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PubMed2005

Changing characteristics of the TDx digoxin II assay in detecting bufadienolides in a traditional Chinese medicine: for better or worse?

In 1992, apparent digoxin concentrations determined by the Abbott TDx II assay 5 hours after the ingestion of 10 pills of traditional Chinese medicine containing toad secretions (chan su) by 7 volunteers, yielded results that were equimolar to bufalin measured by 2 in-house bufalin radioimmunoassays (RIAs). Recently, a 17-year-old Chinese female unintentionally took 100 (instead of 10) of these pills for a sore throat but suffered no ill effects. The blood bufalin concentration at 3 hours by 1 of the 2 RIAs was 10.93 nmol/L, which was commensurate with the dose. However, the apparent digoxin measured by a TDx II assay produced in 2004 was only 3.08 nmol/L, which probably reflects the change in the specificity of the polyclonal digoxin antisera used in the assay over the years. In 1989, the TDx assay was commended for its ability to detect poisoning from plant and animal cardenolides, a property that seems to be waning and, thus, bad news for those wishing to use the assay to detect alternative cardenolides. But, on the other hand, it possibly eliminates the "specter" of digoxin-like immunoreactive substance (DLIS) that has afflicted some digoxin assays, which can only be good news.

Adolescent↗
PubMedDate not supplied

Application of two-point assay of digoxin serum concentration in studying population pharmacokinetics in Egyptian pediatric patients with heart failure: does it make sense?

Digoxin pharmacokinetics (PK) was studied among a selected group of Egyptian pediatric patients (n = 40) with an age range of 0.33 to 15 years. All the patients had heart failure and were maintained on i.v. digoxin (10 microg/kg/d in 2 equal doses). For population PK analysis, 2 serum samples of digoxin were taken per patient. From 30 patients' trough (before the next dose) and 4 hours postdose samples were obtained, while in the other 10 patients, 0.5- and 6-hour postdose samples were taken. Serum concentrations were measured by fluorescence polarization immunoassay. PK modeling was performed using NONMEM software on log-transformed serum digoxin data. The best structural covariate-free model was a linear 2-compartment model with an exponential error model for intersubject variability and an additive model for intrasubject variability. Serum creatinine (SCR) was a significant covariate for clearance. The final population PK parameters were CL (L/h) = 0.388 - [0.78 x (SCR-0.6)], V1 (L/kg) = 1.38, Q (L/h/kg) = 0.48, V2 (L/kg) = 9.11, where CL is the total body clearance, V1 and V2 are the apparent volumes of distribution in the central and peripheral compartments, and Q is intercompartment clearance. A bootstrap resampling for internal validation achieved excellent agreement with the original data sets for PK parameters. In conclusion, 2 points of digoxin concentration allow good regression analysis for clearance-covariate relationship. The inclusion of SCR into the final model might allow better selection of initial maintenance dose of the drug. A prospective study on larger sample size of pediatric patients is recommended for clinical validation of the final model.

Adolescent↗
PubMed1984

Nicholson score for prescribing digoxin compared with Jellife nomogram.

A series of 84 medical inpatients were treated in random order with oral digoxin in doses calculated according to the newly introduced Nicholson score and the Jellife formula and nomogram. The daily dose of digoxin was lower (p less than 0.01) according to the Nicholson score (mean 2.1 digoxin tablets of 62.5 micrograms daily). The mean serum concentration of digoxin was also lower (p less than 0.01) according to the Nicholson score (1.27 nmol/l) than according to the Jellife nomogram (1.84 nmol/l). Estimated by the Nicholson score the serum concentration of digoxin was not optimal (p less than 0.01) and not within an acceptable therapeutic range (p less than 0.01) in more patients than when estimated by the Jellife nomogram. It is concluded that the Nicholson score is not suitable for medical inpatients.

Aged↗
PubMed1977

Monitoring digoxin therapy: II. Determinants of the apparent volume of distribution.

1 In eighteen subjects receiving digoxin therapy the apparent volume of distribution (Vd) of the drug has been calculated. 2 For each subject the sensitivity of the 86Rb transport mechanism of his pre-treatment erythrocytes to in vitro inhibition by digoxin has been measured (IC50). 3 The Vd of digoxin correlates both with the age of the patients and with the IC50 of their pre-treatment erythrocytes. 4 The implications of these findings are discussed in terms of the possible determinants of the Vd of digoxin. 5 Digoxin requirements may be predictable before therapy commences if IC50 measurements are performed.

Adult↗
PubMed1978

Digoxin compliance in patients from general practice.

1. Compliance with digoxin therapy has been assessed in a group of fifty patients receiving the drug in general practice but not attending hospital. 2. Compliance was estimated by comparing plasma digoxin concentrations before and after a 10 day period of measured digoxin consumption and by tablet counting. 3. Twelve patients had plasma concentrations which increased by more than 0.4 ng/ml during monitored intake and eight other patients took less than 80% of their tablets. These twenty patients were considered non-compliant. 4. A further three patients in whom plasma digoxin levels were zero when first seen but increased substantially during the run-in period were also adjudged non-compliant. 5. Non-compliance with prescribed digoxin dosage occurred, therefore, in 46% of the patients studied.

Aged↗
PubMed1979

Changes in cardiac glycoside receptor sites, 86rubidium uptake and intracellular sodium concentrations in the erythrocytes of patients receiving digoxin during the early phases of treatment of cardiac failure in regular rhythm and of atrial fibrillation.

1 Measurements of the binding of 12-alpha-[3H]-digoxin to the membranes of intact erythrocytes, erythrocytic 86rubidium uptake and intraerythrocytic sodium concentrations have been made in the red cells of patients receiving digoxin in the short-term for atrial fibrillation or cardiac failure in regular rhythm. 2 During the first few days of treatment [3H]-digoxin binding and 86rubidium uptake fall and intraerythrocytic sodium concentrations rise. 3 Subsequently parallel fluctuations occur in [3H]-digoxin binding and 86rubidium uptake but not in intraerythrocytic sodium concentrations and the significance of the fluctuations is discussed. 4 The values of all three measurements correlate significantly with the response of the heart in sinus rhythm as measured by QS2I. 5 Plasma digoxin concentrations do not correlate with QS2I.

Adult↗
PubMed1983

Skeletal muscle digoxin binding in patients with renal failure.

For digoxin analyses blood and skeletal muscle samples were taken from seven digoxin-treated patients with chronic renal failure. The ratio between skeletal muscle and serum digoxin concentration in the patients with renal failure was not significantly different from the ratios in two control groups consisting of subjects with normal renal function. In the group of patients with renal failure there was no relationship between the glomerular filtration rate and muscle digoxin binding (specific plus unspecific). The present study does not indicate reduced skeletal muscle digoxin binding in patients with chronic renal failure.

Adult↗
PubMed1986

Influence of nisoldipine on haemodynamic effects and plasma levels of digoxin.

In a placebo controlled double-blind study including 10 patients with heart failure the nisoldipine/digoxin interaction was studied. Nisoldipine was shown to elevate digoxin plasma concentrations significantly by about 15% (trough levels). During chronic combination therapy with nisoldipine trough levels and plasma concentrations 4 h after the morning dose of digoxin were 1.35 +/- 0.14 and 1.92 +/- 0.16 ng ml-1 respectively, whereas they averaged to 1.16 +/- 0.14 and 1.52 +/- 0.16 ng ml-1 with digoxin and placebo (P less than 0.05; mean +/- s.e. mean). Systolic time intervals were significantly altered by nisoldipine co-administration compared with digoxin plus placebo. In certain patients the elevation of digoxin plasma levels due to nisoldipine co-administration could be of clinical relevance.

Adult↗
PubMed1989

The need for reassessment of digoxin prescribing for the elderly.

1. The prevalence and circumstance of digoxin prescribing was assessed in five private nursing homes. 2. Forty-one patients (21% residents) were taking digoxin. 3. Seventeen patients were in atrial fibrillation and the remainder in sinus rhythm. The ventricular rate exceeded 100 beats min-1 in eight of the 17 patients in atrial fibrillation. 4. Thirty-seven patients were prescribed 0.0625 mg digoxin daily and serum digoxin concentrations were subtherapeutic in 20 of 32 patients in whom concentrations were measured. 5. These data indicate a need for more careful review of the need for maintenance digoxin and illustrate the inappropriateness of routinely prescribing very low doses in all elderly patients.

Aged↗
PubMed1977

The effects of digoxin and beta-methyldigoxin on the heart rate of decompensated patients with atrial fibrillation.

Eighteen patients with atrial fibrillation were given digoxin 0.13 mg twice daily for 3 weeks and beta-methyldigoxin 0.10 mg twice daily for another 3 weeks. At the end of each 3 week period an exercise test was performed and the effects on the heart rate of the two drugs were compared. No difference in heart rate was obtained at rest, whereas the heart rate after 6 min of exercise was higher during treatment with digoxin (131 beats/min) than when the patients were taking beta-methyldigoxin (124 beats/min). There were no significant differences between digoxin and beta-methyldigoxin in their effects on the ECG (R-R intervals, T-wave, Q-T duration). The plasma concentrations of the two glycosides were determined by radioimmunoassay and by 86Rb-uptake inhibition assay. Comparable plasma concentration values (1.0 ng/ml for digoxin, 1.1 ng/ml for beta-methyldigoxin, mean values) were obtained by radioimmunoassay, but the 86Rb-technique gave significantly higher values (mean 1.5 ng/ml) for beta-methyldigoxin. It is concluded that beta-methyldigoxin is equal to digoxin for producing slowing of the heart rate in patients with atrial fibrillation.

Aged↗
PubMed1987

Prescribing digoxin in geriatric units--exercise and redistribution of drug.

In subjects capable of normal everyday activity, exercise has been shown to lower the serum digoxin concentration by increasing uptake into skeletal muscle. A randomized cross-over study of the effect on the serum digoxin concentration of treatments consisting of rest for, or exercise during, 30 min was carried out in 20 elderly patients undergoing rehabilitation. In one patient exercise was associated with a marked (40%) reduction in the serum digoxin concentration. In the remainder there was a very small, but statistically significant, fall in concentration in the exercise as compared with the rest period. Unexpectedly low serum digoxin concentrations in in-patients of geriatric units, may occasionally be an artefact due to temporary redistribution of digoxin.

Aged↗
PubMed1981

Digoxin-quinidine interaction in the dog.

In seven healthy dogs, digoxin was given as an oral loading dose (0.05 mg/kg/day) on the first day, followed by an oral maintenance dose (0.02 mg/kg/day) during the next 14 days. On the sixth day of digoxin treatment, oral quinidine (200 mg b.i.d.) was added until the tenth day. Plasma concentrations of digoxin and quinidine were measured; in three of the seven dogs ECG and physical signs of digitalis toxicity were evaluated. The average steady state plasma concentration of digoxin increased significantly (P less than 0.01) during quinidine administration (from 1.4 to 2.3 ng/ml). On the days that digoxin was administered without quinidine, none of the dogs vomited nor was anorectic; the PQ-interval increased significantly (P less than 0.01) between 0.01 and 0.03 s. When quinidine was added, vomiting and anorexia occurred but no further increases in the PQ-interval were seen.

Animals↗
PubMedDate not supplied

Digitalis 'receptors' during chronic digoxin treatment.

The effect of digoxin treatment on Mg-dependent [Na+-K+]-ATPase (the receptor for cardiac glycosides) was assessed by comparison of intracellular Na+-K+, 86Rb uptake and number of digoxin binding sites in the erythrocytes of 138 patients on long term digoxin and of 133 control subjects. The parameters were also assessed in thirty-two patients followed longitudinally for 1 y. The results indicate that the cells adapt to chronic exposure to 'therapeutic' dosage of digoxin with an overcompensatory synthesis of new receptors, a possible mechanism through which the normal intraerythrocytic ionic equilibrium is re-established. The process of synthesis of new receptors appears to be completed in erythrocytes in a period of 4 months after the start of digoxin treatment.

Adolescent↗
PubMed1976

Placental transfer and fetal uptake of 3H-digoxin in humans.

Placental transmission and fetal distribution of 3H-digoxin were studied in seven pregnant women undergoing legal termination of pregnancy during the first half of gestation. The radioactivity in fetal and maternal plasma and in fetal tissues was estimated using the oxidation method, and the integrity of the labelled drug by thin layer chromatography. The 3H-digoxin activity was clearly demonstrated in the umbilical cord blood five minutes after injection of the drug into the maternal blood, and the fetal plasma concentrations of 3H-digoxin approximated to the maternal value 30 minutes after drug administration. The distribution of 3H-digoxin in the fetal tissues was relatively even, with the highest 3H concentrations found in the heart and placenta, the lowest in the brain. The results suggest that the capacity of human fetal heart to bind digoxin during the first half of gestation is limited.

Digoxin↗
PubMed1999

Ketanserin inhibits digoxin-induced arrhythmias in the anaesthetized guinea-pig.

Digoxin inhibits the membrane-bound ATPase enzyme, resulting in a rise in intracellular sodium and activated outward potassium current, predisposing to arrhythmias. In this study, the effect of ketanserin, thought to block outward potassium currents, was investigated on digoxin-induced arrhythmias. Twenty-four guinea-pigs were studied in four groups (control, ketanserin 0.5 mg/kg, ketanserin 1 mg kg, ketanserin 2 mg/kg). Under pentobarbital anaesthesia (40 mg/kg), 15 min after injection of saline or ketanserin, digoxin (0.6 mg/kg) was administered through the jugular vein. Carotid artery blood pressure and electrocardiogram (ECG) were recorded. The time for the onset of the first arrhythmia and incidence of ventricular tachycardia (VT), ventricular fibrillation (VF), and premature ventricular contraction (PVC) were determined. Arrhythmias were scored according to the MacLeod scale. Ketanserin produced minor haemodynamic effects and lacked, by itself, arrhythmogenic effects at the doses studied. However, it increased the time for the onset of the first digoxin-induced arrhythmia and decreased the incidence of VT, VF and PVC. We conclude that ketanserin inhibits digoxin-induced arrhythmias in guinea-pigs.

Animals↗
PubMed1986

Beta-blockade and binding of digoxin to skeletal muscle.

The effect of beta-blockade and a 1-h bicycle exercise test on the digoxin concentration in skeletal muscle (thigh) and serum was studied in 10 healthy men, who had ingested 0.5 mg digoxin daily for 2 weeks. Each subject performed two exercise tests at 100-140 W during maintenance digoxin treatment and 24 h after the latest dose. They rested in the supine position for 2.5 h before the exercise. Sixty minutes before the start of the exercise 0.25 mg/kg b.w. propranolol or saline (control) were injected (single-blind). At the end of the exercise the mean heart rate was 30% lower with beta-blockade (P less than 0.001). During exercise the mean skeletal muscle digoxin concentration increased by 29% (P less than 0.01) in the control situation and by 12% (NS) with beta-blockade. The results indicate that propranolol partly inhibits the exercise-induced increase in skeletal muscle digoxin binding. This might be due to inhibition of a catecholamine-induced stimulation of Na+-K+ATPase during exercise.

Adult↗
PubMed1987

Interactions of amiodarone with digoxin in rats.

1. The influence of oral amiodarone treatment on the blood and tissue concentrations of digoxin was investigated in the anaesthetized rat by use of unlabelled and [3H]-digoxin. 2. Amiodarone diminished the total body clearance and the apparent volume of digoxin distribution by 60%. This reduction was due to a 50% reduction of the hepatobiliary clearance, whereas the renal clearance did not change. 3. Amiodarone treatment increased blood, myocardial and skeletal muscle [3H]-digoxin concentrations by 200% indicating passive equilibration between blood and these tissues, and resulting in unaltered tissue to blood ratios. In contrast, the liver concentration increased by 70% only and the liver to blood ratio therefore decreased under amiodarone treatment. 4. It is concluded that the hepatobiliary elimination of digoxin is decreased in amiodarone-treated rats compared to controls and is responsible for the increased levels of blood and tissue glycoside.

Amiodarone↗
PubMed1979

Digoxin removal from a patient with renal failure by hemoperfusion with Amberlite XAD-4 resin.

A digitoxic patient with severe renal failure underwent two hemoperfusion treatments with Amberlite XAD-4 resin. Digoxin clearances calculated from plasma flow rates and plasma digoxin concentrations, as well as from the amount of digoxin eluted from the used columns, were superior to those previously described for peritoneal dialysis, hemodialysis and charcoal hemoperfusion. There was a temporary improvement in the patient's life-threatening digitoxic cardiac rhythm with the first hemoperfusion, and a permanent improvement after the second hemoperfusion. It is submitted that hemoperfusion with this resin may significantly lessen manifestations of digoxin poisoning and may hasten digoxin elimination in digitoxic patients with renal failure.

Aged↗