in free repaglinide. No reduction was found using 0.1 microgram/ml repaglinide. Diazepam, glibenclamide and nicardipine hydrochloride had no significant effects on the in vitro protein binding of repaglinide. These data suggest that the binding of repaglinide to HSA in human plasma has potential clinical significance, and that within the therapeutic range for repaglinide, the presence of the test drugs has no clinically relevant effects on repaglinide binding to plasma proteins.