Comparison of cefadroxil and ampicillin in the treatment of urinary tract infections in children.

The therapeutic efficacy of 25 mg/kg of cefadroxil administered once daily was compared with that of 50 mg/kg/day of ampicillin administered in four equal doses in the treatment of acute uncomplicated urinary tract infections (UTIs) in children. Nineteen girls and seven boys (mean age, 5.5 years) received cefadroxil, and 18 girls and eight boys (mean age, 5.9 years) received ampicillin. The clinical and bacteriological characteristics, as well as the demographic characteristics, of both populations were well matched. Patients with structural anomalies or with a history of hypersensitivity to cephalosporins or penicillins or abnormal hepatorenal function were excluded from the trial. Only patients with at least two consecutive positive cultures of a single pathogen, obtained in clean-catch midstream urine samples (greater than or equal to 10(5) colony-forming units per ml urine) and susceptible to the respective antibiotic, were admitted to the study. Urine cultures were repeated during the ten days of treatment and ten days after the completion of treatment. All patients in the cefadroxil group were evaluated as clinically and bacteriologically cured. Three (12%) of the patients in the ampicillin group had positive cultures in the immediate post-treatment period. The differences in the cure rates of the two groups were not statistically significant. No adverse effects of either antibiotic were observed.

Serum gamma-glutamyl transpeptidase, D-glucaric acid excretion and plasma half-life of antipyrine in newborns with severe jaundice of unknown etiology and due to glucose-6-phosphate dehydrogenase deficiency in Greece.

Serum gamma-glutamyl transpeptidase (gamma-GT) activity, urinary D-glucaric acid (D-GA) excretion and plasma half-life of antipyrine were measured in 22 healthy children as well as in 45 full-term newborns on the 10th day of life. Of these 45 newborns, 20 had jaundice of unknown etiology, 14 had jaundice due to G-6 PD deficiency, and 11 were normal and served as controls. Serum gamma-GT activity was found to be within the normal range in the 22 healthy children, whereas it was in the upper range of the norm in all newborns during the neonatal period. Urinary D-GA excretion was normal in the healthy children and in control known etiology and in 57% of babies with jaundice due to G-6-PD deficiency. Plasma half-life of antipyrine was normal (less than 30 h) in the 22 healthy children, whereas it was prolonged (greater than 30 h) in 9% of the normal newborns, in 60% of the newborns with jaundice of unknown etiology and in 7% of the newborns with jaundice due to G-6-PD deficiency. These findings suggest that in severe neonatal jaundice of unknown etiology there is a greatly reduced excretion of endogenously formed D-GA as well as prolongation of the plasma half-life of antipyrine. This is probably due to decreased activity of the liver enzymes involved in the metabolism of glucuronic acid and the oxidation of antipyrine. These defects probably contributed to the unconjugated hyperbilirubinemia observed in these newborns.

D-Glucaric acid excretion in newborns with severe jaundice of unknown etiology and due to glucose-6-phosphate dehydrogenase deficiency in Greece.

The urinary D-glucaric acid of 86 full-term newborns was determined on the 10th day of life. Of these, 28 had jaundice due to glucose-6-phosphate dehydrogenase (G-6-PD) deficiency, 24 jaundice of unknown etiology and 18 Rhesus incompatibility. Practically all the cases of the first two groups had a greatly decreased D-glucaric acid excretion whereas this was not a constant finding in the 18 cases with Rh-incompatibility. Normal values were found in 16 healthy controls of the same age. These findings suggest that in severe neonatal jaundice due to G-6-PD deficiency and in jaundice of unknown etiology, there is a greatly reduced excretion of endogenously formed D-glucaric acid, due probably to decreased activity of liver enzymes involved in the metabolism of glucuronic acid. This defect probably contributes to the unconjugated hyperbilirubinemia in these newborns.