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PubMed1980

Clinical studies on digoxin intoxication II. Relationship between plasma and erythrocyte digoxin concentrations.

We measured the digoxin concentration in both plasma and erythrocytes in 75 patients by radioimmunoassay during digoxin maintenance therapy. Mean plasma digoxin concentration was 0.90 ng/ml and mean erythrocyte digoxin concentration was 1.44 ng/ml in 75 patients. The ratio of digoxin concentration of erythrocyte to plasma during maintenance therapy was 2.24 in all patients, 1.63 in patients with therapeutic plasma digoxin levels, and 3.52 in patients with subtherapeutic plasma levels. There was a significant correlation between erythrocyte and plasma digoxin concentrations in therapeutic plasma levels (r=0.53, p<0.001). Patients on maintenance digoxin therapy were classified into 6 groups according to plasma and erythrocyte digoxin concentrations; in group I, 7 patients with both low plasma and erythrocyte digoxin concentrations, were poorly controlled in respect to heart failure; in group II, 19 patients with low plasma and medium erythrocyte digoxin concentrations failed to show compliance; in group III also, 3 patients with therapeutic plasma and low erythrocyte digoxin levels showed poor compliance; in group IV, 41 patients with both medium plasma and erythrocyte digoxin levels, were well controlled in respect to heart failure and all were compliant. Careful observation was required to avoid digoxin intoxication in group V with therapeutic plasma and high erythrocyte digoxin concentrations, and in group VI with high plasma and high erythrocyte digoxin concentrations.

Digoxin↗
PubMed1999

Time- and dose-dependent digoxin redistribution by digoxin-specific antigen binding fragments in a rat model.

To study the influence of the interval between digoxin intake and digoxin-specific antigen binding fragment (DSFab) administration, we developed a rat kinetic model. 3H-digoxin (0.77 nmol/kg) was injected by intravenous route and DSFab was injected at different times (12, 30 or 60 min) corresponding to different levels of 3H-digoxin distribution (50, 83 and 100%). The effect of increasing the molar DSFab/3H-digoxin ratio from 1 to 5 was also investigated. To evaluate DSFab effect on the 3H-digoxin pharmacokinetics, we also investigated the pharmacokinetics of the 125I-DSFab and DSFab-3H-digoxin complex. 3H-digoxin and DSFab-3H-digoxin complex pharmacokinetics showed that DSFab altered immunoreactive 3H-digoxin pharmacokinetics. In redistribution studies performed 12, 30 or 60 min after 3H-digoxin injection, DSFab bound immunoreactive 3H-digoxin including native 3H-digoxin and active metabolites of 3H-digoxin. This binding induced a redistribution process of immunoreactive 3H-digoxin in the DSFab distribution compartment and was evaluated by the redistribution fraction (F(R)). F(R) was 23% lower at 60 min than at 12 and 30 min, and by increasing the DSFab/3H-digoxin ratio from 1 to 5, F(R) increased by 60%. In conclusion, the longer the time interval between digoxin intake and DSFab administration, the lower the efficacy of the redistribution process. This effect could be reduced by increasing the DSFab dose.

Animals↗
PubMed1997

Effects of digoxinlike immunoreactive substances and digoxin FAB antibodies on the new digoxin microparticle enzyme immunoassay.

Digoxin-like immunoreactive substance (DLIS) is known to interfere with fluorescence polarization immunoassay (FPIA) (Digoxin II, Abbott Laboratories) and falsely elevates the total digoxin concentrations. Digoxin FAB antibody (Digibind) is also known to affect digoxin results by FPIA assay. The authors studied the effects of DLIS and Digibind on a new microparticle enzyme immunoassay (MEIA) for digoxin recently introduced by Abbott Laboratories, compared with the standard FPIA method and chemiluminescence assay (ACS-digoxin, Ciba-Corning). They studied 30 volume-expanded patients (term pregnancy, liver and renal disease) for the presence of DLIS. None of these patients received digoxin. They observed measurable DLIS concentrations in 12 of 30 patients by the FPIA assay and in only 1 patient by both MEIA and ACS assays. The concentration of DLIS in that patient was 0.31 ng/ml of digoxin equivalent by the MEIA assay, 0.36 ng/ml by the ACS assay, and 1.15 ng/ml by the FPIA assay. When they supplemented serum containing digoxin with low to high concentrations of digibind (0.5, 1.0, 2.0 and 4.0, 10, and 20 micrograms/ml), and measured digoxin concentrations by FPIA, MEIA, and ACS assays, they observed lower than expected values of total digoxin. However, when they supplemented serum containing no digoxin with high concentration of digibind (5.0, 10.0 and 20.0 micrograms/ml) and supplemented protein-free ultrafiltrates with digoxin, they observed expected digoxin concentrations in the ultrafiltrates by all three assays, indicating that the ultrafiltrates are essentially free of digibind.

Antibodies↗
PubMed1995

Problems in determining levels of free digoxin in patients treated with digoxin immune FAb.

Determination of free digoxin levels in patients treated with digoxin immune FAb has long been a problematic area in clinical laboratory testing. The older radioimmunoassays resulted in inaccurate and variable results due to the competition of the administered drug with the radioactively labelled forms. The 1995 Physicians' Desk Reference continues to state that digoxin immune FAb will interfere with digitalis immunoassay measurements. This statement, however, is based primarily on the RIA methods. We evaluated the Stratus digoxin assay and the TDX digoxin II assay. Increasing amounts of immune FAb were added in a stepwise fashion to 12 patient samples containing high normal to elevated digoxin levels. Results showed a progressive decrease in digoxin levels when assayed with the Stratus kit. However, five patient samples tested with the TDX kit resulted in constant digoxin values despite the presence of increasing digibind levels. These results suggest that the Stratus method measures free digoxin, whereas the TDX method measures the total digoxin. Measurement of digoxin by the Stratus method is simple and quick. The Stratus digoxin assay may be an accurate and objective way of measuring free digoxin levels in patients on digoxin immune FAb.

Digoxin↗
PubMed1976

Tissue digoxin concentrations at digoxin intoxication in normal, acutely hypokalemic, and acutely hyperglycemic dogs.

Thirty intact dogs were studied to determine digoxin concentration in various tissues after ventricular tachycardia had been induced by digoxin infusion. A control group was infused solely with digoxin. A second group was made acutely hypokalemic by glucose-insulin infusion before the digoxin infusion. A third group was infused with glucose and digoxin to determine the effect of increased blood glucose levels and osmalarity on the induction of ventricular tachycardia. Results were: (1) The amount of digoxin infused to produce ventricular tachycardia did not differ getween the normal and hypokalemic groups. (2) The concentration of digoxin in various parts of the heart, other muscle tissue, renal cortex, and liver did not differ between the normal and acutely hypokalemic dogs although the amount excreted in bile and urine was reduced in hypokalemia. (3) Acute hypokalemia did not sensitize the myocardium to the arrhythmogenic effects of digoxin. (4) Ventricular tachcardia occurred at a similar plasma digoxin level in normal and acutely hypokalemic dogs. (5) In dogs with a lowered plasma potassium level, junctional tachycardia occurred whereas it did not occur in normal dogs or those with only a high blood glucose level. (6) Ventricular tachycardia occurred in the hyperglycemic dogs at a plasma digoxin level of 170 ng/ml, which was significantly greater than in the other experiments (7) Acute hyperglycemia reduced the mean rate of myocaridal uptake of digoxin into atria and right and left ventricular tissue; and the concentration of digoxin in atria, left ventricle, and interventricular septum was lower at the time of ventricular tachycardia than occurred in normal dogs. (8) Lowering the plasma potassium level in the presence of acute hyperglycemia, which occurred with the glucose-insulin infusion, did increase the myocardial uptake of digoxin. Similar effects of hyperglycemia were noted on mean hepatic uptake and excretion of digoxin and also the renal uptake of the glycoside.

Animals↗
PubMed1981

Pharmacokinetics of digoxin in patients subjected to the quinidine-digoxin interaction.

1 This study was designed to evaluate pharmacokinetically the digoxin-quinidine interaction in patients with atrial fibrillation. 2 Five patients on maintenance digoxin therapy were given [3H]-digoxin as a single i.v. dose before and during quinidine therapy and the elimination of [3H]-digoxin from plasma and excretion in urine were determined. 3 The mean steady state plasma concentration of digoxin increased from 0.7 to 1.3 nmol/l after quinidine administration. 4 The apparent volume of distribution of digoxin decreased on the average 38%. Renal clearance and the total body clearance of digoxin decreased 51 and 56% respectively (mean values). Also non renal clearance was reduced. The fraction of digoxin excreted unmetabolised in urine did not change during quinidine treatment. The mean elimination half life of digoxin increased from 49 to 72 h during quinidine. 5 In two patients the DC-shock did not cause a conversion to sinus rhythm. However, the quinidine induced changes in the pharmacokinetics of digoxin in these patients did not differ from the others. 6 Quinidine appears to decrease the amount of digoxin distributed to body tissue(s). In addition, the reduction of renal clearance of digoxin and the observed unchanged clearance of creatinine suggests an inhibition of the renal secretion of digoxin.

Adult↗
PubMed1970

Digoxin intoxication: the relationship of clinical presentation to serum digoxin concentration.

A radioimmunoassay for serum digoxin concentration has been used to study the interrelationships of circulating levels of the drug and various factors in the clinical setting in 48 hospitalized patients with cardiac rhythm disturbances due to digoxin intoxication. 131 patients on maintenance doses of digoxin without toxicity and 48 patients with equivocal evidence of digoxin excess were also studied and compared with the toxic group. Patients with cardiac rhythm disturbances due to digoxin intoxication tended to be older and to have diminished renal function compared with the nontoxic group; body weight, serum potassium concentration, underlying cardiac rhythm, and nature of cardiac disease were not significantly different for the groups as a whole. Despite comparable mean daily digoxin dosages, digoxin intoxicated patients had a mean serum digoxin concentration of 3.7 +/-1.0 (SD) ng/ml, while nontoxic patients had a mean level of 1.4 +/-0.7 ng/ml (P < 0.001), 90% of patients without evidence of toxicity had serum digoxin concentrations of 2.0 ng/ml or less, while 87% of the toxic group had levels above 2.0; the range of overlap between the two groups extended from 1.6 to 3.0 ng/ml. Patients with atrioventricular block as their principal toxic manifestation had a significantly lower mean serum digoxin concentration than those in whom ectopic impulse formation was the chief rhythm disturbance. Patients with equivocal evidence of digoxin excess had received comparable daily maintenance doses of digoxin but had a mean serum concentration of 1.9 +/-0.8 ng/ml, intermediate between those of the nontoxic (P < 0.005) and toxic (P < 0.001) groups. Renal function as judged by mean blood urea nitrogen concentration was also intermediate. The data indicate that knowledge of the serum digoxin concentration, weighed in the clinical context, is useful in the management of patients receiving this drug.

Age Factors↗
PubMed1976

A comparison of the bioavailability of digoxin in capsule, tablet, and solution taken orally with intravenous digoxin.

Six healthy volunteers were given five single-dose treatments of 0.40 mg digoxin either intravenously, in liquid form, in conventional tablet form (dissolution rate 76 per cent in 1-hour), or in new capsule preparations containing 0.05, 0.10, or 0.20 mg digoxin per capsule. Serum levels, area under the concentration-time curve, and daily urinary digoxin excretion were measured for six days. Higher serum digoxin levels were seen after ingestion of the capsules than after the tablets, with peak levels for the former being 2.2-2.8 times higher than after tablet digoxin. Bioavailability was assessed further by comparing the area under a six-hour concentration-time curve, and again the capsules gave a consistently higher value than the tablets. In addition, the absorption of 0.40 mg digoxin from any of the capsule preparations was much greater than 0.50 mg digoxin in commercially available tablets. The six-day cumulative urinary digoxin excretion was also greater for the capsules than for the 0.20-mg tablets. In comparison with intravenous digoxin, tablets provide 75 per cent maximum bioavailability, whereas the capsule preparations of digoxin improve the bioavailability of digoxin and the 0.20-mg digoxin capsule is absorbed better than 0.25-mg digoxin tablet.

Adult↗
PubMed1985

Serum digoxin concentrations in a representative digoxin-consuming adult population.

As part of health examination of a representative sample of an adult population (n = 8000) serum digoxin concentration was measured in 661 patients on continuous digoxin therapy. The prescribed mean daily dose of digoxin was significantly higher in men (223 micrograms) than in women (201 micrograms); the dose significantly decreased with increasing age. The mean serum digoxin concentration was the same in men and women and it differed insignificantly between age groups, although older persons tended to have a higher concentration. The age - adjusted mean steady state digoxin concentration was 1.02 ng/ml in men and 0.98 ng/ml in women; in about 60% the concentration was within the "therapeutic" range (0.80-2.00 ng/ml). The concentrations were clearly related to daily dose of digoxin. At equal dose levels old persons tended to have higher concentrations than younger persons. The interindividual variation in serum digoxin concentrations was very wide. However, when digoxin measurements in the same subjects were repeated about three months later, a good correlation between the two measurements was found. The interval between the last dose of digoxin and the collection of blood (up to 41 h) had relatively little effect on individual serum digoxin concentrations. Patients on concomitant thiazide or loop diuretic therapy had the same mean serum digoxin concentration as those not-receiving a diuretic. The mean concentration was significantly higher in patients taking a thiazide or loop diuretic combined with triamterene. The difference may have been due to an interaction between triamterene and digoxin.

Adult↗
PubMed1997

[Estimating concentrations of serum total digoxin and digoxin-like immunoreactive substances in patients of cardiac failure with renal insufficiency].

Measurement of serum digoxin concentration is recommended as a routine in patients undergoing digoxin therapy because its therapeutic range is narrow. The presence of a high concentration of digoxin-like immunoreactive substances(DLIS) in human serum have been reported in a number of pathophysiological conditions. DLIS which cross-react with anti-digoxin antibodies, can falsely elevate the total digoxin concentration and is troublesome in the therapeutic monitoring of digoxin. The concentrations of serum total digoxin and DLIS in twelve patients of cardiac failure with renal insufficiency were estimated after determination of free digoxin by ultrafiltration with fluorescence polarization immunoassay. In these patients, the free digoxin concentration in serum determined was 0.79 +/- 0.48 (0.46-2.10) nmol.L-1. The total digoxin determined(1.31 +/- 0.80 nmol.L-1) was significantly higher than the calculated total digoxin(1.05 +/- 0.64 nmol.L-1) (P < 0.01), suggesting the presence of elevated DLIS in serum for these patients. The calculated DLIS concentration was 0.27 +/- 0.19(0.07-0.76) nmol.L-1. The results were well consistent with that obtained by recently published method of Dasgupta et al. In conclusion, the approach presented in this paper can estimate the true serum concentrations of digoxin and DLIS in patients of chronic cardiac failure with renal insufficiency.

Cardenolides↗
PubMed1989

Beta-methyl digoxin: a better absorbable digoxin.

Since Megges and Repke [1961] showed that acetylation of the hydroxyl groups in the aglycone or the sugar side chain of the digitalis molecule results in a derivative with enhanced and more complete absorption from the gastrointestinal tract, several new compounds resulting from acetylation or methylation of digoxin molecule have been developed. Beta-methyl digoxin (beta-methyl digoxin) is a methyl derivative (methyl group in position 4 of the digitoxose residue) of digoxin. Enhanced and more complete gastrointestinal absorption of tritium labeled beta-methyl digoxin [Rennekamp et al. 1972] has been confirmed. Weiss et al. [1975], based on the serum levels following oral administration, calculated that to achieve comparable levels, digoxin dose would have to be increased by 1.55 times compared to that of beta-methyl digoxin. These and other studies supported an earlier notion that beta-methyl digoxin was a better and desirable cardiotropic agent than the digoxin. Comparison of cardiac effects using equivalent doses of the two compounds however, showed no difference [Das et al. 1977]. Following oral administration, the serum glycoside levels to beta-methyl digoxin indeed were significantly greater than those with digoxin. However, these differences in serum levels were not of sufficient magnitude to influence detectable cardiac inotropic effects, hence, the search for a better digoxin should continue.

Digoxin↗
PubMed1987

Determination of free digoxin concentrations in serum for monitoring Fab treatment of digoxin overdose.

A rapid method for assessing the free digoxin concentration in the serum of digoxin-overdosed patients receiving treatment with digoxin-specific Fab fragments has been developed. For this method, a protein-free ultrafiltrate is prepared from the patient's serum, and the digoxin in the ultrafiltrate (free digoxin) is measured by fluorescence polarization immunoassay. Both the inaccuracies associated with measurements of total digoxin by immunoassay in the presence of Fab and the long turnaround time associated with measurements of free digoxin by equilibrium dialysis were avoided. Good correlation was observed between measurements of free digoxin by this ultrafiltration technique and by equilibrium dialysis. The ultrafiltration method was used to evaluate the concentrations of free digoxin in a digoxin-overdosed patient treated with Fab at our hospital. In retrospect, the results suggest that her hospital stay could have been shortened by a timely appreciation of her increased concentration of free digoxin. Using the ultrafiltration method, one can determine free digoxin concentrations quickly, conveniently, and accurately in the clinical laboratory. This procedure therefore should be a valuable aid in monitoring the efficacy and adequacy of Fab treatment.

Adolescent↗
PubMed1985

The influence of digoxin antibodies on digoxin disposition and effect: studies in guinea-pigs and HeLa cells.

Pretreatment of guinea-pigs with digoxin-specific Fab (fragment antigen binding) fragments reduced the cardiotoxicity of intravenously infused digoxin (the lethal doses in Fab-treated and control animals were 1.0 and 0.6 mgkg-1, respectively). At death the serum digoxin concentration was elevated 2 fold in the Fab-treated animals, while the tissue concentrations were generally lower. The 30-40% lower cardiac digoxin concentration (seen in whole homogenate and throughout the subcellular fractions examined) was surprising; presumably this reflects a difference from the controls in the proportion of pharmacologically active/inactive digoxin in this organ. Adding digoxin-specific immunoglobulin G or the Fab fragments to HeLa cells before incubation with digoxin, reduced specific digoxin binding (Na pump-bound) slightly more than the non-specific binding. Adding specific antibody after digoxin, however, did not reduce digoxin binding or effect a recovery in Na pump activity. It seems that the protective effect of digoxin-specific antibodies seen in the guinea-pig can to some extent be simulated using HeLa cells. However, this is apparently not so regarding the widely-reported ability of these antibodies to reverse the action of digoxin.

Animals↗
PubMed1984

Characteristics of the digoxin-quinidine and digoxin-verapamil interactions in the rat kidney.

Recently quinidine and verapamil have been reported to cause toxic accumulation of digoxin due to mainly decrease in the renal secretion of the cardiac glycoside. Because these drugs do not alter GFR, it was assumed that the renal tubular secretion of digoxin is inhibited by them. We studied the characteristics of the renal cortical specific binding for digoxin in the rat kidney, and the antagonistic effects of quinidine and verapamil on digoxin uptake by the kidney slices. Specific binding of digoxin was documented in the renal slices with B max of 42.34 pmol/gr and Kd of 7.6 pmol/gr. The addition of quinidine in therapeutic concentrations (6.7 microM) caused a mean 23% reduction of digoxin uptake by the kidney slice (p less than 0.01). When quinidine concentrations were elevated above the therapeutic range there was additional reduction in digoxin uptake; 84 mM quinidine caused a mean 61% reduction (p less than 0.0001). A similar interaction was documented with verapamil; therapeutic concentrations (550 mM) of the drug caused 15% reduction in digoxin uptake. Further increase in verapamil concentration resulted in additional reduction in digoxin uptake; the maximal concentration used (42 microM) caused 60% decrease in uptake (p less than 0.0001). The inhibition of the renal uptake of digoxin caused by quinidine and verapamil in conjunction with the pharmacokinetic studies, which have shown that both drugs decrease the renal clearance of digoxin without changing GFR, support the suggestion that they inhibit the renal tubular secretion of digoxin.

Animals↗
PubMed1981

The use of brain digoxin concentrations to confirm blood digoxin concentrations.

Recent research suggests that the cardiotoxic as well as the neurotoxic effects of digitalis may be mediated by the central nervous system. Therefore brain regions implicated in the genesis of cardiac rhythm disorders were assayed for digoxin. An 125I-labeled radioimmunoassay was used to determine blood and tissue digoxin concentrations. Digoxin was found in the optic tract and optic chiasm in each of four persons who had been taking digoxin regularly. Digoxin is apparently concentrated from blood by the choroid plexus of the fourth ventricle but not by the choroid plexus of the lateral ventricle. However, digoxin was present in the area postrema and nucleus of the vagus only in the two digoxin overdose cases. Digoxin was not detected in any of the other brain regions analyzed. The presence of digoxin in the area postrema (the chemoreceptor trigger zone) and the nucleus of the vagus in the toxic but not in the therapeutic cases suggests a mechanism for the emesis and cardiac arrest brought about by digoxin toxicity in humans. The digoxin content of the medulla, especially the surface of the medulla under the obex, may be useful in confirmation of elevated blood digoxin concentrations.

Aged↗
PubMed1996

Elevated serum digoxin levels in a patient taking digoxin and Siberian ginseng.

A 74-year-old man taking a constant dose of digoxin for many years was found to have an elevated serum digoxin level with no signs of toxic effects. Common causes of elevated serum digoxin were ruled out, and the patient's digoxin level remained high after digoxin therapy was stopped. The patient then revealed that he was taking Siberian ginseng, a popular herbal remedy. The patient stopped taking ginseng, and the serum digoxin level soon returned to an acceptable level. The digoxin therapy was resumed. The patient resumed taking ginseng several months later, and the serum digoxin level again rose. Digoxin therapy was maintained at a constant daily dose, the ginseng was stopped once more, and the serum digoxin levels again returned to within the therapeutic range. It is unclear whether some component of the ginseng was converted to digoxin in vivo, interfered with digoxin elimination or caused a false serum assay result. The author cautions physicians to be alert to the potential for herbal remedies to interact with prescribed medications and to affect biochemical analyses.

Aged↗
PubMed1989

Pharmacokinetics and efficacy of digoxin specific Fab fragments in a child following massive digoxin overdose.

The use of digoxin-specific Fab fragments (d-Fab) to treat life-threatening digitalis intoxication has been widely substantiated in adults. This reports a case of a 2-year-old girl who ingested 90-92, 0.25 mg tablets of digoxin and within four hours, developed vomiting, lethargy, tachycardia and AV block (Mobitz type I and II). These symptoms were associated with total and free serum digoxin concentrations of 17.1 and 12.4 ng/ml, respectively. Following GI decontamination, a total dFab dose of 1280 mg (32 vials) was given with resolution of electrocardiographic abnormalities within 40 minutes and a concomitant reduction in the free serum digoxin concentration to 0.11 ng/ml. Repeated blood sampling over 19 days revealed an apparent elimination half-life (t1/2) of 134.9 and 129.9 hr for total and free digoxin, respectively. The long t1/2 for digoxin corresponded to a low apparent renal clearance of total digoxin which ranged from 0.56 to 0.82 ml/minute over four separate collection intervals. The free serum digoxin concentration never exceeded 3% of the total concentration and the patient did not develop a recurrence of toxic symptoms or any adverse effects (e.g. fever) attributable to dFab. Administration of an equimolar dFab dose to children following acute, massive digoxin intoxication represents safe, effective treatment which produces a prompt, sustained reversal of toxic effects. Digoxin specific Fab fragments should be promptly administered to any infant or child with significant, life-threatening symptoms following acute digoxin intoxication.

Child, Preschool↗
PubMed1981

Skeletal muscle digoxin concentration during digitalization and during withdrawal of digoxin treatment.

Blood samples and skeletal muscle biopsies (m. quadriceps femoris, vastus lateralis) were taken from 15 patients during digitalization or during withdrawal of digoxin treatment for analysis of serum and skeletal muscle digoxin concentrations. A percutaneous needle biopsy technique was used for muscle sampling and digoxin was analysed by radioimmunoassay. During "slow" digitalization with 0.25 mg digoxin daily the skeletal muscle digoxin concentrations after 2 and 4 days were 45% (range 19%--62%; n = 3) and 78% (range 56%--92%; n= 3) respectively, of the steady state concentration (defined as the digoxin concentration after 25--40 days of treatment). After 9 and 11 days of treatment the skeletal muscle digoxin concentrations were 106% (range 84%--133%; n = 5) and 116% (range 72%--164%; n = 3) respectively, of the steady state concentration. A doubling of the digoxin dose gave a proportional increase in skeletal muscle digoxin concentration (three patients). The magnitude of the estimated half-life of skeletal muscle digoxin was the same as previously reportedly in healthy subjects. No significant correlations were found between changes in systolic time intervals and steady state serum or skeletal muscle digoxin concentrations.

Adult↗