Journal articles: 'Digoxin (digitalis)'

1

Hollman, A. "Digoxin comes from Digitalis lanata." BMJ 312, no. 7035 (April 6, 1996): 912. http://dx.doi.org/10.1136/bmj.312.7035.912.

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Sharma, Anup, and Bulbul Purkait. "Quality Assessment of Serially Ultradiluted and Agitated Drug Digitalis purpurea by Emission Spectroscopy and Clinical Analysis of Its Effect on the Heart Rate of Indian Bufo melanostictus." Journal of Pharmaceutics 2013 (December 27, 2013): 1–6. http://dx.doi.org/10.1155/2013/571464.

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The investigation of ultradiluted (homeopathic) drugs is extremely interesting and challenging, and from that point of view this study shows novelty. A study of in vivo changes in heart rate of the Indian Bufo melanostictus caused by commercially available serially ultra-diluted and agitated extract of Digitalis purpurea has been tried in order to understand their pharmacological role. RR interval (of ECG) was compared after intraperitoneal administration of serially diluted and agitated Digitalis purpurea extract, diluent rectified spirit, and Digoxin in anesthetized animals. The study revealed statistically significant changes in the heart rate after application of these drugs except in case of Digoxin and the 200th serial dilution of Digitalis purpurea. The duration of RR intervals after application of the drugs was corroborative of the effect of Digoxin and Digitalis purpurea extract up to 30th dilution. Emission spectra were obtained for the experimental ultra-diluted Digitalis purpurea extract and Digoxin to identify and characterize them. The observed RR pattern and emission spectra show an association. The quality assessment of the commercial ultra-diluted organic drugs obtained from natural products may be initiated by monitoring in vivo studies on animal models.

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3

Scherrmann, Jean Michel, Pierre Sandouk, and Xavier Guedeney. "Digitalis-like Factors and Digoxin Pharmacokinetics." Chest 89, no. 3 (March 1986): 468–69. http://dx.doi.org/10.1378/chest.89.3.468.

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4

Cole, Patricia L., and Thomas W. Smith. "Use of Digoxin-Specific Fab Fragments in the Treatment of Digitalis Intoxication." Drug Intelligence & Clinical Pharmacy 20, no. 4 (April 1986): 267–70. http://dx.doi.org/10.1177/106002808602000403.

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The narrow margin between therapeutic and toxic effects of digitalis glycosides renders patients taking these drugs particularly susceptible to serious consequences of accidental or deliberate overdosage, including life-threatening arrhythmias. Until recently, the treatment of digitalis intoxication has been largely supportive. In the past decade, however, digoxin-specific antibodies have been developed and have proven to be effective in rapidly reversing the electrophysiologic and metabolic manifestations of digitalis intoxication, both in vitro and in vivo. Enzymatic cleavage of the intact antibody population into Fab fragments results in a more rapidly effective and less immunogenic antidote to digitalis excess. More recently, monoclonal antibodies with high affinity and specificity for digoxin have been produced by the technique of somatic cell fusion; application of this technique to the production of anti-digoxin antibodies has potential implications for the production of a highly purified homogeneous product, but this approach has not yet been tested clinically.

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5

Rabkin, Simon W., and Mark Redston. "The effect of inhibitors of endogenous opioid degradation, bacitracin, bestatin, captopril, and D-phenylalanine, on digoxin-induced arrhythmias in guinea pigs." Canadian Journal of Physiology and Pharmacology 67, no. 8 (August 1, 1989): 857–63. http://dx.doi.org/10.1139/y89-134.

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The purpose of this study was to investigate the effect of inhibition of endogenous opioid degradation on digitalis-induced arrhythmias, utilizing the inhibitors bacitracin, bestatin, captopril, and D-phenylalanine. Guinea pigs, anesthetized with pentobarbital, 50 mg/kg i.p., and breathing spontaneously received intracerebroventricular (i.c.v.) injection of bacitracin (6.8 mg/kg), bestatin (1 mg/kg), captopril (2 mg/kg), D-phenylalanine (1.2 mg/kg) or the diluent, saline. Digitalis arrhythmias were induced by a 50 μg/kg i.v. bolus of digoxin followed by 500 μg∙kg−1∙h−1 i.v. Bacitracin and bestatin, but not captopril or D-phenylalanine, significantly (p < 0.05) altered the relationship between the digoxin dose and the first occurrence of arrhythmias, i.e., digoxin-induced ventricular arrhythmias became manifest at lower digoxin doses. The mean digoxin dose and ED50s, at which arrhythmias first occurred, were significantly (p < 0.05) reduced by bacitracin and bestatin. The findings were similar for fatal arrhythmias, although D-phenylalanine appeared to decrease the digoxin dose at the development of fatal arrhythmias. The opioid antagonist naloxone, in a 50 μg/kg bolus and 50 μg∙kg−1∙h−1 i.c.v., completely prevented these effects of bacitracin and reduced the effect of bestatin. The relationship to arrhythmias could not be ascribed to an effect on blood pressure, as the blood pressure response to digoxin was the same in bestatin, D-phenylalanine, and control groups. To examine whether systemic administration of an inhibitor of opioid degradation had similar effects, a second protocol was selected with systemic administration of bacitracin because it altered the dose effect relationship after i.c.v. administration and systemic concentrations could be readily attained. Bacitracin, in a 13.5 mg/kg i.v. bolus and 135 mg∙kg−1∙h−1 i.v., was followed by 100 μg/kg digoxin i.v. every 15 min. Bacitracin significantly (p < 0.05) reduced the digoxin dose at the development of arrhythmias. This was reversed by naloxone, given as 2 mg/kg i.v. plus 10 mg∙kg−1∙h−1. Thus, these data indicate that inhibitors of degradation of some opioid potentiate digitalis arrhythmias in a manner that is inhibited by naloxone, and provide evidence that implicates a role for endogenous opioids in digitalis arrhythmias.Key words: digitalis arrhythmias, aminopeptidase inhibitors.

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Rodríguez-Calvo, María S., Rosa Rico, Manuel López-Rivadulla, José M. Suárez-Peñaranda, José I. Muñoz, and Luis Concheiro. "2. Report of a Suicidal Digoxin Intoxication: A Case Report." Medicine, Science and the Law 42, no. 3 (July 2002): 265–68. http://dx.doi.org/10.1177/002580240204200313.

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Digoxin is a cardiotonic glycoside that is primarily used in the treatment of heart failure, atrial fibrillation or flutter, and paroxysmal atrial tachycardia. Intoxication due to digitalis excess is a common problem in clinical practice because it is therapeutically effective within a narrow dose range. However, massive intoxication with digitalis glycosides following a suicidal attempt is a rare event. In this report we describe an overdose fatality involving digoxin in a suicidal 82-year-old man, in whom measurement of serum digoxin concentration is available. A toxicological study of our patient, approximately two and a half hours after ingestion of the drug, revealed digoxin concentrations within 12.2–13.2 ng/ml in the blood, while the mean therapeutic serum concentration ranged from 0.5 to 2 ng/ml.

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Sabatini, Diletta, Giovanni Truscelli, Antonio Ciccaglioni, Carlo Gaudio, and Maria Caterina Grassi. "Bidirectional Tachycardia after an Acute Intravenous Administration of Digitalis for a Suicidal Gesture." Case Reports in Psychiatry 2014 (2014): 1–3. http://dx.doi.org/10.1155/2014/109167.

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Acute digoxin intoxication is a life-threating condition associated with severe cardiotoxicity. Female gender, age, low lean body mass, hypertension, and renal insufficiency may worsen the prognosis. Arrhythmias caused by digitalis glycosides are characterized by an increased automaticity coupled with concomitant conduction delay. Bidirectional tachycardia is pathognomonic of digoxin intoxication, but it is rarely observed. An 83-year-old woman was admitted to the Emergency Department after self-administration of 5 mg of digoxin i.v. for suicidal purpose. Her digoxin serum concentration was 17.4 ng/mL. The patient developed a bidirectional tachycardia and the Poison Control Center of the hospital provided digoxin immune fab. Bidirectional tachycardia quickly reversed and the patient remained stable throughout the hospital stay. This case shows that a multiple disciplinary approach, involving cardiologists and toxicologists, is essential for the management of digoxin intoxication. The optimal treatment of this rare event depends on the clinical conditions and on the serum drug concentration of the patient. Digoxin immune fab represents a safe, effective, and specific method for rapidly reversing digitalis cardiotoxicity and should be started as soon as the diagnosis is defined.

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8

Longerich, L., S. Vasdev, E. Johnson, and M. H. Gault. "Disposable-column radioimmunoassay for serum digoxin with less interference from metabolites and endogenous digitalis-like factors." Clinical Chemistry 34, no. 11 (November 1, 1988): 2211–16. http://dx.doi.org/10.1093/clinchem/34.11.2211.

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Abstract A preparative extraction step using disposable C18 low-pressure chromatography columns greatly improved the specificity of a commercially prepared digoxin radioimmunoassay (RIA). Elution solvents were isopropanol/water (15/85 by vol), which extracted most immunoreactive digitalis-like factors and metabolites, and methanol, which extracted digoxin for RIA. Many different digoxin RIA kits could be used. The coefficients of variation for replicates and duplicates were 4.6% and 5.2%. Analytical recoveries of digoxin standards in serum of 1.0, 0.5, and 0.1 microgram/L were 96%, 95%, and 88%, respectively. Serum digoxin was assayed by this method in 200 patients, 47 of whom were studied by HPLC-RIA. Values correlated better with "true digoxin" by HPLC-RIA (r = 0.93) than did values found by direct assay (r = 0.63). The mean for the isopropanol fraction as a percentage of the mean direct RIA value was higher for the 21 dialysis-dependent patients than was that found for the 179 nondialysis patients (P less than 0.004). The method is suggested as being most useful when metabolites or digitalis-like factors are known to be often high and values for digoxin are disproportionate to the dose.

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9

Malini, Pier Luigi, Enrico Strocchi, Giorgio Feliciangeli, Andrea Buscaroli, Vittorio Bonomini, and Ettore Ambrosioni. "DIGITALIS RECEPTORS AND DIGOXIN SENSITIVITY IN RENAL FAILURE." Clinical and Experimental Pharmacology and Physiology 12, no. 2 (April 1985): 115–20. http://dx.doi.org/10.1111/j.1440-1681.1985.tb02313.x.

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10

Lengel, Matthew J., Kun Xiang, Vincent F. Mauro, Blair P. Grubb, and Christopher J. Cooper. "Acute Digitalis Delirium Associated with Intravenous Digoxin Administration." Arrhythmia grand rounds 1, no. 1 (April 27, 2015): 3–6. http://dx.doi.org/10.12945/j.agr.2015.0002-14.

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11

Rutledge, Joe. "Digitalis toxicity in infants and plasma digoxin levels." Pediatric Cardiology 6, no. 1 (March 1985): 51. http://dx.doi.org/10.1007/bf02265409.

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12

Balzan, Sllvana, Serglo Ghione, Pascal Biver, Psolo Gazzetti, and Umberto Montali. "Partial purification of endogenous digitalis-like compound(s) in cord blood." Clinical Chemistry 37, no. 2 (February 1, 1991): 277–81. http://dx.doi.org/10.1093/clinchem/37.2.277.

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Abstract Increasing evidence indicates the presence of endogenous digitalis-like compound(s) in human body fluids. In this preliminary report, we describe a study of the partial purification by HPLC of these compounds in the plasma of neonates (who have particularly high concentrations of this substance) and adults. Plasma samples from neonates (cord blood) and adults, lyophilized and extracted with methanol, were applied on a 300 x 3.9 mm C18 Nova Pak column and eluted with a mobile phase of acetonitrile/methanol/water (17/17/66 or 14/14/72 by vol) and, after 30 min, with 100% methanol. We assayed eluted fractions for inhibitory activity of 86Rb uptake and for digoxin-like immunoreactivity. The elution profile revealed a first peak of inhibitory activity of 86Rb uptake at the beginning of the chromatography; another peak was eluted with the 100% methanol. The two peaks also cross-reacted with antidigoxin antibodies. Because the second peak could possibly reflect the nonspecific interference of various lipophilic compounds, we focused our attention on the first peak. For these fractions dose-response curves for 86Rb uptake and for displacement of digoxin were parallel, respectively, to those of ouabain and digoxin, suggesting similarities of digoxin-like immunoreactive substance to cardiac glycosides. Similar chromatographic profiles were also obtained for plasma from adults, suggesting that the endogenous glycoside-like compound(s) in the neonate may be the same as those in the adult.

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13

Clerico, A., A. Paci, M. G. Del Chicca, P. Biver, and O. Giampietro. "Endogenous Digitalis-Like Factors in Human Milk." Clinical Chemistry 38, no. 4 (April 1, 1992): 504–6. http://dx.doi.org/10.1093/clinchem/38.4.504.

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Abstract We measured the concentration of endogenous digitalis-like factors (EDLFs) in milk or colostrum of women during nursing on different days after delivery. EDLF concentrations were assayed by a solid-phase RIA involving antidigoxin antibodies and by a radioreceptor assay (RRA) involving human placenta Na+/K(+)-ATPase. The mean (SD) EDLF concentrations as measured by RIA were 35.6 (19.4) ng of digoxin equivalents per liter in milk samples (n = 37) and 61.3 (12.5) ng/L in colostrum samples (n = 5); the mean EDLF concentration as measured by RRA in milk samples (n = 11) was 573 (717) ng/L (range 0-2098). EDLF concentration in milk is greater than circulating concentrations in healthy adults but is comparable with serum concentration in the third trimester of pregnancy. In milk and serum samples (n = 8) collected at the same time, heating and (or) extracting with Sep-Pak C18 cartridges before the RIA produced significantly different EDLF values from those in untreated serum (P less than 0.001) and milk (P = 0.035). EDLF in milk appeared to be not bound or weakly bound to milk protein, as indicated by the fact that boiling did not increase the digoxin-like immunoreactivity.

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14

Paci, A., F. Cocci, F. Piras, G. Ciarimboli, and A. Clerico. "Specific binding of cardiac glycoside drugs and endogenous digitalis-like substances to particulate membrane fractions from human placenta." Clinical Chemistry 35, no. 10 (October 1, 1989): 2093–97. http://dx.doi.org/10.1093/clinchem/35.10.2093.

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Abstract We studied the characteristics of binding of cardiac glycosides to particulate membrane fractions from human placenta, to demonstrate that placental tissue is a suitable source of receptors for digitalis drugs. Moreover, we performed preliminary experiments with 125I-labeled digoxin and placental particulates to develop a radioreceptor assay for measurement of endogenous substances with activity similar to cardiac glycoside drugs (EDLS). Placental membrane fractions were incubated with [3H]ouabain (10 nmol/L) or 125I-labeled digoxin (50 pmol/L). With both ligands, binding followed a pseudo-first-order reaction kinetics and was saturable. Scatchard analysis revealed a single class of sites [for ouabain, KD = 20.2 +/- 5.8 nmol/L (mean +/- SEM), Bmax = 3.1 +/- 0.9 nmol per gram of protein; for digoxin, KD = 29.7 +/- 1.9 nmol/L, Bmax = 24.3 +/- 1.1 nmol per gram of protein]. As expected, digoxin was less potent than ouabain in displacing both tracers from digitalis drugs receptors; progesterone, cortisone, digitoxose, furosemide, bumetanide, and propranolol had no or little effect. Specific 125I-labeled digoxin binding was competitively inhibited by plasma and (or) urine extracts from newborns, adults, pregnant women, and patients with renal insufficiency. Inhibition of binding and volume of plasma and urine assayed were linearly related. These findings support the hypothesis that cardiac glycosides and EDLS can interact with the human placenta and suggest placental tissue to be a suitable source of receptors for cardiac glycosides.

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15

Bauer, N., G. Scheiner-Bobis, and W. Schoner. "„Endogenes Digitalis” – der lange Weg vom herzwirksamen pflanzlichen Toxin zum Hormon der Säuger." Tierärztliche Praxis Ausgabe K: Kleintiere / Heimtiere 34, no. 06 (2006): 389–97. http://dx.doi.org/10.1055/s-0037-1622553.

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ZusammenfassungEndogene Herzglykoside wurden kürzlich aus Blut, Urin, Nebennieren und Hypothalamus von Säugetieren isoliert und in ihrer Struktur aufgeklärt. Zu den endogenen Herzglykosiden zählen so gut bekannte Hemmstoffe der Natriumpumpe wie Ouabain (g-Strophanthin), Digoxin und Marinobufagenin. Endogenes Ouabain und Digoxin werden in der Nebennierenrinde der Säuger aus Progesteron und Pregnenolon synthetisiert. Ouabain wird bei Kreislaufbelastung rasch freigesetzt, seine Konzentration fällt bei Ruhe innerhalb weniger Minuten wieder ab. ACEInhibitoren und β-Blocker verhindern bei Hunden diesen Anstieg. Ouabain wird durch ACTH, Adrenalin und Angiotensin II aus Nebennierenrindenzellen in Kultur freigesetzt. Nanomolare Ouabain-Konzentrationen stimulieren die Proliferation von glatten Muskelzellen. An schwerer dilatativer Kardiomyopathie erkrankte Hunde haben im Vergleich zu gesunden Hunden signifikant erniedrigte Ouabain-Blutwerte. Beim Menschen und Ratten führt eine lang dauernde zu hohe NaCl-Zufuhr über die Nahrung zum Konzentrationsanstieg von endogenem Ouabain im Blut und zum Bluthochdruck. Eine über lange Zeit durchgeführte Infusion von Ouabain, aber nicht von Digoxin, erzeugt bei Ratten Bluthochdruck. Digoxin senkt den Ouabain-induzierten Bluthochdruck. Da bei ca. 50% der Hochdruckpatienten erhöhte Ouabain-Werte vorliegen, ist es von großer medizinischer Bedeutung, dass mit dem Ouabain-Antagonisten Rostafuroxin ein neues Prinzip und eine neue Gruppe von Blutdrucksenkern gefunden wurde. Marinobufagenin, dessen Konzentration bei Herzinfarkt akut ansteigt, hat auf die Niere eine natriuretische Wirkung. Im Gehirn wird Ouabain im Hypothalamus synthetisiert und bei einer erhöhten intrazellulären Natriumkonzentration freigesetzt.

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16

Gault, M. H., L. Longerich, M. Dawe, and S. C. Vasdev. "Combined liquid chromatography/radioimmunoassay with improved specificity for serum digoxin." Clinical Chemistry 31, no. 8 (August 1, 1985): 1272–77. http://dx.doi.org/10.1093/clinchem/31.8.1272.

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Abstract This method for assaying digoxin in serum with improved specificity combines small-column extraction of serum, "high-performance" liquid chromatography, and RIA of the eluted fractions. Analytical recoveries of 1.0, 0.5, and 0.1 microgram/L standards were 95%, 93%, and 84%, respectively. The CVs for duplicates and replicates of sera with values of 0.5 to 1 microgram/L were 4 to 6%. Fifty-nine sera from 50 patients receiving digoxin were so studied. All digoxin metabolites appear to cross react with antibody to digoxin to various degrees. The most polar metabolites were quantitatively the most important, their average cross reactivity being 33%. For eight patients the value for digoxin by the present method was less than 60% of the RIA value. Sera from nine patients not taking digoxin but with falsely high digoxin values were also studied by the present method. The digoxin peak was well resolved from those for (a) digoxin metabolites (except dihydrodigoxin), (b) digitalis-like factors in neonates and in patients with renal failure or combined hepatic and renal failure, and (c) two cross reacting drugs and their metabolites.

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17

Mordel, Amnon, Hillel Halkin, Lea Zulty, Shlomo Almog, and David Ezra. "Quinidine enhances digitalis toxicity at therapeutic serum digoxin levels." Clinical Pharmacology and Therapeutics 53, no. 4 (April 1993): 457–62. http://dx.doi.org/10.1038/clpt.1993.51.

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18

Tröster, Sibille, K. F. Bodmann, and H. P. Schuster. "Schwere Digitalis-Intoxikation nach Ingestion von 1 g Digoxin." DMW - Deutsche Medizinische Wochenschrift 117, no. 30 (March 25, 2008): 1149–52. http://dx.doi.org/10.1055/s-2008-1062424.

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19

Andjelic, Sladjana. "Bigeminy: A result of digoxin and St John’s wort interaction." Vojnosanitetski pregled 60, no. 3 (2003): 361–64. http://dx.doi.org/10.2298/vsp0303361a.

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A case of an by digoxin under unusual circumstances is reported. An 80-year-old man, previously on long-term digoxin treatment, started consuming St John?s wort herbal tea (2 000 ml/daily) because of frequent episodes of depression. After the cessation of consuming herbal tea containing Hypericum perforatum, digoxin poisoning developed in our patient. Electrocardiography revealed nodal bradicardia 36/min and bigeminy. Manifested symptoms were the consequence of interaction between digoxin and Hypericum perforatum which were consumed simultaneously, and the cessation of consuming St John?s wort herbal tea afterwards. Therapy was the same as in the standard digitalis poisoning. Consumers of St John?s wort combined with medical products are advised not to discontinue tea consumption on their own, without consulting their physician.

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20

Kelly, R. A. "Excretion of artifactual endogenous digitalis-like factors." American Journal of Physiology-Heart and Circulatory Physiology 251, no. 1 (July 1, 1986): H205—H209. http://dx.doi.org/10.1152/ajpheart.1986.251.1.h205.

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Radioimmunoassays have been used to detect digoxin-like immunoreactive factors (DLF) in the plasma and urine of hypertensive patients and rats with deoxycorticosterone acetate (DOCA)-salt hypertension. Uninephrectomized rats (n = 9), given 15 mg DOCA . kg-1 . wk-1, were fed a standard rat chow supplemented with 2% NaCl (DOCA-HS); control animals (n = 15) were given vehicle injection and a specially formulated low-salt diet (0.05% NaCl). At 4 wk, DOCA-HS rats were hypertensive (121.4 +/- 10.1 vs. 88 +/- 4.4 Torr, mean +/- SEM, P less than 0.05) and excreted more DLF (2.7 +/- 1.1 vs. 0.2 +/- 0.1 ng digoxin equivalents . day-1, P less than 0.001) compared with control rats. DLF, partially purified from DOCA-HS urine by antidigoxin antibody immunoaffinity chromatography, was found to have a molecular weight less than 2,000, was resistant to acid hydrolysis or proteases, and had many properties of the cardiac glycosides, including inhibition of Na+-K+-ATPase activity, displacement of ouabain from human erythrocyte membranes, and inhibition of 86Rb influx into red blood cells. When DOCA-HS rats were switched to the low-sodium chow, DLF excretion dropped precipitously. No measurable DLF (less than 10 pg/ml) was detected in the plasma of rats eating either chow. However, greater than 95% of the urinary DLF could be attributed to a contaminant in the standard laboratory chow; rats fed the low-salt chow supplemented with 2% NaCl excreted much less DLF, and DLF was isolated from the standard chow.(ABSTRACT TRUNCATED AT 250 WORDS)

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A. van Wietmarschen, Herman, Hansj謗g Hagels, Ron Peters, Jolanda Heistek, Jan van der Greef, and Mei Wang. "Optimizing Growth Conditions for Digoxin Production in Digitalis lanata Ehrh." World Journal of Traditional Chinese Medicine 2, no. 2 (2016): 24–35. http://dx.doi.org/10.15806/j.issn.2311-8571.2016.0010.

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MARTINY, SABRENA SALUK, STEPHANIE J. PHELPS, and KENNETH L. MASSEY. "Treatment of severe digitalis intoxication with digoxin-specific antibody fragments." Critical Care Medicine 16, no. 6 (June 1988): 629–35. http://dx.doi.org/10.1097/00003246-198806000-00014.

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23

Gault, M. H., S. Vasdev, and L. Longerich. "Higher values for digitalis-like factors with TDx Digoxin II." Clinical Chemistry 32, no. 10 (October 1, 1986): 2000–2001. http://dx.doi.org/10.1093/clinchem/32.10.2000a.

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Goto, A., T. Ishiguro, K. Yamada, M. Ishii, M. Yoshioka, C. Eguchi, M. Shimora, and T. Sugimoto. "Isolation of a urinary digitalis-like factor indistinguishable from digoxin." Biochemical and Biophysical Research Communications 173, no. 3 (December 1990): 1093–101. http://dx.doi.org/10.1016/s0006-291x(05)80898-8.

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Varriale, Philip, and Ahmad Mossavi. "Rapid reversal of digitalis delirium using digoxin immune fab therapy." Clinical Cardiology 18, no. 6 (June 1995): 351–52. http://dx.doi.org/10.1002/clc.4960180611.

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Souza, Felipe C., Emiliana B. Marques, Rogério B. M. Scaramello, and B. V. Christianne. "Study of digoxin use in a public health unit." Anais da Academia Brasileira de Ciências 87, no. 2 (May 15, 2015): 1033–40. http://dx.doi.org/10.1590/0001-3765201520140133.

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Digoxin is used for heart failure associated to systolic dysfunction and high ventricular rate. It has a narrow therapeutic range and intoxication may occur due to drug interactions or comorbidities. The aim of this work was to study digoxin use in a public health unit delineating the profile of patients susceptible to digitalis intoxication. Medical records belonging to patients admitted to the cardiomyopathy ward of the health unit (2009-2010) and in use of digoxin were analyzed. Among 647 patients admitted, 185 individuals using digoxin and possessed records available. The registration of plasma digoxin concentration was found in 80 records and it was out of the therapeutic range in 42 patients (52.5%). This group of individuals was constituted mainly by males patients (79%), functional class III of heart failure (65%), exhibiting renal failure (33%). The evaluated sample reflects the epidemiology of heart failure in Brazil and, although pharmacotherapy had been according to Brazilian Guidelines, apparently the monitoring was not performed as recommended. This work highlighs the necessity of plasma digoxin constant monitoring during pharmacotherapy and the development of protocols that enable a safer use, especially in male patients, functional class III and with renal dysfunction.

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Konstantinou, Dimitrios M., Haralambos Karvounis, and George Giannakoulas. "Digoxin in Heart Failure with a Reduced Ejection Fraction: A Risk Factor or a Risk Marker?" Cardiology 134, no. 3 (2016): 311–19. http://dx.doi.org/10.1159/000444078.

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Digoxin is one of the oldest compounds used in cardiovascular medicine. Nevertheless, its mechanism of action and most importantly its clinical utility have been the subject of an endless dispute. Positive inotropic and neurohormonal modulation properties are attributed to digoxin, and it was the mainstay of heart failure therapeutics for decades. However, since the institution of β-blockers and aldosterone antagonists as part of modern heart failure medical therapy, digoxin prescription rates have been in free fall. The fact that digoxin is still listed as a valid therapeutic option in both American and European heart failure guidelines has not altered clinicians' attitude towards the drug. Since the publication of original Digitalis Investigation Group trial data, a series of reports based predominately on observational studies and post hoc analyses have raised concerns about the clinical efficacy and long-term safety of digoxin. In the present review, we will attempt a critical appraisal of the available clinical evidence regarding the efficacy and safety of digoxin in heart failure patients with a reduced ejection fraction. The methodological issues, strengths, and limitations of individual studies will be highlighted.

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Cha, Kyungman, Byung Hak So, and Won Jung Jeong. "Bufotoxin poisoning that showed the sign of acute digitalis overdose in the patient of Kyushin® intoxication." Hong Kong Journal of Emergency Medicine 27, no. 3 (October 23, 2018): 180–84. http://dx.doi.org/10.1177/1024907918807526.

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Introduction: Kyushin® is a widely used herbal medicine in East Asia for heart failure. Toad venom in present in Kyushin®, which has positive inotropic effect as digitoxin. Case presentation: An 81-year-old, female patient presented with decreased mental status after overdose of Kyushin®. The first electrocardiogram showed junctional tachycardia with 142/min, suddenly dropped to 27/min and followed by ventricular fibrillation. After one cycle of CPR, spontaneous circulation returned but junctional bradycardia, tachycardia, and ventricular fibrillation appeared. After six times of defibrillation, spontaneous circulation returned, and mechanical ventilator and transcutaneous pacing were applied. Plasma toxicology test revealed digitoxin 66.90 ng/mL by cloned enzyme donor immunoassay and digoxin 0.76 ng/mL by kinetic interaction of microparticles in solution immunoassay. After 8 h from presentation, the patient’s mental status came to be alert, and then transcutaneous pacing was removed. Discussion: Cloned enzyme donor immunoassay has been reported to be highly cross-reactive with digoxin-like substances, which strongly supports bufotoxin to be responsible for arrhythmia of the patient. Conclusion: Poisoning of bufotoxin in Kyushin® can cause cardiac arrhythmia, even arrest, but without digoxin-specific Fab, conventional therapy could be successful.

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Jortani, S. A., R. A. Helm, and R. Valdes. "Inhibition of Na,K-ATPase by oleandrin and oleandrigenin, and their detection by digoxin immunoassays." Clinical Chemistry 42, no. 10 (October 1, 1996): 1654–58. http://dx.doi.org/10.1093/clinchem/42.10.1654.

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Abstract Ingestion of oleander plant, containing the cardiac glycoside oleandrin, has been reported to induce fatal poisonings. Derivatives of oleandrin are structurally similar to digoxin. We investigated the cross-reactivities of oleandrin and its aglycone metabolite, oleandrigenin, in several commercially available digoxin immunoassays; assessed their ability to inhibit Na,K-ATPase catalytic activity; and measured their binding to proteins in serum. As assayed with ACS:180, Stratus, RIA, On-Line, and TDx digoxin assays, oleandrin at 100 micromol/L in digoxin-free serum gave apparent digoxin values of 0, 0.83, 2.24, 2.37, and 5.34 nmol/L, respectively, whereas oleandrigenin at that concentration gave results of 0, 0.52, 0.77, 4.94, and 1.40 nmol/L. Study of Na,K-ATPase inhibition showed IC50 values (micromol/L) of 0.22 for ouabain, 0.62 for oleandrin, 1.23 for oleandrigenin, and 2.69 for digoxin. At 25 degrees C, 96% of oleandrin and 48% of oleandrigenin were bound to serum proteins. Because detection of oleandrin and oleandrigenin by digoxin immunoassays is variable between assays as well as between congeners, assessment of cross-reactivity is warranted for each assay. The inhibition of Na,K-ATPase by oleandrin and oleandrigenin confirms that they likely exert their toxic effects through inhibition of sodium pump activity. In cases of digitalis-like poisoning with suspicion of oleander ingestion, a combination of digoxin immunoassays may be useful to effectively rule out the presence of oleander.

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Bekhit, M. H. "INCREASING PRODUCTIVITY OF DIGOXIN CONTENT IN DIGITALIS LANATA EHRH "IN VITRO"." Journal of Plant Production 34, no. 1 (January 1, 2009): 333–45. http://dx.doi.org/10.21608/jpp.2009.116616.

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Springer, martin, Kent R. Olson, and William Feaster. "Acute massive digoxin overdose: Survival without use of digitalis-specific antibodies." American Journal of Emergency Medicine 4, no. 4 (July 1986): 364–68. http://dx.doi.org/10.1016/0735-6757(86)90311-6.

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Erdmann, E., W. Mair, M. Knedel, and W. Schaumann. "Digitalis intoxication and treatment with digoxin antibody fragments in renal failure." Klinische Wochenschrift 67, no. 1 (January 1989): 16–19. http://dx.doi.org/10.1007/bf01736529.

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Rojas-Fernandez, Carlos H., Luis Viana, and Farzan Dadfar. "Contemporary Considerations for the Use of Digoxin for Heart Failure in Older Patients." Canadian Pharmacists Journal / Revue des Pharmaciens du Canada 144, no. 6 (November 2011): 265–69. http://dx.doi.org/10.3821/1913-701x-144.6.265.

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Background: Digoxin has been used in older people for over 200 years to treat heart failure. Research over the past 15 years has caused the place of digoxin in therapy to evolve. This review was conducted in order to describe the role of digoxin in the care of older patients with heart failure. Methods: This review was conducted by systematically searching the literature using MEDLINE via Ovid, Cochrane Library, Pub Med and EMBASE, with the search terms “heart failure” and “digoxin.” Studies published after publication of the Digitalis Investigation Group (DIG) trial (conducted from February 1997 to October 2010) were selected for possible inclusion in the review. Results: The majority of data regarding the use of digoxin for heart failure in older people originates from the DIG trial and the various post-hoc analyses of this dataset. When considered in unison with evidence for other heart failure therapies (e.g., angiotensin-converting enzyme inhibitors), the place of digoxin is clear, in that it should be used for patients in sinus rhythm who are symptomatic despite therapy with first-line agents or for those with concomitant atrial fibrillation whose heart rate is not well controlled by, or cannot tolerate, beta-adrenergic blockers. There are various safety and monitoring parameters that should be considered in older people when using this drug. Conclusions: Digoxin is a drug that still demonstrates value for heart failure in older patients when used appropriately, and after first-line agents have been maximized.

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Aubier, M., N. Viires, D. Murciano, J. P. Seta, and R. Pariente. "Effects of digoxin on diaphragmatic strength generation." Journal of Applied Physiology 61, no. 5 (November 1, 1986): 1767–74. http://dx.doi.org/10.1152/jappl.1986.61.5.1767.

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Contrary to hindlimb muscle, extracellular calcium plays an important role in diaphragmatic strength generation (J. Appl. Physiol. 58: 2054–61, 1985). Since the inotropic effect of digitalis appears to be related to cell membrane transport of calcium, we studied the effect of digoxin on diaphragmatic contractility in 20 anesthetized dogs. The diaphragm was electrically stimulated with intramuscular electrodes. The transdiaphragmatic pressure (Pdi) during supramaximal (50 V) 2-s stimulations applied over a frequency range of 10–100 Hz was measured with balloon catheters at functional residual capacity. Cardiac output was measured with a Swan-Ganz catheter and diaphragmatic blood flow (Qdi) by timed volume collections of left inferior venous effluent. The force generated by the sartorius muscle during electrical stimulations was studied concomitantly to Pdi. In 10 dogs (group A) 0.04 mg/kg of digoxin was infused in 10 min. In 10 other dogs (group B) 0.2 mg/kg was administered. All measurements were performed during control and 30, 60, 90, and 120 min after digoxin administration. In group A, digoxin plasmatic level at 60 min reached a therapeutic range in all dogs (1.8 +/- 0.3 ng/ml), whereas in group B, digoxin plasmatic level was higher (8 +/- 1.3 ng/ml). No significant change in cardiac output and Qdi was noted after administration of digoxin, either in the dogs of group A or those of group B.(ABSTRACT TRUNCATED AT 250 WORDS)

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Haddy, FJ. "Humoral Factors in Hypertension." Physiology 4, no. 5 (October 1, 1989): 202–5. http://dx.doi.org/10.1152/physiologyonline.1989.4.5.202.

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Acute volume expansion and low-renin hypertension endow the plasma with the capacity to inhibit Na+-K+-ATPase, cause natriuresis, sensitize blood vessels to vasoconstrictor agents, and raise blood pressure. Digoxin-like immunoreactivity has been detected in the plasma under both circumstances. These findings suggest the existence of an endogenous "digitalis" that is relevant to volume and blood pressure control.

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Aguirre Dávila, Lukas, Kristina Weber, Udo Bavendiek, Johann Bauersachs, Janet Wittes, Salim Yusuf, and Armin Koch. "Digoxin–mortality: randomized vs. observational comparison in the DIG trial." European Heart Journal 40, no. 40 (June 18, 2019): 3336–41. http://dx.doi.org/10.1093/eurheartj/ehz395.

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Abstract Aims The Digitalis Investigation Group (DIG) trial, the only large randomized trial of digoxin in heart failure, reported a neutral effect on mortality and a significant reduction in heart failure hospitalizations. Recent observational studies reported increased mortality with digoxin treatment. We present further analyses of the DIG trial displaying the inability to control bias in observational treatment comparisons despite extensive statistical adjustments. Methods and results Forty-four percent of the 6800 patients in the DIG trial had been treated with digoxin before randomization, and half of them were randomly withdrawn from digoxin treatment. We contrast the main randomization-based result of the DIG trial with the observational non-randomized comparison of patients pre-treated or not pre-treated with digoxin. Mortality [hazard ratio (HR) 1.22, 95% confidence interval (CI) 1.12–1.34; P < 0.001] and heart failure hospitalizations (HR 1.47, 95% CI 1.33–1.61; P < 0.001) were significantly higher in patients pre-treated with digoxin even after adjustment for baseline population differences. The higher risks for both outcomes in those who had previously received digoxin persisted even if they received placebo during the trial (HR 1.24, 95% CI 1.10–1.40; P < 0.001). This sharply contradicts the neutral effect on mortality and the significant reduction in heart failure hospitalizations observed in the randomized comparison. Conclusion Prescription of digoxin is an indicator of disease severity and worse prognosis, which cannot be fully accounted for by covariate adjustments in the DIG trial where patients were well-characterized. It is unlikely that weaker research approaches (observational studies of administrative data or registries) can provide more reliable estimates of the effects of cardiac glycosides.

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Cooper, D. M., J. D. Maloney, L. A. Cooper, J. R. Hodgman, and L. W. Castle. "Immunological reversal of digitalis toxicity by Fab fragments of digoxin-specific antibodies." Cleveland Clinic Journal of Medicine 54, no. 1 (January 1, 1987): 43–48. http://dx.doi.org/10.3949/ccjm.54.1.43.

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Smolarz, A., E. Roesch, E. Lenz, H. Neubert, and P. Abshagen. "Digoxin Specific Antibody (Fab) Fragments in 34 Cases of Severe Digitalis Intoxication." Journal of Toxicology: Clinical Toxicology 23, no. 4-6 (January 1985): 327–40. http://dx.doi.org/10.3109/15563658508990641.

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Wenger, Thomas L., Vincent P. Butler, Edgar Haber, and Thomas W. Smith. "Treatment of 63 severely digitalis-toxic patients with digoxin-specific antibody fragments." Journal of the American College of Cardiology 5, no. 5 (May 1985): 118A—123A. http://dx.doi.org/10.1016/s0735-1097(85)80471-x.

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Hunt, Michael. "Digoxin specific antibody (Fab) fragments in 34 cases of severe digitalis intoxication." Annals of Emergency Medicine 15, no. 9 (September 1986): 1129–30. http://dx.doi.org/10.1016/s0196-0644(86)80166-4.

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Lapostolle, Frédéric, Stephen W. Borron, Carine Verdier, Pierre Taboulet, Gilles Guerrier, Frédéric Adnet, Jean-Luc Clemessy, Chantal Bismuth, and Frédéric J. Baud. "Digoxin-specific Fab fragments as single first-line therapy in digitalis poisoning." Critical Care Medicine 36, no. 11 (November 2008): 3014–18. http://dx.doi.org/10.1097/ccm.0b013e31818b341c.

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Stolshek, Bradley S., Shirley K. Osterhout, and Gary Dunham. "The Role of Digoxin-Specific Antibodies in the Treatment of Digitalis Poisoning." Medical Toxicology 3, no. 3 (June 1988): 167–71. http://dx.doi.org/10.1007/bf03259880.

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Shilo, L., A. Pomeranz, M. Rathaus, J. Bernheim, and L. Shenkman. "Endogenous digoxin-like factor raises blood pressure and protects against digitalis toxicity." Life Sciences 44, no. 24 (January 1989): 1867–70. http://dx.doi.org/10.1016/0024-3205(89)90304-4.

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Hutomo, Suryo Ardi, and Agus Subagjo. "Difficult Atrial Fibrilation Rate-Control and Digitalis Toxicity in Mitral-Valve Prolapse Patient with Hyperthyroidism." Cardiovascular and Cardiometabolic Journal (CCJ) 1, no. 2 (September 19, 2020): 57. http://dx.doi.org/10.20473/ccj.v1i2.2020.57-68.

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Rate-control is important management in patient with atrial fibrillation. The optimum rate control provides a decrease of symptoms, improves hemodynamics and prevents tachycardia-induced cardiomyopathy. Rate-control could be difficult to achieve because of patient's comorbidities and special treatment strategy is needed to resolve it. A-46-yo. male, came to ER with palpitation. Holosystolic murmur was heard at apex, radiating to axilla. ECG showed atrial fibrillation, with rapid ventricular response 180 bpm. Echocardiography showed dilated LA and LV, false-normal LV function with EF 59% and anterior mitral-valve prolapse with moderate mitral regurgitation. Acute treatment was administration of digoxin and beta blockers, but ventricular rate wasn’t controlled, until 1.5 mg doses of digoxin was administered. Then patient develops acute digitalis intoxication. After toxicity management, rapid ventricular rate recurs. Patient reevaluation showed hyperthyroidism with low TSH and high T4. Methimazole and propranolol was given and rate-control was achieved shortly after euthyroid state, in 2 months treatment. This patient suffered difficult rate-control despite guidelines-based management. Digitalis intoxication was developed after administration of several therapeutic doses. The diagnosis of hyperthyroidism is central in management of this case. Coexistent of hyperthyroidism and mitral-valve prolapse may be explained by genetic, autoimmune, and thyroid hormone effects in myocardium.

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Negroni, Maria Silvia, Arianna Marengo, Donatella Caruso, Alessandro Tayar, Patrizia Rubiolo, Flavio Giavarini, Simone Persampieri, et al. "A Case Report of Accidental Intoxication following Ingestion of Foxglove Confused with Borage: High Digoxinemia without Major Complications." Case Reports in Cardiology 2019 (November 29, 2019): 1–6. http://dx.doi.org/10.1155/2019/9707428.

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Foxglove (Digitalis purpurea L.) leaves are frequently confused with borage (Borago officinalis L.), which is traditionally used as a food ingredient. Due to the presence of the cardiac glycosides, mostly digitoxin, foxglove leaves are poisonous to human and may be fatal if ingested. A 55-year-old Caucasian woman complaining weakness, fatigue, nausea, and vomiting was admitted to the Emergency Department. Her symptoms started following consumption of a home-made savory pie with 5 leaves from a plant bought in a garden nursery as borage. Digoxinemia was high (10.4 μg/L). The patient was admitted to the cardiac intensive care unit for electrocardiographic monitoring. Two days after admission, a single episode of advanced atrioventricular (AV) block was recorded by telemetry, followed by a second-degree AV block episode. Plasma samples at day 11 were analysed by LC-MS spectrometry, and gitoxin was identified suggesting that this compound may be responsible for the clinical toxicity rather than digoxin. In the case of Digitalis spp. poisoning, laboratory data should be interpreted according to the clinical picture and method of analysis used since a variety of glycosides, which are chemically similar to the cardioactive glycosides but without or with fewer cardiac effects, may be incorrectly recognized as digoxin by the test, giving misleading results.

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Paci, A., G. Ciarimboli, and P. Biver. "Human placenta radioreceptor assay with digoxin and ouabain to detect endogenous digitalis-like factor(s) in human plasma and urine." Clinical Chemistry 42, no. 2 (February 1, 1996): 270–78. http://dx.doi.org/10.1093/clinchem/42.2.270.

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Abstract We describe the optimization and validation of a clinically feasible radioreceptor assay to detect endogenous digitalis-like factor(s) (EDLF) in human plasma and urine. The assay is based on the competitive replacement of 125I-labeled digoxin on human placenta membranes by ligands present in sample extracts. Digoxin and ouabain were used as calibrators. We also describe simple and effective methods for extraction and enrichment of EDLF from human plasma and urine. Assay sensitivity and precision were enhanced by using a sequential saturation technique with appropriate concentrations of tracer and receptors. Filtration was used to separate bound from free ligand. A two-step solid-state extraction with acetonitrile allowed the separation of two EDLFs with different polarity (EDLF-1 and EDLF-2) from the same plasma sample. A one-step solid-state extraction with methanol was suitable for urine. EDLF-1 and EDLF-2 in healthy adults were respectively 204 +/- 155 and 207 +/- 423 pmol/L ouabain equivalents, or 312 +/- 241 and 302 +/- 581 pmol/L digoxin equivalents. Plasma concentrations of EDLFs in newborns and pregnant women were higher than in healthy adults, and the concentrations in urine were higher than in plasma. Several cross-reactivity experiments showed that physiological concentrations of endogenous steroids and lipids did not inhibit binding, and supported the hypothesis that EDLFs are endogenous compounds other than the steroids and lipids also investigated.

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Zulian, Alessandra, Cristina I. Linde, Maria V. Pulina, Sergey G. Baryshnikov, Italia Papparella, John M. Hamlyn, and Vera A. Golovina. "Activation of c-SRC underlies the differential effects of ouabain and digoxin on Ca2+ signaling in arterial smooth muscle cells." American Journal of Physiology-Cell Physiology 304, no. 4 (February 15, 2013): C324—C333. http://dx.doi.org/10.1152/ajpcell.00337.2012.

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Cardiotonic steroids (CTS) of the strophanthus and digitalis families have opposing effects on long-term blood pressure (BP). This implies hitherto unrecognized divergent signaling pathways for these CTS. Prolonged ouabain treatment upregulates Ca2+ entry via Na+/Ca2+ exchanger-1 (NCX1) and TRPC6 gene-encoded receptor-operated channels in mesenteric artery smooth muscle cells (ASMCs) in vivo and in vitro. Here, we test the effects of digoxin on Ca2+ entry and signaling in ASMC. In contrast to ouabain treatment, the in vivo administration of digoxin (30 μg·kg−1·day−1 for 3 wk) did not raise BP and had no effect on resting cytolic free Ca2+ concentration ([Ca2+]cyt) or phenylephrine-induced Ca2+ signals in isolated ASMCs. Expression of transporters in the α2 Na+ pump-NCX1-TRPC6 Ca2+ signaling pathway was not altered in arteries from digoxin-treated rats. Upregulated α2 Na+ pumps and a phosphorylated form of the c-SRC protein kinase (pY419-Src, ∼4.5-fold) were observed in ASMCs from rats treated with ouabain but not digoxin. Moreover, in primary cultured ASMCs from normal rats, treatment with digoxin (100 nM, 72 h) did not upregulate NCX1 and TRPC6 but blocked the ouabain-induced upregulation of these transporters. Pretreatment of ASMCs with the c-Src inhibitor PP2 (1 μM; 4-amino-5-(4-chlorophenyl)-7-( t-butyl)pyrazolo[3,4- d]pyrimidine) but not its inactive analog eliminated the effect of ouabain on NCX1 and TRPC6 expression and ATP-induced Ca2+ entry. Thus, in contrast to ouabain, the interaction of digoxin with α2 Na+ pumps is unable to activate c-Src phosphorylation and upregulate the downstream NCX1-TRPC6 Ca2+ signaling pathway in ASMCs. The inability of digoxin to upregulate c-Src may underlie its inability to raise long-term BP.

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Ujhelyi, Michael R., and Sylvie Robert. "Pharmacokinetic Aspects of Digoxin-Specific Fab Therapy in the Management of Digitalis Toxicity." Clinical Pharmacokinetics 28, no. 6 (June 1995): 483–93. http://dx.doi.org/10.2165/00003088-199528060-00006.

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Widman, Ron. "The use of digoxin-specific Fab fragments for severe digitalis intoxication in children." Annals of Emergency Medicine 21, no. 11 (November 1992): 1409. http://dx.doi.org/10.1016/s0196-0644(05)81922-5.

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Woolf, Alan D., Thomas Wenger, Thomas W. Smith, and Frederick H. Lovejoy. "The Use of Digoxin-Specific Fab Fragments for Severe Digitalis Intoxication in Children." New England Journal of Medicine 326, no. 26 (June 25, 1992): 1739–44. http://dx.doi.org/10.1056/nejm199206253262604.

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Journal articles on the topic 'Digoxin (digitalis)'

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