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At least 109 records · Page 6Linked to original sources
PubMed1986

Interference of digoxin-like immunoreactive substances with three digoxin immunoassays in patients with various degrees of renal function.

The effect of renal function and digoxin use in adult patients on interference from digoxin-like immunoreactive substances (DLIS) with three digoxin immunoassays was studied. Hospital patients entered into the study were categorized into the following groups according to renal function: group I (serum creatinine less than 1.5 mg/dL), group II (serum creatinine 1.5-2.5 mg/dL), group III (serum creatinine greater than 2.5 mg/dL, not on hemodialysis), and group IV (serum creatinine greater than 2.5 mg/dL, on maintenance hemodialysis). Medical records were reviewed to determine whether or not patients were receiving digoxin. Excess sera for analysis of serum digoxin concentrations (SDCs) was collected from routine laboratory tests. Serum samples were assayed singly by fluorescence polarization immunoassay (FPIA, Digoxin I, Abbott), radioimmunoassay (RIA, Micromedic), and affinity-column-mediated immunoassay (ACMIA, aca, E.I. du Pont). Correlation of SDCs obtained by RIA and ACMIA with FPIA results was determined using linear-regression analysis. A total of 177 patients met the study criteria; 98 were receiving digoxin. In patients on digoxin, SDCs by RIA were significantly higher than those obtained by FPIA in group II and III patients. SDCs obtained by ACMIA correlated well with and were not significantly different from those obtained by FPIA in any of the patient groups. Maximum differences and mean absolute differences in SDCs obtained by RIA were greater than those for ACMIA when compared with FPIA values in all patient groups. Over 40% of patients with renal dysfunction not on digoxin had false-positive SDCs by RIA; the highest of these values was seen in groups II and III.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Measuring endogenous digoxin-like substance and exogenous digoxin in the serum of low-birth-weight infants.

The interference with three serum digoxin assay methods of endogenous digoxin-like substance (EDLS) in the serum of low-birth-weight (LBW) infants was assessed. The serum from 5-mL blood samples obtained from each of 19 LBW infants was divided into four 0.5-mL portions. Each portion was spiked with 10 microL of a distilled water-ethanol solution with or without digoxin to produce final digoxin concentrations of 0 (control), 0.49, 0.98, or 1.96 ng/mL. Each portion in each patient was then analyzed by radioimmunoassay (RIA), fluorescence polarization immunoassay (FPIA), and radial partition immunoassay (RPIA) using the control portions to measure EDLS. Serum digoxin concentrations measured by each assay method were calculated by subtracting the EDLS concentrations in the control portions from the measured digoxin concentrations in the spiked samples. The mean +/- S.D. concentrations of EDLS measured by RIA and FPIA were 0.26 +/- 0.13 ng/mL and 0.33 +/- 0.16 ng/mL, respectively. Of the 19 control samples assayed by RPIA, 18 had EDLS concentrations less than 0.1 ng/mL; one sample reflected an apparent concentration of 0.11 ng/mL. Mean recovered digoxin concentrations by RIA at each spiked digoxin concentration were significantly different from those obtained by FPIA and RPIA. A low but significant correlation was noted between EDLS concentrations in serum samples assayed by RIA and FPIA. The RPIA method appears to be preferred over the RIA and FPIA methods used in this study for serum digoxin analysis in LBW infants because of acceptable accuracy and minimal interference by EDLS.

Blood Proteins↗
PubMed1978

[Digoxin intoxication in newborns correlation with digoxin plasma concentration (author's transl)].

During childhood digitalis glycosides are most frequently used during the newborn period. Within two years, we found evidence of digoxin intoxication in eight newborns. This was suspected when specific electrocardiographic signs developed under digoxin treatment and disappeared either after discontinuation of digoxin alone, or in combination with specific treatment. These eight newborns had plasma digoxin concentrations of 5 ng/ml or more, while the concentrations in unaffected newborns averaged 2.4 ng/ml (premature newborns) and 2.2 ng/ml, (mature newborns). The clinical and pathophysiological features of digoxin intoxication specific to the newborn period are discussed. Despite certain limitations it seems reasonable to check plasma digoxin concentrations during the newborn period, since clinical and electrocardiographic manifestations of a digoxin intoxication are frequently unspecific at this age. A digoxin intoxication is very likely with plasma digoxin concentrations of 5 ng/ml or more, but unlikely with concentrations below 3 ng/ml.

Digoxin↗
PubMed1980

The renal clearance of digoxin is dependent upon the serum digoxin concentration.

The effect of alterations of serum digoxin concentrations on the renal clearance of digoxin (CDIG) was studied in seven dogs. Digoxin, 0.016 microgram/kg/min (low dose) in normal saline was infused at the rate of 1 ml/min. After 60 min of equilibration, five 15-min urine collections were made. The digoxin infusion was then increased to 0.112 microgram/kg/min (high dose) and five additional collections were made after equilibration. Digoxin was measured by 125I radioimmunoassay whose specificity was confirmed by high-pressure liquid chromatography. With low dose digoxin, the serum digoxin concentration was 0.5 +/- 0.2 (S.D.) ng/ml, CDIG 58 +/- 26 ml/min, inulin clearance (CIN) 48 +/- 8 ml/min and CDIG/CIN 1.2 +/- 0.5. With high dose infusion, the serum digoxin concentration rose to 5.2 +/- 1.4 ng/ml, CDIG decreased 43% to 33 +/- 13 ml/min and CDIG/CIN decreased 48% to 0.6 +/- 0.2 (P < .05 for both compared to control, while CIN remained constant. We conclude that CDIG is not as dependent upon glomerular filtration as previously thought. Increases in serum digoxin concentrations can significantly reduce CDIG without altering glomerular filtration rate.

Animals↗
PubMed1997

Multicenter study of Abbott AxSYM Digoxin II assay and comparison with 6 methods for susceptibility to digoxin-like immunoreactive factors.

Performance characteristics of the Abbott nonpretreatment AxSYM Digoxin II assay were evaluated for quantification of digoxin at four independent sites. Correlation of digoxin measurements with the Abbott pretreatment AxSYM, Baxter Stratus II, Abbott TDx/ TDxFLx II, Abbott IMx, Emit 2000, and Beckman Synchron CX digoxin assays showed acceptable agreement, as indicated by: slope values > 0.84, r > 0.90, y-intercepts for all comparisons at or below the assay detection limit, and Sy/x ranging between 7.5% and 15.4% of the average digoxin value. Susceptibility to interference from digoxin-like immunoreactive factors (DLIFs) was examined in 233 samples from renal patients, liver disease patients, cord blood, and third-trimester pregnancies; the AxSYM Digoxin II assay demonstrated the least DLIFs interference. DLIF susceptibility for four of the methods was significantly greater (P < 0.05) than in the AxSYM Digoxin II assay; susceptibilities of the Stratus II and Emit 2000 methods were similar to the AxSYM Digoxin II assay.

Autoanalysis↗
PubMed1992

Digoxin-interactions in man: spironolactone reduces renal but not biliary digoxin clearance.

The possibility of an inhibitory effect of spironolactone on the biliary clearance of digoxin has been investigated in 6 healthy subjects. Plasma clearance and the renal and biliary clearance of digoxin were determined twice at steady state (digoxin 0.5 to 1 mg.d-1 p.o. for 6 days), alone or in combination with spironolactone 200 mg daily, after an intravenous dose of digoxin (0.7 x oral dose) on Day 7. Plasma and urine were collected for 48 h. Biliary clearance of digoxin was determined on Day 8 by a duodenal perfusion technique. During spironolactone treatment plasma digoxin clearance tended to be lower (255 vs 224 ml/min; P = 0.057) and renal clearance significantly lower (166 vs 144 ml/min), while the biliary clearance of digoxin remained unchanged (106 vs 103 ml/min). Thus, spironolactone reduced the renal clearance of digoxin by an average of 13%, without affecting its biliary clearance.

Adult↗
PubMed1982

Renal digoxin clearance: dependence on plasma digoxin and diuresis.

The renal handling of digoxin in animals involves glomerular filtration, tubular secretion and tubular reabsorption, while only glomerular filtration and tubular secretion have been described in humans. The influence of plasma digoxin and urine flow on the renal handling of digoxin was investigated in 6 healthy volunteers. Non-glomerular renal excretion of digoxin (tubular secretion minus tubular reabsorption) was inversely correlated with plasma digoxin concentration and directly with urine flow. Hence, the present study demonstrated the occurrence of tubular reabsorption in addition to glomerular filtration and tubular secretion of digoxin. The results suggest that renal clearance of digoxin should be increased by increased urine flow, which might be of importance during digoxin toxicity.

Adult↗
PubMed1987

Reversal of toxic and non-toxic effects of digoxin by digoxin-specific Fab fragments in isolated human ventricular myocardium.

The time course of the reversal of toxic and nontoxic effects of digoxin by digoxin-specific antibody fragments (Fab) was measured in isolated human ventricular myocardium. A concentration of 2 X 10(-6) mol/l digoxin was used to produce positive inotropy followed by mechanical signs of toxicity. After addition of a 1.5-fold higher molar concentration of digoxin-specific Fab, signs of toxicity disappeared within 30 min and digoxin-induced force of contraction decayed with a monoexponential time course with a half-life of 52 min. This rate of decay was almost identical to that observed for the dissociation of the digoxin-(Na+ + K+)-ATPase complex in human heart cell membranes. It is concluded that digoxin-specific Fab are capable of completely removing digoxin from its binding sites, the maximal rate of removal of digitalis glycosides from the (Na+ + K+)-ATPase is limited by the dissociation rate constant, and there is a close correlation between the degree of binding of digitalis glycosides to the (Na+ + K+)-ATPase and the increase in force of contraction.

Binding Sites↗
PubMed1982

Use of control steady-state serum digoxin levels for predicting serum digoxin concentration after quinidine administration.

Serum digoxin and/quinidine concentration were measured before and following the institution of quinidine therapy in 11 patients who were receiving maintenance oral digoxin therapy and who required quinidine therapy for suppression of extrasystoles. Steady-state serum digoxin concentrations after quinidine administration were found to correlate well with serum digoxin concentrations before quinidine therapy and with peak serum digoxin concentrations after the first dose of quinidine sulfate, but not with serum quinidine concentrations. Thus steady-state serum digoxin concentration after quinidine (Y) could be estimated from the steady-state serum digoxin concentration before quinidine (X) as expressed by the regression formula Y = 2.6X - 0.6, with Syx2 - 0.21, and r = 0.96 (p less than 0.01). Based on these observations, guidelines for administering digoxin with concomitant quinidine therapy are presented.

Aged↗
PubMed1994

High-performance thin-layer chromatographic determination of digoxin and related compounds, digoxigenin bisdigitoxoside and gitoxin, in digoxin drug substance and tablets.

A high-performance thin-layer chromatographic (HPTLC) method for the determination of digoxin and its related compounds digoxigenin bisdigitoxoside (DBD) and gitoxin in digoxin drug substance and tablets was developed. Separation of the three compounds was accomplished on a C18 wettable reversed-phase plate using water-methanol-ethyl acetate (50:48:2, v/v/v) as the mobile phase. The analytes were determined by densitometry using absorbance for digoxin and fluorescence for the two related compounds. All peaks were quantified by peak-height analysis. Linear regression analysis of the data was performed for all three compounds. The calibration range for digoxin was set at 320-480 ng per 5-mm band, equivalent to 80-120% (w/w) of a 400-ng band load, that for DBD was set at 4-12 ng per 5-mm band, equivalent to 1-3% (w/w) of the digoxin load, and that for gitoxin was set at 0.4-1.6 ng per 5-mm band, equivalent to 0.1-0.4% (w/w) of the digoxin load. The limit of quantification (LOQ) for digoxin was 64 ng per 5-mm band with a limit of detection (LOD) of 8 ng per 5-mm band. The LOQs for both DBD and gitoxin were 0.12 ng per 5-mm band with LODs of 0.4 ng per 5-mm band. The linearity range for the digoxin peak height in the absorbance mode was 0-5000 ng per 5-mm band. The linearity range for DBD and gitoxin peak heights in the fluorescence mode was 0-2000 ng per 5-mm band.

Carbohydrate Sequence↗
PubMed1990

Effect of endogenous digoxin-like substances on the interpretation of high concentrations of digoxin in children.

The objective of this study was to assess the effect of endogenous digoxin-like substances on the interpretation of excessive concentrations of digoxin in children. After the development of a high-pressure liquid chromatography (HPLC) method for digoxin in our laboratories, we analyzed sera of children in whom the fluorescence polarization immunoassay identified potentially toxic concentrations of the glycoside (greater than 3 nmol/L; 2.3 ng/ml). Sixteen of them were receiving long-term digoxin therapy, and one had an accidental overdose. The immunoassay yielded significantly higher concentrations (4.1 +/- 1.2 nmol/L; 3.2 +/- 0.9 ng/ml) than the HPLC method (3.3 +/- 1.6 nmol/L; 2.6 +/- 1.2 ng/ml; p less than 0.01). In five cases (30%) these differences were clinically significant because administration of digoxin had been discontinued in the presence of true digoxin concentrations within the therapeutic range and the lack of clinical toxic effects. These data suggest that therapeutic drug monitoring using immunoassays of digoxin may be too inaccurate to detect potential toxic effects, and that much more weight should be focused on clinical monitoring. The HPLC method for assay of digoxin is extremely meticulous and will not become clinically available; therefore the development of better immunoassays should be encouraged.

Adolescent↗
PubMed1995

Monoclonal digoxin-specific antibodies induce dose- and affinity-dependent plasma digoxin redistribution in rats.

The effect of three monoclonal digoxin-specific antibodies on total and free digoxin plasma disposition was studied in rats in order to determine the role of affinity constant (Ka) and dose. Thirty minutes after digoxin infusion, administration of a stoichiometrical dose of the ICIO, 6C9 and 9F5 IgG (Ka = 6 10(9), 3.1 10(8) and 2.5 10(7) M-1, respectively) resulted in a plasma digoxin increase linearly related to Ka. The mean free plasma digoxin was 0.6 +/- 0.4, 7.8 +/- 3.3 and 43 +/- 22% respectively after 1C10, 6C9, and 9F5 IgG infusion in comparison to 70 +/- 9% in the control group. When the IgG:digoxin ratio increased from 1 to 5, plasma digoxin Cmax and AUCT also increased as a function of both affinity (Ka) and dose (N), but not linearly. The product of NKa defined an immunoreactivity factor that was well fitted to the digoxin redistribution parameters (Cmax and AUCT) by a Hill equation.

Animals↗
PubMed1988

Effects of amlodipine on steady-state digoxin concentrations and renal digoxin clearance.

The effect of oral amlodipine on steady-state digoxin concentrations and renal clearance was studied in 21 healthy male subjects. After 2-week digitalization (digoxin, 0.375 mg/day), they were randomized in a single-blind crossover protocol to receive either placebo or amlodipine (5 mg/day) in combination with digoxin for the following two 2-week periods. Mean (+/- SD) digoxin concentrations of 0.64 +/- 0.19 ng/ml after 2-week digoxin monotherapy and 0.61 +/- 0.23 ng/ml during placebo were not altered by amlodipine (0.60 +/- 0.18 mg/ml). Renal digoxin clearance was 202 +/- 44 ml/min on placebo and 207 +/- 55 ml/min during amlodipine coadministration. No change in pharmacologic effect of digoxin was noted during amlodipine coadministration, nor was blood pressure or heart rate changed. These data indicate that oral amlodipine does not significantly influence steady-state digoxin concentrations in healthy subjects.

Adult↗