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PubMed1977

Serum glycoside concentrations after single or repeated intravenous doses of beta-methyl-digoxin and digoxin.

The aim of the present investigation was to estimate the ratio of the intravenous doses of beta-methyl-digoxin and digoxin required to produce identical serum glycoside concentrations in man. 20 patients on intravenous maintenance therapy were changed from beta-methyl-digoxin to the identical dose of digoxin or vice versa. Each drug was given for 7 days. Serum concentrations 13% higher were found during administraton of beta-methyl-digoxin. Assuming a half life of 60 h after withdrawal, the dose of digoxin producing the same minimum serum concentration was estimated to be 1.16 times higher than that of beta-methyl-digoxin. 18 healthy volunteers received 0.4 mg beta-methyl- digoxin, and 23 the same dose of digoxin, as an intravenous infusion over 2 h. The serum concentrations and urinary glycoside excretion were measured over a period of 32 hrs. During the first hour after the infusion the serum concentration of digoxin declined more rapidly than that of beeta-methyl-digoxin. Thereafter, the ratio of the serum concentrtions did not change appreciably up to the end of the investigation. The area under the serum concentration/time curve was about 13% greater for beta-methyl-digoxin than for digoxin; this difference was not significant. The average renal clearance was 96 +- 9 ml for beta-methyl-digoxin, 151 +- 13 ml for digoxin. Since the total body clearance of digoxin is only about 1.16 times higher than that of beta-methyl-digoxin, the lower renal clearance of beta-methyl-digoxin must partly be compensated by higher extrarenal clearance. From the ratios of the areas under the serum concentration/time curves after single doses of beta-methyl-digoxin and digoxin, and the minimum serum concentrations during maintenance therapy, it was concluded that the dose of digoxin to produce the same average serum concentrations would be about 1.15 times higher than that of beta-methyl-dogoxin. In comparison wtih the large variations in individual dosage of digoxin and beta-methyl-digoxin, this difference is too small to be of practical importance.

Aged↗

PubMed1987

Increase in serum digoxin concentration produced by quinidine does not increase the potential for digoxin-induced ventricular arrhythmias in dogs.

Chronic treatment of dogs with digoxin alone, quinidine alone and digoxin in combination with quinidine was initiated in dogs to assess changes in arrhythmogenic potential associated with the quinidine-induced increase in serum digoxin concentration observed during combined digoxin and quinidine treatment. The arrhythmogenic potential of digoxin was evaluated through the use of the acetylstrophanthidin (AcS) tolerance test. AcS was infused at a rate of 5 micrograms/kg/min until ventricular arrhythmias occurred during a drug-free period and during chronic treatment with digoxin, quinidine and digoxin plus quinidine. The dose of AcS required to initiate ventricular arrhythmias is inversely related to the arrhythmogenic potential of digoxin present at the time of AcS infusion. Administration of quinidine alone in two different dosage regimens produced serum quinidine concentrations of 5.99 +/- 1.18 and 2.99 +/- 0.43 micrograms/ml and significantly increased AcS tolerance, whereas digoxin alone, over a wide range of serum digoxin concentrations, significantly decreased AcS tolerance. This decrease in AcS tolerance was linearly related to the serum digoxin concentration. The addition of quinidine treatment to animals receiving digoxin resulted in a significant elevation in the steady-state serum digoxin concentration. However, the AcS tolerance determined during the elevated serum digoxin concentration induced by quinidine was greater than that determined during treatment with the same dose of digoxin alone. Thus, quinidine administration to animals receiving digoxin resulted in a significant increase in the steady-state serum digoxin concentration but did not increase the arrhythmogenic potential of digoxin over that observed during treatment with the same dose of digoxin alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Influence of digoxin immune Fab therapy and renal dysfunction on the disposition of total and free digoxin.

OBJECTIVE: To characterize the disposition of total and free serum digoxin following the administration of digoxin Fab antibody in patients with varying degrees of renal function. DESIGN: Observational study of pharmacokinetics and pharmacodynamics. SETTING: Critical care and telemetry units of two university-affiliated teaching institutions, Hartford Hospital and Henry Ford Hospital. PATIENTS: Fourteen digoxin-intoxicated patients (baseline total digoxin > 3.2 nmol/mL) with mean (+/- SD) serum creatinine of 380.1 +/- 212.2 mumol/L who received digoxin Fab antibody therapy. MEASUREMENTS: Serum was drawn every 12 to 24 hours for 80 to 327 hours after Fab administration. Total and free digoxin were assayed in serum by fluorescence polarization immunoassay or modified immunofluorometric assay. RESULTS: Before Fab was administered, total digoxin ranged from 3.5 to 10.5 nmol/mL. After treatment with Fab, total digoxin increased rapidly to a mean (+/- SD) maximum of 51.8 +/- 22.7 nmol/mL and decreased to 7.2 +/- 4.7 nmol/mL at the last measurement. Total digoxin was eliminated in a two-phase fashion. The half-life of the initial phase of total digoxin decline was 11.6 +/- 4.1 hours, and the half-life of the second or terminal elimination phase was 118 +/- 57 hours. Free digoxin levels decreased rapidly following Fab therapy, to a mean nadir of 0.6 +/- 1.1 nmol/mL, but rebounded to a mean maximum free digoxin concentration of 1.7 +/- 1.3 nmol/mL in 77 +/- 46 hours. The time to maximum free digoxin rebound occurred later in patients with end-stage renal disease (n = 4) compared with other patients (127 +/- 40 hours compared with 55 +/- 28 hours). CONCLUSION: Elimination of digoxin following Fab therapy is prolonged in digoxin-toxic patients with renal dysfunction. In addition, rebound of free digoxin is delayed in anephric patients. Monitoring free digoxin following the administration of Fab may be of value in selected patients to guide additional Fab dosing, confirm possible rebound toxicity, or guide the reinitiation of digoxin therapy.

Adult↗

PubMed2005

New enzyme-linked immunosorbent digoxin assay on the ADVIA IMS 800i system is virtually free from interference of endogenous digoxin-like immunoreactive factors.

Endogenous digoxin-like immunoreactive factors (DLIF) may crossreact with antidigoxin antibody and falsely elevate immunoassay results. Recently, a new enzyme-linked immunosorbent chemiluminescent assay for digoxin has been available for use on the ADVIA IMS (Integrated Modular System) 800i analyzer (Bayer Diagnostics). We studied potential interference of DLIF with this new digoxin assay. We analyzed 30 serum specimens from patients who have pathologic conditions that may increase serum DLIF concentrations. These patients were never exposed to digoxin or other agents that may lead to a measurable digoxin concentration. We also analyzed 10 specimens from neonates, 10 cord blood specimens, and 10 amniotic fluid specimens. Apparent digoxin concentrations were measured using the new enzyme-linked immunosorbent digoxin assay (IMS-Digoxin), a fluorescence polarization immunoassay (FPIA), and also a chemiluminescent immunoassay (CLIA, run on ACS:180(R) system from Bayer Diagnostics). We observed measurable apparent digoxin levels with the FPIA in 4 uremic patients (range 0.21-0.36 ng/mL, digoxin equivalent), 7 patients with liver disease (range 0.21-0.72 ng/mL), and 3 patients in the third trimester of pregnancy (0.22-0.66 ng/mL). We also observed measurable DLIF concentrations with the FPIA in 2 neonates (0.22 and 0.36 ng/mL), 5 cord blood specimens (range 0.21-1.18 ng/mL), and 5 amniotic fluid specimens (0.21-0.50 ng/mL). None of these DLIF-positive specimens showed any measurable digoxin concentration using the IMS-Digoxin or the CLIA assay. When serum specimens containing elevated concentrations of DLIF but no digoxin (as measured by FPIA) were supplemented with known concentrations of digoxin, we observed falsely elevated digoxin concentrations, as expected, only by the FPIA. In contrast, we observed a good agreement between the target and observed concentrations when the new IMS-Digoxin or the CLIA assay was used. We conclude that the IMS-Digoxin assay is free from interference of DLIF.

Adult↗

PubMed1998

Unexpected suppression of total digoxin concentrations by cross-reactants in the microparticle enzyme immunoassay: elimination of interference by monitoring free digoxin concentration.

The microparticle enzyme immunoassay (MEIA for digoxin (Abbott Laboratories, Abbott Park, Ill) requires no sample pretreatment and is widely used in clinical toxicology laboratories for monitoring serum digoxin concentrations. One advantage of the new MEIA is the lower cross-reactivities with such cross-reactants as digitoxin, oleandrin, and bufalin compared with the fluorescence polarization immunoassay (FPIA)for digoxin. Digitoxin, oleandrin, and bufalin showed positive cross-reactivity with MEIA and FPIAs for digoxin in the absence of the primary analyte, digoxin. A surprising finding was that digoxin concentrations were falsely decreased by these cross-reactants when serum pools containing digoxin were supplemented with various concentrations of these cross-reactants and when digoxin concentrations were measured by the MEIA. In contrast, digoxin concentrations were falsely elevated when measured by the FPIA. For example, when a serum pool containing 2.15 nmol/L of digoxin was supplemented with 129.5 nmol/L of bufalin, the apparent digoxin concentrations were 1.45 nmol/L with the MEIA and 3.00 nmol/L with the FPIA. Taking the advantage of only 25% protein binding of digoxin and more than 95% protein binding of digitoxin and bufalin, we demonstrated that monitoring free digoxin instead of total digoxin eliminated negative interference of digoxin by these cross-reactants in the MEIA and positive interference in the FPIA. Although oleandrin is also strongly bound to serum protein, high concentrations of oleandrin still modestly affect the free digoxin assay for both MEIA and FPIAs.

Bufanolides↗

PubMed1973

Effects of digoxin-specific antibodies on accumulation and binding of digoxin by human erythrocytes.

THE PRESENT STUDIES INDICATE THAT ACCUMULATION OF DIGOXIN BY INTACT HUMAN ERYTHROCYTES IS THE RESULT OF TWO PROCESSES: binding of digoxin to the erythrocyte membrane and uptake of digoxin across the membrane into the cell. In contrast, accumulation of ouabain by human erythrocytes is entirely attributable to binding of this glycoside to the plasma membrane. Digoxin binding to the erythrocyte membrane involves a single class of binding sites, is a saturable function of the extracellular digoxin concentration, reversible, temperature-sensitive, dependent on the cation composition of the incubation medium, inhibited by other cardioactive steroids, and correlates with the inhibition of erythrocyte potassium influx. Digoxin uptake across the membrane into the cell is also temperature-sensitive and reversible but is a linear function of the extracellular digoxin concentration, not altered by changes in the cation composition of the incubation medium, not inhibited by other cardioactive steroids, and does not correlate with inhibition of erythrocyte potassium influx. Digoxinspecific antibodies can both prevent and reverse effects of digoxin on potassium influx in human erythrocytes by virtue of the capacity of the antibodies to decrease the amount of digoxin that is bound to the erythrocyte membrane. These antibodies also reduce uptake of digoxin across the plasma membrane into the erythrocyte; however, this portion of cellular digoxin is not responsible for the observed inhibition of potassium influx. In the presence of digoxin-specific antibodies, the changes in digoxin binding to the erythrocyte membrane and in digoxin uptake across the membrane into the cell reflect the ability of the antibodies to form complexes with "free" digoxin molecules in the incubation medium and thereby decrease the effective concentration of digoxin.

Adult↗

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↗

PubMed2003

Effect of the traditional Chinese medicines Chan Su, Lu-Shen-Wan, Dan Shen, and Asian ginseng on serum digoxin measurement by Tina-quant (Roche) and Synchron LX system (Beckman) digoxin immunoassays.

Chan Su, Lu-Shen-Wan, Dan Shen, and Asian ginseng are traditionally used to treat a number of conditions, including cardiovascular disease. All of these traditional Chinese medicines exhibit cardioactive properties. Digoxin is a cardioactive drug with a narrow therapeutic range (0.8-1.9 ng/mL). A patient taking digoxin may also take these Chinese medicines for their cardiotonic effects. Moreover, the active components of these medicines that are responsible for cardiotonic effects bear structural similarities to digoxin. Therefore, we studied the potential interference of these Chinese medicines with two digoxin immunoassays--the Tina-quant (Roche Diagnostics) and the Beckman (Synchron LX system)--and compared the values with the fluorescence polarization immunoassay (FPIA; Abbott Laboratories). When very small amounts (2-5 microL) of aqueous extract of Chan Su or Lu-Shen-Wan were added to drug-free serum, we observed high digoxin-like immunoreactivity with the FPIA. In contrast, when ethyl acetate extract of Dan Shen or microliter amounts of ginseng extract were added to drug-free serum, we observed modest digoxin-like immunoreactivity with the FPIA, but no apparent digoxin activity with the Roche and Beckman digoxin immunoassays. When aliquots of a digoxin pool prepared from patients receiving digoxin were supplemented with these Chinese medicines, we observed the most significant interference with the FPIA. The presence of endogenous digoxin-like immunoreactive substances can have additive effects with these Chinese medicines and falsely increase apparent digoxin levels by the FPIA. On the other hand, the Roche and Beckman assays were free from interference from DLIS but showed significant interference from Chan Su and Lu-Shen-Wan. We conclude that the FPIA showed the most significant interference from all four of the Chinese medicines we studied. However, the Roche and Beckman assays showed no interference from two (Dan Shen and Asian ginseng) of the four Chinese medicines we studied.

Bufanolides↗

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↗

PubMed2001

Removal of digoxin by column for specific adsorption of beta(2)-microglobulin: a potential use for digoxin intoxication.

BACKGROUND: A beta(2)-microglobulin adsorption column used for the treatment of dialysis-related amyloidosis removes serum beta(2)-microglobulin by recognition of lipophilic residue in the protein. No data are available for the adsorption of the highly lipophilic drug digoxin. METHODS: In vivo clearance of digoxin with the beta(2)-microglobulin column was measured by a single use of the column in 8 patients receiving hemodialysis with a therapeutic level of digoxin. In vitro adsorption was evaluated by use of incubation with adsorbent of the column and digoxin or ranitidine, a hydrophilic drug. Clearance with the beta(2)-microglobulin column was further compared with that obtained by use of activated charcoal in the dogs intoxicated with digoxin. RESULTS: Digoxin concentration was reduced from 1.11 +/- 0.25 ng/mL to 0.57 +/- 0.15 ng/mL at 240 minutes after initiation of hemoperfusion with the column in the patients. Digoxin clearance with the beta(2)-microglobulin column was about 145 +/- 20 mL/min, with a blood flow rate of 160 to 220 mL/min (80% of plasma flow rate). Eighty-five percent of digoxin was adsorbed in vitro, and the capacity of the beta(2)-microglobulin column was not saturated until a toxic level was reached (50 ng/mL). This value was higher than that obtained with use of charcoal. In dogs with digoxin intoxication, digoxin clearance was 38.9 +/- 1.5 mL/min, with a blood flow rate of 50 mL/min (95% of plasma flow rate), which was almost twice as that achieved with charcoal. The degree of thrombocytopenia and leukopenia was small with use of the beta(2)-microglobulin column. CONCLUSION: These data suggested that the beta(2)-microglobulin column selectively adsorbs digoxin. This column is a promising tool for the treatment of digoxin intoxication, especially in patients undergoing hemodialysis.

Adsorption↗

PubMed2005

Effect of Brazilian, Indian, Siberian, Asian, and North American ginseng on serum digoxin measurement by immunoassays and binding of digoxin-like immunoreactive components of ginseng with Fab fragment of antidigoxin antibody (Digibind).

We compared Brazilian, Indian, Siberian, Asian, and North American ginseng for potential interference with 3 digoxin immunoassays: fluorescence polarization (FPIA), microparticle enzyme (MEIA), and Tina-quant (Roche Diagnostics, Indianapolis, IN). We supplemented aliquots of a drug-free serum pool with ginseng extracts representing expected in vivo concentrations and overdose. We observed apparent digoxin-like immunoreactivity with FPIA, modest immunoreactivity with MEIA, and no apparent digoxin immunoreactivity with the Tina-quant with all ginsengs except Brazilian, which showed no immunoreactivity with any assay. When aliquots of serum pools prepared from patients receiving digoxin were supplemented with ginsengs, we observed falsely elevated digoxin values with FPIA, falsely lower digoxin values (negative interference) with MEIA, and no interference with the Tina-quant. Digoxin-like immunoreactive components of various ginsengs have moderate protein binding; monitoring free digoxin concentrations does not eliminate such interference. We also observed that Digibind (Burroughs Wellcome, Research Triangle Park, NC) can bind free digoxin-like immunoreactive components of ginsengs; such effects can be monitored by measuring apparent free digoxin concentrations. Indian, Asian, and North American ginsengs interfere with serum digoxin measurement by FPIA and MEIA; the Tina-quant is free of such interference. Digibind can bind free digoxin-like immunoreactive components of ginseng.

Amaranthaceae↗