RESUMEN
Aztreonam was administered to 25 neonates (16 term, 9 premature) with clinically and bacteriologically proved gram-negative infections. Ten patients had meningitis, 9 had septicemia and 6 had urinary tract infections. Patients were between 1 and 28 days of age. Aztreonam was administered intravenously in doses ranging from 40 to 120 mg/kg/day for 10-30 days, depending on the causative organism. All CSF, blood and urine cultures were sterile 48 h after drug treatment had begun. There was no incidence of bacteriologic relapse. Body temperature returned to normal in 96% of patients within 3-4 days of therapy. Aztreonam was well tolerated. One infant experience nausea and vomiting, but no patient was withdrawn from therapy due to adverse reactions.
Asunto(s)
Aztreonam/uso terapéutico , Infecciones Bacterianas/tratamiento farmacológico , Enfermedades del Prematuro/tratamiento farmacológico , Bacterias Gramnegativas , Humanos , Recién Nacido , Meningitis/tratamiento farmacológico , Pronóstico , Sepsis/tratamiento farmacológico , Infecciones Urinarias/tratamiento farmacológicoRESUMEN
Changes in uridine-diphosphate glucuronyl transferase activity (UDP-GT) in liver homogenates of hamsters treated with different doses of isoniazid (INH), rifampicin (RMP), para-aminosalicylic acid (PAS) and hydrocortisone for several periods of time were studied and expressed as mg of bilirubin conjugated per g of protein per h. INH, RMP, PAS and hydrocortisone induced UDP-GT activity to a statistically significant degree. The optimum dose for high induction was 20 mg for INH, RMP and hydrocortisone, and 200 mg for PAS per kg of body weight. The optimum time of treatment for high induction was 10 consecutive days of intraperitoneal administration for all drugs examined. Such data, particularly for INH and RMP, indicate why patients who receive these drugs show no clinical jaundice, although they develop an hepatitis-like disease with elevation of serum transaminase of hepatic origin. This could be the result of stimulation of the hepatic smooth endoplasmic reticulum which produces rapid conjugation and therefore excretion of bilirubin. Similarly, the antituberculous drugs may cause liver dysfunction by inducing other liver enzymes.
Asunto(s)
Antituberculosos/farmacología , Glucuronosiltransferasa/metabolismo , Hígado/enzimología , Ácido Aminosalicílico/farmacología , Animales , Bilirrubina/metabolismo , Cricetinae , Activación Enzimática/efectos de los fármacos , Hidrocortisona/farmacología , Isoniazida/farmacología , Masculino , Rifampin/farmacología , Factores de TiempoRESUMEN
Ascorbic acid (AsA) concentrations in plasma exert a modulating effect on the activity of liver enzymes. Since UDP-glucuronyl transferase is a liver enzyme, which is responsible for bilirubin glucuronidation, the effect of varied amounts of AsA on this enzyme activity was studied. Sixty male guinea-pigs were randomly allocated to the following six groups: controls, scorbutic and groups given 2, 5, 10 or 20 mg of ascorbic acid, respectively. All the animals with the vitamin C deficient diet presented clinical signs of scurvy at the end of the experimental period, and had lost both body and liver weight compared to all other groups. Scorbutic animals had very low levels of AsA in the liver compared with controls (0.20 +/- 0.10 and 1.65 +/- 0.45 mg/g liver, respectively) (p less than 0.001). Liver AsA levels increased as the AsA dose increased. The UDP-glucuronyl transferase activity was lower in scorbutic animals than in controls (6.20 +/- 1.95 and 23.85 +/- 4.20 mg bilirubin/g protein/h, respectively) (p less than 0.001). The other groups C, D, E and F also had higher mean levels of UDP-GT activity than the scorbutic group B. Finally, no correlation was found between UDP-glucuronyl transferase activity and ascorbic acid intake.