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Biomedical subjects

G Karlaganis

Publications and source records attributed to G Karlaganis.

47 records · Page 3Linked to original sources
PubMed1978

Bile acid pattern in human amniotic fluid.

Individual bile acids were determined in twenty-nine amniotic fluid specimens obtained from twenty-six women between the 32nd and 41st week of gestation. Total bile acid concentration ranged from 0.4 to 4.8 mumol/l with a mean of 1.57 mumol/l. Besides the two major bile acids of man, cholic acid and chenodeoxycholic acid, 3beta-hydroxy-5-cholenoic acid was found in all, lithocholic acid in ten and deoxycholic acid in nine of the twenty-nine amniotic fluid samples. 3beta-Hydroxy-5-cholenoic acid averaged 39.8% of total bile acids during 32-37 weeks of gestation and 20.2% at term (P less than 0.01). These findings point towards important differences between fetal and adult bile metabolism and may reflect maturation of hepatic bile acid biosynthesis near term.

Amniotic Fluid↗
PubMed1978

Analysis of bile acids in serum and bile by capillary gas-liquid chromatography.

Various liquid phases for glass capillary columns have been evaluated for gas-liquid chromatographic analysis of methyl ester trimethylsilylether derivatives of bile acids from serum and bile. Bile acid analysis is rapid and exhibits high separation efficiency with a 20 X 0.3 mm glass capillary column whose internal surface is covered with a crystal layer of barium carbonate and coated with polyethyleneglycol 20000 as liquid phase according to Grob et al.

Bile↗
PubMed1977

[Detection of 3 beta-hydroxy-5-cholenoic acid in human amniotic fluid].

Studies of the bile acids of human meconium suggest that a fetal pathway of bile acid synthesis exists which leads to formation of 3beta-hydroxy-5-cholenoic acid, a bile acid not found in serum of healthy pregnant women. To obtain additional support for this hypothesis, cholic, chenodeoxycholic, and 3beta-hydroxy-5-cholenoic acid were measured in amniotic fluid specimens from 18 pregnant women without liver disease. The finding of a considerable percentage of 3beta-hydroxy-5-cholenoic acid (mean: 34 molar %; range 3-71 molar % of total bile acids) in amniotic fluid strengthens the hypothesis that a fetal pathway of bile acid synthesis exists which begins with oxidation of the cholesterol side chain.

Adolescent↗
PubMedDate not supplied

Mechanism of the excessive sedative response of cirrhotics to benzodiazepines: model experiments with triazolam.

Mechanisms responsible for disproportional sedation resulting from triazolam administration to patients with cirrhosis were investigated. Ordinary sedative doses (0.25 mg) were given p.o. to 8 cirrhotics and 18 controls. Plasma concentrations of unbound drug were assessed by capillary gas chromatography and equilibrium dialysis. Median apparent oral clearances of unbound triazolam were 14.8 ml per min per kg in cirrhotics and 23.9 ml per min per kg in controls (p less than 0.01). Clearances were significantly correlated with severity of liver disease as assessed by the aminopyrine breath test (Rs = 0.77, n = 17, p less than 0.001). At a time when plasma concentrations of unbound triazolam were the same in both groups, i.e., 2.25 hr after dosing, flicker sensitivity at 5 Hz which was used as an index of CNS performance was impaired by a factor of 3.2 in cirrhotics and 1.4 in controls (p less than 0.01 for group difference). Performance was also significantly lower in cirrhotics with the digit symbol substitution test (p less than 0.05). It is concluded that, in patients with cirrhosis, disproportional sedation after benzodiazepine administration may be due not only to impaired drug elimination, but also to hypersensitivity of the brain.

Adult↗
PubMedDate not supplied

Bile acids and bile alcohols in two patients with Zellweger (cerebro-hepato-renal) syndrome.

The Zellweger cerebro-hepato-renal syndrome (CHRS) is a rare hereditary disease in which there is a generalized deficiency of peroxisomal function. Liver peroxisomes are important for the conversion of 3 alpha,7 alpha,12 alpha-trihydroxy-5 beta-cholestanoic acid into cholic acid, and, consequently, 3 alpha,7 alpha,12 alpha-trihydroxy-5 beta-cholestanoic acid and metabolites of this bile acid precursor accumulate in serum and bile of patients with CHRS. Little is known about the urinary excretion of bile acids in this disease. Using gas chromatography-mass spectrometry we have analyzed serum bile acids and urinary excretion of bile acids and bile alcohols in two Swiss male CHRS patients. As expected, serum concentrations and urinary excretions of 3 alpha,7 alpha,12 alpha-trihydroxy-5 beta-cholestanoic acid and 3 alpha,7 alpha,12 alpha,24-tetrahydroxy-5 beta-cholestanoic acid were elevated, which is probably an obligatory finding in CHRS. In addition, the urinary excretion of 1,3,7,12-tetrahydroxy-5 beta-cholanoic acid (a very polar unusual bile acid) was increased (99-1556 nmol/24 h). In contrast, the excretion of the major urinary bile alcohol, 27-nor-5 beta-cholestane-3 alpha, 7 alpha,12 alpha,24,25-pentol was found to be normal. 3 alpha, 7 alpha,12 alpha-Trihydroxy-5 beta-C29-dicarboxylic acid, a metabolite of 3 alpha,7 alpha,12 alpha-trihydroxy-5 beta-cholestanoic acid previously believed to be obligatory in CHRS, was found only in one of our patients.

Abnormalities, Multiple↗
PubMedDate not supplied

Identification of mephenytoin metabolites in the dog.

In two dogs p-hydroxymephenytoin, m-hydroxymephenytoin, 5-ethyl-5-phenylhydantoin (nirvanol), and 5-ethyl-5-(p-hydroxyphenyl)hydantoin (p-hydroxynirvanol) were identified by use of synthetic metabolites as standards for comparison.

Animals↗