Disease relevance of digoxin

• Asymptomatic digoxin toxicity [1].
• In one case the available Fab fragment supply was inadequate to reverse a massive suicidal ingestion of digoxin, and the patient died after recurrent ventricular arrhythmias [2].
• Using a randomized, double-blind, crossover protocol, we compared the effects of oral digoxin and placebo on the clinical courses of 25 outpatients without atrial fibrillation [3].
• This improvement demonstrated the value of long-term oral digoxin therapy in congestive heart failure [4].
• Digoxin therapy and mortality after myocardial infarction. Experience in the MILIS Study [5].
• The effect of digoxin use in women being treated for breast cancer or in survivors is unknown [6].

Psychiatry related information on digoxin

• The serum digoxin test and digoxin toxicity: a Bayesian approach to decision making [7].
• In a previous study using somatic cell fusion for Ig chain recombination we demonstrated that a recombinant antibody consisting of the H chain of antibody 26-10 and the L chain of antibody 40-20 retained digoxin binding and the 26-10 Id, but displayed a binding specificity pattern dominated by the 26-10 H chain donor [8].
• Resumption of physical activity resulted in gradual decline of plasma digoxin, and subsequent strenuous exercise reduced the value to preimmobilization level [9].
• Visual hallucinations as the earliest symptom of digoxin intoxication [10].
• This approach has been less successful with digoxin because patient compliance, the proportion absorbed and liver clearance are not yet predictable [11].

High impact information on digoxin

• In a doubleblind study, we enrolled 1663 patients who had severe heart failure and a left ventricular ejection fraction of no more than 35 percent and who were being treated with an angiotensin-converting-enzyme inhibitor, a loop diuretic, and in most cases digoxin [12].
• Images in clinical medicine. Digoxin-induced bidirectional ventricular tachycardia [13].
• Carvedilol reduces the risk or death as well as the risk of hospitalization for cardiovascular causes in patients with heart failure who are receiving treatment with digoxin, diuretics, and an angiotensin-converting-enzyme inhibitor [14].
• In the digoxin group, valve replacement (in a total of 20 patients) was performed because of left ventricular dysfunction (ejection fraction < 50 percent) in 75 percent, left ventricular dysfunction plus symptoms in 10 percent, and symptoms alone in 15 percent [15].
• By actuarial analysis, we determined that after six years a mean (+/- SD) of 34 +/- 6 percent of the patients in the digoxin group had undergone valve replacement, as compared with only 15 +/- 3 percent of those in the nifedipine group (P < 0.001) [15].

Chemical compound and disease context of digoxin

• Effect of quinidine on digoxin concentration in skeletal muscle and serum in patients with atrial fibrillation. Evidence for reduced binding of digoxin in muscle [16].
• Purified Fab fragments of digoxin-specific antibodies obtained from sheep were used to treat 26 patients with advanced, life-threatening digoxin (23 cases) or digitoxin (3 cases) toxicity [2].
• The hemodynamic effects of dobutamine were compared with those of digoxin in six patients with cardiac failure within 24 hours of onset of acute myocardial infarction [17].
• Our data suggest that the addition of hydralazine and isosorbide dinitrate to the therapeutic regimen of digoxin and diuretics in patients with chronic congestive heart failure can have a favorable effect on left ventricular function and mortality [18].
• The other patient, who had never taken methyldopa alone, did not demonstrate bradycardia with digoxin alone [19].

Biological context of digoxin

• The dose was adjusted on the basis of pharmacokinetics to achieve a mean steady-state concentration of 1.6 +/- 0.3 ng of digoxin per milliliter of serum [20].
• Decreased bioavailability of digoxin due to antacids and kaolin-pectin [21].
• In addition, the patients switched from digoxin to placebo had lower quality-of-life scores (P = 0.04), decreased ejection fractions (P = 0.001), and increases in heart rate (P = 0.001) and body weight (P < 0.001) [22].
• A digoxin-antibiotic drug interaction [23].
• Unlike other investigations, our studies provided no evidence that quinidine displaced digoxin at specific cardiac binding sites [24].

Anatomical context of digoxin

• One of these fetuses responded to cardioversion at birth, another responded to transplacental digoxin therapy, and the third died with atrial flutter and high-grade atrioventricular block before delivery [25].
• The hybrid VDJH-C alpha protein is expressed on a subset of T cells in these mice, and we have shown that it forms part of a functional TCR complex by the criteria of coprecipitation and comodulation of CD3 and TCR beta chain components and T cell activation with anti-idiotypic antibodies or digoxin [26].
• RESULTS--Five major preoperative predictors of postoperative myocardial ischemia were identified: (1) left ventricular hypertrophy by electrocardiogram; (2) history of hypertension; (3) diabetes mellitus; (4) definite coronary artery disease; and (5) use of digoxin [27].
• In each patient, normal sinus node function was demonstrated after methyldopa and digoxin therapy was discontinued [19].
• We show here that the mouse mdr1a and the human MDR1 P-glycoprotein actively transport ivermectin, dexamethasone, digoxin, and cyclosporin A and, to a lesser extent, morphine across a polarized kidney epithelial cell layer in vitro [28].

Associations of digoxin with other chemical compounds

• We studied 178 patients with New York Heart Association class II or III heart failure and left ventricular ejection fractions of 35 percent or less in normal sinus rhythm who were clinically stable while receiving digoxin, diuretics, and an angiotensin-converting-enzyme inhibitor (captopril or enalapril) [22].
• However, the clinical condition of 20 percent of the patients taking milrinone deteriorated within two weeks after treatment was begun, as compared with only 3 percent of those taking digoxin (P less than 0.05) [29].
• To determine whether a single dose of quinidine sulfate might alter serum digoxin levels, patients receiving maintenance digoxin therapy who required quinidine had their serum digoxin levels measured after oral administration of digoxin, quinidine, or both [30].
• Absence of the mdr1a P-Glycoprotein in mice affects tissue distribution and pharmacokinetics of dexamethasone, digoxin, and cyclosporin A [28].
• When neomycin was given after a 9-day period of digitalization, the terminal serum digoxin half-life was not significantly shortened [31].

Gene context of digoxin

• Furthermore, unlike other subtypes, OATP2 did not transport digoxin or aldosterone [32].
• Involvement of Cdk5/p25 in digoxin-triggered prostate cancer cell apoptosis [33].
• None of the tested endogenous steroids or synthetic glucocorticoids or digoxin, however, were transported substrates of BCRP [34].
• In the presence of digoxin, secretory transport of vinblastine and erythromycin, substrates for both Pgp and cytochrome P450 3A4 (CYP3A4), was significantly reduced, whereas absorptive transport was unaffected [35].
• In addition, CYP3A substrates and inhibitors varied widely in their ability to inhibit the P-gp-mediated transport of digoxin [36].

Analytical, diagnostic and therapeutic context of digoxin

• Spurious results of digoxin radioimmunoassay [37].
• Employing a Latin-square design and single-dose studies of bioavailability in 10 normal human volunteers, we tested the hypothesis that antacids and kaolin-pectin might interfere with the bioavailability of orally administered digoxin [21].
• According to a clinicoradiographic scoring system, the severity of heart failure was reduced by digoxin in 14 patients; in nine of these 14, improvement was confirmed by repeated trials (five patients) or right-heart catheterization (four patients) [3].
• Upon withdrawal of digoxin, pulmonary capillary-wedge pressure increased from 21 +/- 8 to 29 +/- 10 mm Hg, and cardiac index decreased from 2.4 +/- 0.7 to 2.1 +/- 0.6 liters per minute per square meter of body-surface area, suggesting a deterioration in left ventricular function [4].
• When starting quinidine therapy in patients who are taking digoxin, the clinical course, ECG, and serum digoxin level should be followed closely [38].

References