RESUMEN
There have been controversies on the effect of albumin in treating edema in nephrotic syndrome patients. We evaluated the additive diuretic effect of coadministration of furosernide with albumin in the six patients with nephrotic syndrome. We administered 160mg of furosemide intravenously for 1 hour with 100rnl of 20% albumin or 5% dextrose by random cross-over design. The urine and plasma furosemide concentrations were measured by HPLC. After the administration of furosemide alone, urine volume, urinary excretions of sodium and chloride were increased significantly compared to those of basal state (P<0.05). But, coadministration of furose-mide with albumin did not increase significantly the urine voume (2285+/-445ml vs. 3023+/-715ml), urinary excretions of sodium (194+/-58rnmol/day vs. 282+/-85 mmol/day) and chloride (213+/- 54mmoVday vs. 286+/- 74mmoVday) comparing to those of furosemide only cases. Addition of albumin to furosemide did not significantly changed pharmacokinetic parameters such as AUC (28.3+/-5.5ug/ml hr vs 36.0+/-6.7ug/ml hr), total plasma clearance (115+/-30mVmin vs 108+/-41ml/min), volume of distribution (0.13+/-0.02L/kg vs 0.10+/- 0.01L/kg), elirnination half life (1.4+/-0.3hr vs 1.5+/-0.3hr), and urine furosemide excretion (44+/-8% vs 43+ 10%). We concluded that albumin infusion did not enhance the diuretic action of furosemide pharmacodynamically and pharmacokinetically in patients with nephrotic syndrome.
Asunto(s)
Humanos , Área Bajo la Curva , Cromatografía Líquida de Alta Presión , Estudios Cruzados , Diuréticos , Edema , Furosemida , Glucosa , Semivida , Síndrome Nefrótico , Farmacocinética , Plasma , SodioRESUMEN
It is important to predict time to reach therapeutic concentration in phenytoin toxicity. In tradition, frequent drug monitoring is inevitable until the therapeutic serum level is reached. A method of estimating Vmax and Vd of phenytoin with application to estimating time to reach therapeutic concentration of phenytoin is described. We evaluated the usefulness of that method in twelve patients with phenytoin toxicity whose initial levels ranging from 27.7 to 74.0 ug/ml. We compaired the observed time defined as the time of returning from the initial toxic level to the optimum therapeutic level by serial measurement of serum concentration with the calculated time by using the modified Michaelis-Menten equation (Km x In (C1/C2) +Cl-C2=Vmax/vd x T). We determined individual patient's Vmax (maximal metabolic rate of concentration), Vd(volume of distribution of concentration), and Km(constants of Michaelis-Menten equation) for phenytoin, using data obtained from two consecutive serum concentration and known value of Km in Korean. And then, we calculated the decline time of phenytoin. The calculated decline time did not differ significantly from observed decline time (P=0.830). It is possible to predict the time to the therapeutic range and to reduce the unnecessarily frequent drug monitoring.