The influence of kidney or liver disorders on the serum concentration and urinary excretion of 3H-peruvoside, a tritium-labelled cardiac glycoside

1968 ◽  
Vol 3 (2) ◽  
pp. 147-152 ◽  
Author(s):  
Hg. Lahrtz ◽  
P.A. Van Zwieten
1976 ◽  
Vol 4 (5) ◽  
pp. 352-354
Author(s):  
L Padeletti ◽  
F Fantini ◽  
P Cinelli ◽  
C Gremigni

In a randomized crossover study the bioavailability of a single dose of digoxin and of beta-methyl-digoxin tablets was tested in four normal volunteers. No difference was found between the two products in the rate and extent of drug absorption using 6 day cumulative urinary excretion and serial serum concentration measurements.


Chemotherapy ◽  
1974 ◽  
Vol 20 (3) ◽  
pp. 129-140 ◽  
Author(s):  
N.K. Ao ◽  
O.P. Taneja ◽  
V.N. Bhatia ◽  
D.S. Aggarwal

1981 ◽  
Vol 96 (4) ◽  
pp. 444-450 ◽  
Author(s):  
Bjarne Lund ◽  
Peter Claes Eskildsen ◽  
Birger Lund ◽  
Anthony W. Norman ◽  
Ole Helmer Sørensen

Abstract. Acromegalic subjects were found to have elevated serum levels of both 1,25-dihydroxyvitamin D (1,25-(OH)2D), (67 ± 22 (sd) pg/ml) and 24,25-dihydroxyvitamin D (24,25-(OH)2D), (6.9 ± 1.5 (sd) ng/ml). The serum concentration of 1,25-(OH)2D correlated positively (P < 0.02, R = 0.56) to the 24 h urinary excretion of growth hormone, but not to the serum levels of parathyroid hormone, prolactin, thyroid hormones or the urinary excretion of free cortisol. Fourteen patients were treated with bromocriptine at doses from 15–45 mg/day for a period of about 6 months. This was accompanied by a significant decrease in the urinary excretion of growth hormone and calcium and in the serum concentrations of 1,25-(OH)2D and 24,25-(OH)2D. A relationship was demonstrated between the decrease in urinary calcium excretion and the decrease in serum 1,25-(OH)2D (P < 0.02, R = 0.64). It is concluded that the serum concentration of 1,25-(OH)2D is elevated in acromegaly, perhaps as a consequence of a direct action of growth hormone on the renal lα-hydroxylase activity.


PEDIATRICS ◽  
1983 ◽  
Vol 71 (1) ◽  
pp. 59-63
Author(s):  
Dagfinn Aarskog ◽  
Lage Aksnes ◽  
Trond Markestad

Studies were carried out to compare the effects of parathyroid extract (PTE) on the serum concentration of 1,25-dihydroxyvitamin D (1,25[OH]2D), 24,25-dihydroxyvitamin D (24,25[OH]2D), 25,26-dihydroxy vitamin D (25,26[OH]2D) and cAMP, and the urinary excretion of calcium, phosphorus, and cAMP in two normal adult subjects, and in a girl with vitamin D-dependent rickets. The concentration of 1,25[OH]2D was markedly decreased even when she was receiving a daily dose of 25,000 IU of ergocalciferol. PTE infusion resulted in a prompt and distinct increase in the serum levels and the urinary excretion of cAMP in the patient and control subjects. In the control subjects the serum concentration of 1,25[OH]2D increased after the PTE infusion, whereas there was no response in the patient with vitamin D-dependent rickets. The two other dihydroxylated metabolites of vitamin D showed no consistent response to the PTE infusion in the control subjects or the patient. The patient showed no phosphaturic response to PTE while she was receiving high-dosage ergocalciferol treatment. By contrast, when the patient was re-studied after therapy with lα-hydroxyvitamin D, PTE infusion resulted in an increase in urinary phosphate excretion. These findings might lend support for the notion that 1,25[OH]2D has an effect on tubular phosphate resorption and has a permissive role in the phosphaturic effect of parathyroid hormone. The present findings also confirm that the formation of 1,25[OH]2D is impaired in vitamin D-dependent rickets and indicate that the renal 25-hydroxyvitamin D-lα-hydroxylase is unresponsive to the stimulatory effect of parathyroid hormone in this condition.


PEDIATRICS ◽  
1985 ◽  
Vol 75 (6) ◽  
pp. 1032-1037
Author(s):  
Gideon Koren

Quinidine and digoxin had been coadministered in cardiac patients for several decades before their interaction was reported in 1978. During the last few years, monitoring of increased digoxin serum concentration when several drugs are commonly coadministered with digoxin has led to reports of toxic accumulation of the cardiac glycoside. Because digoxin toxicity is frequently associated with severe morbidity and mortality, close monitoring of clinical and laboratory signs are mandatory whenever the cardiac glycoside is coadministered with quinidine, verapamil, amiodarone, nifedipine, and indomethacin. Because many of the children receiving a combination of digoxin and interacting drugs are outpatients, it is mandatory to take steps to ensure that toxicity will be detected and treated in its early stages.


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