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Biomedical subjects

E Forster

Publications and source records attributed to E Forster.

At least 37 records · Page 2Linked to original sources
PubMed1981

6 beta-Hydroxycortisol: a noninvasive indicator of enzyme induction.

We measured urinary 6 beta-hydroxycortisol (6 beta OHF) excretion in normal children and in children receiving anticonvulsant therapy with phenobarbital or diphenylhydantoin, 6 beta OHF excretion increased 4- to 7-fold during anticonvulsant therapy. The marked increase in the ratios of 5 beta OHF to 17-hydroxycorticosteroid and 6 beta OHF to free cortisol suggests that the measured increase in urinary 6 beta OHF may serve as an index of induction of the microsomal mixed function oxidase system. This noninvasive approach allows rapid assessment of the effects of drugs and foreign compounds on microsomal hydroxylation of cortisol. This convenient probe can be applied, with particular ease, to further studies in children in whom characterization of the effects of drugs and xenobiotic compounds on hepatic hydroxylation is of interest.

17-Hydroxycorticosteroids↗
PubMed1980

Aldosterone response to prolonged ACTH infusion in juvenile hypertension.

The effects of a continuous 5-day ACTH infusion (40 units/24 hr) on plasma aldosterone (aldo) concentration and urinary excretion of aldosterone pH 1 conjugate, tetrahydroaldosterone and free aldo were investigated in 6 normotensive children, and 7 children with hypertension of unknown origin. In both groups, an initial rise of plasma aldo and all urinary aldo metabolites and a subsequent fall were observed during the ACTH test. The decline in plasma aldo correlated significantly with a decrease in plasma renin activity and serum K+. There was, however, evidence for another regulatory factor of aldo secretion during ACTH infusion because on a low salt diet. ACTH produced a similar aldo pattern which could not be attributed to the changes in plasma renin activity or serum K+. Urinary excretion of both free aldo and tetrahydroaldosterone, a metabolite formed in the liver, showed a slower decrease during ACTH infusion than aldosterone pH 1 conjugate, which is of renal origin. The change in pattern of urinary aldo metabolites may be caused by a relative increase of the free, nonprotein bound plasma fraction of aldo and an enhanced metabolism of aldo in the liver during ACTH infusion. Neither in the baseline state nor during the ACTH test was there a difference between the normotensive and the hypertensive group in any of the aldo parameters.

Adolescent↗