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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
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
OBJECTIVE
To determine the extent to which immaturity of hepatic microsomal enzyme activity might contribute to physiological jaundice.
METHODS
Urinary excretion of D-glucaric acid, expressed in mumol glucaric acid/ mmol creatinine, was measured in 122 Chinese full-term healthy newborn babies during
The urinary excretion of D-glucaric acid, a catabolite of glucuronic acid, is considered to be a reliable index of the state of hepatic microsomal enzyme activity. Because enzyme activity may be altered in liver disease, we examined the effect of liver disease on the excretion of this metabolite and
The excretion of D-glucaric acid (DGA), a metabolite of the cytochrome P-450 pathway, is considered a marker of the viability of hepatocytes. Twelve cases of biliary atresia (BA) have been investigated, correlating the level of DGA, degree of histological alteration of liver parenchyma, and clinical