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Artykuły w czasopismach na temat „Digoxin”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 25 lipca 2025

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1

Masse, Ève, Michel Germain, Marie-Sophie Lambert, Jacinthe Leclerc, Maude Lavallée, and Julie Méthot. "Analyse descriptive de l’efficacité et de la toxicité de la dose de charge intraveineuse de digoxine à l’Institut universitaire de cardiologie et de pneumologie de Québec–Université Laval." Pharmactuel 58, no. 1 (2025): 13–21. https://doi.org/10.63209/1545.

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Objectifs : Les objectifs de l’étude sont de déterminer la proportion de dose de charge de digoxine par voie intraveineuse associée à un contrôle satisfaisant de la fréquence cardiaque en contexte de fibrillation auriculaire ou de flutter auriculaire, d’identifier les doses de charge suivies d’une digoxinémie et de déterminer les facteurs associés à l’efficacité et à la toxicité de la digoxine. Méthode : Étude rétrospective descriptive de population longitudinale menée entre le 1er mai 2019 et le 1er mai 2023. Les variables comprenaient des données relatives au patient, à la prescription, ains

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2

Wang, Kai-di, Xiang Ding, Nan Jiang, et al. "Digoxin targets low density lipoprotein receptor-related protein 4 and protects against osteoarthritis." Annals of the Rheumatic Diseases 81, no. 4 (2021): 544–55. http://dx.doi.org/10.1136/annrheumdis-2021-221380.

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ObjectivesDysregulated chondrocyte metabolism is closely associated with the pathogenesis of osteoarthritis (OA). Suppressing chondrocyte catabolism to restore cartilage homeostasis has been extensively explored, whereas far less effort has been invested toward enhancing chondrocyte anabolism. This study aimed to repurpose clinically approved drugs as potential stimulators of chondrocyte anabolism in treating OA.MethodsScreening of a Food and Drug Administration-approved drug library; Assays for examining the chondroprotective effects of digoxin in vitro; Assays for defining the therapeutic ef

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Wermeling, Daniel P., Carinda J. Feild, Deborah A. Smith, Mary H. H. Chandler, G. Dennis Clifton, and Duane A. Boyle. "Effects of Long‐Term Oral Carvedilol on the Steady‐State Pharmacokinetics of Oral Digoxin in Patients With Mild to Moderate Hypertension." Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy 14, no. 5 (1994): 600–606. http://dx.doi.org/10.1002/j.1875-9114.1994.tb02857.x.

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The effect of multiple oral doses of carvedilol on steady‐state plasma digoxin pharmacokinetics was evaluated in 12 patients with mild to moderate hypertension. Area under the curve (AUC), mean maximum plasma concentration (Cmax), mean time to maximum concentration (Tmax), concentration at 24 hours after the dose (C24), creatinine clearance, renal digoxin clearance, and urinary digoxin excretion were determined after patients took oral digoxin 0.25 mg once/day for 2 weeks. Carvedilol was added to the regimen, and digoxin pharmacokinetics were assessed after 2 weeks of concurrent treatment. The

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4

Scalese, Michael J., and Dominick J. Salvatore. "Role of Digoxin in Atrial Fibrillation." Journal of Pharmacy Practice 30, no. 4 (2016): 434–40. http://dx.doi.org/10.1177/0897190016642361.

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Since its isolation in the 1930s, digoxin has played a pivotal role in the treatment of cardiac conditions including heart failure and supraventricular tachyarrhythmias. The parasympathomimetic activity makes digoxin a reasonable option for controlling ventricular rate in atrial fibrillation (AF). However, the unique pharmacokinetic properties, electrolyte-dependent effects, and P-glycoprotein drug interactions influence the clinical use of digoxin. In addition, the delayed onset and narrow therapeutic index can make digoxin utilization cumbersome and often necessitates serum drug monitoring.

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5

Qadhi, Rawabi, Tran Tran, Stefanie Lip, Ogor Team, Linsay Macallum, and Sandosh Padmanabhan. "ASSESSING THE CLINICAL IMPACT OF PROTON PUMP INHIBITOR-DIGOXIN INTERACTIONS: A RETROSPECTIVE COHORT STUDY OF HOSPITALIZATION AND MORTALITY RISK." Journal of Hypertension 42, Suppl 1 (2024): e253-e254. http://dx.doi.org/10.1097/01.hjh.0001022092.07013.e9.

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Objective: Digoxin pharmacokinetics are altered by co-administration of proton pump inhibitors (PPI). This may have adverse clinical consequences given digoxin's narrow therapeutic index. Our aim was to investigate whether there was evidence for the association of digoxin-PPI interactions with early adverse clinical events. Design and method: A retrospective cohort study was conducted using an anonymised extract of linked routinely collected Greater Glasgow and Clyde hospitals data between 01/01/2014 and 31/12/2022. Patients aged 40 years and over when commencing either a PPI or digoxin were c

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6

Atkins, Clarke E., Patti S. Snyder, Bruce W. Keene, and John E. Rush. "Effects of compensated heart failure on digoxin pharmacokinetics in cats." Journal of the American Veterinary Medical Association 195, no. 7 (1989): 945–50. https://doi.org/10.2460/javma.1989.195.07.945.

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Summary To evaluate the effects of compensated heart failure (hf) on digoxin pharmacokinetic properties in cats, 6 cats with dilated cardiomyopathy were compared with 6 clinically normal (control) cats. Digoxin tablets were administered at a dosage of 0.01 mg/kg of body weight, q 48 h for approximately 10 days, until presumed steady state was reached. Both groups were treated concomitantly with aspirin, furosemide, and a commercial low-salt diet. Retrospectively, control and hf cats were calculated to be at 95% and 97% steady state, respectively. At the time blood samples were collected, hf ca

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7

Ren, Yulin, Sijin Wu, Joanna E. Burdette, Xiaolin Cheng, and A. Douglas Kinghorn. "Structural Insights into the Interactions of Digoxin and Na+/K+-ATPase and Other Targets for the Inhibition of Cancer Cell Proliferation." Molecules 26, no. 12 (2021): 3672. http://dx.doi.org/10.3390/molecules26123672.

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Digoxin is a cardiac glycoside long used to treat congestive heart failure and found recently to show antitumor potential. The hydroxy groups connected at the C-12, C-14, and C-3′a positions; the C-17 unsaturated lactone unit; the conformation of the steroid core; and the C-3 saccharide moiety have been demonstrated as being important for digoxin’s cytotoxicity and interactions with Na+/K+-ATPase. The docking profiles for digoxin and several derivatives and Na+/K+-ATPase were investigated; an additional small Asn130 side pocket was revealed, which could be useful in the design of novel digoxin

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8

Suryoputri, Masita Wulandari, Laksmi Maharani, and Ika Mustikaningtias. "Penyesuaian Dosis Digoxin pada Pasien Gagal Jantung di RSUD Margono Soekardjo Purwokerto." JURNAL ILMU KEFARMASIAN INDONESIA 19, no. 2 (2021): 248. http://dx.doi.org/10.35814/jifi.v19i2.778.

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Tingginya prevalensi penyakit gagal jantung di Indonesia menyebabkan penggunaan obat digoxin semakin meningkat. Digoxin merupakan obat indeks terapi sempit yang perlu dilakukan pemantauan kadar obat dalam darah. Apabila estimasi kadar obat dalam darah tidak sesuai kisaran terapetik maka diperlukan penyesuaian dosis pada pasien, sehingga outcome klinis tercapai dan efek toksik dapat dihindari. Dosis pemeliharaan digoksin oral adalah 0,0625 – 0,125 mg/hari untuk pasien gagal jantung dan diharapkan kadar kisaran terapetik digoksin dalam darah berkisar 0,5-0,9 ng/ml. Tujuan penelitian ini adalah u

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9

Tuffaha, Haya, Laith Alshoaibi, Aya Al-tarawneh, et al. "Therapeutic drug monitoring of digoxin in Jordanian patients: Comparing saliva versus plasma." Journal of Research in Pharmacy 29, no. 4 (2024): 1485–94. https://doi.org/10.12991/jrespharm.1734554.

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Therapeutic drug monitoring (TDM) is measuring drug concentrations in plasma, serum or blood, to assure that drug concentrations can be maintained within a target range and to make sure the amount of medicine being administered is both safe and effective. TDM is essential to avoid digoxin toxicity due to its narrow therapeutic window (therapeutic levels of digoxin are 0.8-2.0 ng/mL. The toxic level is >2.4 ng/mL). TDM of digoxin is currently performed by plasma sampling, which is an invasive and painful procedure. The aim of the study is to study the pharmacokinetics of digoxin in plasma an

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10

Cremer, Edivaldo, Almir Conrrado Rodrigues de Lima, Larissa Laila Cassarotti, Gabrielle Rodrigues Munhoz, Romulo Jordão Barbosa Pedrinho, and Roberto Kenji Nakamura Cuman. "Mortalidade de indivíduos idosos cardíacos tratados com digoxina." Revista Recien - Revista Científica de Enfermagem 10, no. 29 (2020): 120–28. http://dx.doi.org/10.24276/rrecien2358-3088.2020.10.29.120-128.

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Objetivou-se descrever as taxas de mortalidade e sobrevida de idosos com insuficiência cardíaca que fizeram uso de digoxina, bem como identificar os fatores de risco associados à mortalidade. Prontuários de pacientes idosos (≥60 anos) atendidos no ambulatório de cardiologia para insuficiência cardíaca e que fizeram uso de digoxina foram triados e selecionados para este estudo retrospectivo. Variáveis sociodemográficas e clínicas foram mensuradas. A sobrevida foi verificada pelas curvas de Kaplan-Meier e teste log-rank. A regressão logística múltipla ajustada foi utilizada para avaliar os poten

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11

Allen, Nancy M., Gary D. Dunham, Jeffrey M. Sailstad, and John W. A. Findlay. "Clinical and Pharmacokinetic Profiles of Digoxin Immune Fab in Four Patients with Renal Impairment." DICP 25, no. 12 (1991): 1315–20. http://dx.doi.org/10.1177/106002809102501205.

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Minimal pharmacokinetic data on digoxin immune Fab are currently available, especially in patients with impaired renal function. The serum concentration-time profiles of total digoxin, free digoxin, and digoxin immune Fab in four patients with moderate to severe renal impairment who received digoxin immune Fab are presented. The calculated elimination half-life of digoxin immune Fab was 25–73 hours. The calculated elimination half-life of total digoxin was 24–72 hours. Free digoxin concentrations rebounded to a peak of 1–2.9 ng/mL 44–97 hours after the administration of digoxin immune Fab. The

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12

Moffett, Brady S., April Garner, Troy Zapata, Jeffrey Orcutt, Mary Niu, and Keila N. Lopez. "Serum digoxin concentrations and clinical signs and symptoms of digoxin toxicity in the paediatric population." Cardiology in the Young 26, no. 3 (2015): 493–98. http://dx.doi.org/10.1017/s1047951115000505.

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AbstractBackgroundSerum digoxin levels have limited utility for determining digoxin toxicity in adults. Paediatric data assessing the utility of monitoring serum digoxin concentration are scarce. We sought to determine whether serum digoxin concentrations are associated with signs and symptoms of digoxin toxicity in children.MethodsWe carried out a retrospective review of patients <19 years of age who received digoxin and had serum digoxin concentrations assessed between January, 2007 and June, 2013. Data collection included patient demographics, digoxin indication, serum digoxin concentrat

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13

Dasgupta, Amitava, Laura Kidd, Brian J. Poindexter, and Roger J. Bick. "Interference of Hawthorn on Serum Digoxin Measurements by Immunoassays and Pharmacodynamic Interaction With Digoxin." Archives of Pathology & Laboratory Medicine 134, no. 8 (2010): 1188–92. http://dx.doi.org/10.5858/2009-0404-oa.1.

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Abstract Context.—Hawthorn is an herb indicated for treating cardiac illness. Because a patient taking digoxin may also take hawthorn, we investigated potential interference of hawthorn in serum digoxin measurements using immunoassays as well as pharmacodynamic interaction between hawthorn and digoxin. Hawthorn contains alkaloids that are structurally similar to digoxin and may interfere with serum digoxin measurement using immunoassays. In addition, hawthorn has cardioactive properties similar to digoxin. Objective.—To study potential pharmacodynamic interaction between hawthorn and digoxin.

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14

Atkins, Clarke E., Patti S. Snyder, and Bruce W. Keene. "Effect of aspirin, furosemide, and commercial low-salt diet on digoxin pharmacokinetic properties in clinically normal cats." Journal of the American Veterinary Medical Association 193, no. 10 (1988): 1264–68. https://doi.org/10.2460/javma.1988.193.10.1264.

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Summary Steady-state serum digoxin concentration ([digoxin]) was measured for 48 hours in 6 healthy cats after they were treated with digoxin tablets (0.01 mg/kg of body weight, q 48 h) for 10 days and again after concurrent treatment of identical duration with orally administered digoxin, aspirin (80 mg, q 48 h), furosemide (2 mg/kg, q 12 h), and a commercial low-salt diet. The concurrent treatment substantially altered digoxin pharmacokinetic properties, with a resultant increase in peak (mean ± sem; from 2.1 ± 0.35 to 3.3 ± 0.6 ng/ml), 8-hour (from 1.4 ± 0.35 to 2.5 ± 0.64 ng/ml), and 48-ho

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15

Bizjak, Eric D., and Vincent F. Mauro. "Digoxin–Macrolide Drug Interaction." Annals of Pharmacotherapy 31, no. 9 (1997): 1077–79. http://dx.doi.org/10.1177/106002809703100918.

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Macrolide antibiotics appear to be able to enhance the oral bioavailability of digoxin by altering the gastrointestinal flora that metabolize digoxin to less active dihydro metabolites, thus leading to increased serum digoxin concentrations and possible digoxin toxicity in select patients stabilized on digoxin therapy. This interaction may be of clinical importance in up to 10% of the population. Currently, the orally administered erythromycin, clarithromycin, and roxithromycin have been implicated. Although realistically this interaction may be encountered rarely, when it does occur, it can b

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16

&NA;. "Anti-digoxin polyclonal antibody/digoxin." Reactions Weekly &NA;, no. 1283 (2010): 12. http://dx.doi.org/10.2165/00128415-201012830-00041.

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Doolittle, M. H., K. Lincoln, and S. W. Graves. "Unexplained increase in serum digoxin: a case report." Clinical Chemistry 40, no. 3 (1994): 487–92. http://dx.doi.org/10.1093/clinchem/40.3.487.

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Abstract We describe a patient with unexpectedly high serum digoxin after cardiac surgery. To control atrial fibrillation in the immediate postoperative period, she was given a brief trial of digoxin (four 0.25-mg doses) over 12 h. Serum digoxin 6 h later was 2.5 micrograms/L. Two days later, the patient developed ventricular fibrillation, which progressed to cardiac arrest. During or immediately after resuscitation, blood was drawn for a digoxin measurement, and the concentration reported was 9.3 micrograms/L; this result was verified by repeated analysis. Digoxin decreased rapidly and progre

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18

Alderman, Christopher P., and Peter D. Allcroft. "Digoxin–Itraconazole Interaction: Possible Mechanisms." Annals of Pharmacotherapy 31, no. 4 (1997): 438–40. http://dx.doi.org/10.1177/106002809703100410.

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Objective To document a case in which the administration of itraconazole was associated with an apparent decrease in digoxin clearance, resulting in an increase in the serum digoxin concentration. Case Summary A man receiving digoxin for atrial fibrillation was concurrently treated with itraconazole 200 mg/d for esophageal candidiasis. The estimated urinary digoxin clearance was decreased during this combination therapy. Discussion Digoxin is primarily cleared by the kidneys, and the mechanism of renal clearance involves both glomerular filtration and tubular secretion. We postulate that itrac

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Dasgupta, Amitava, Edward Kang, Margaret Olsen, Jeffrey K. Actor, and Pradip Datta. "Interference of Asian, American, and Indian (Ashwagandha) Ginsengs in Serum Digoxin Measurements by a Fluorescence Polarization Immunoassay Can Be Minimized by Using a New Enzyme-Linked Chemiluminescent Immunosorbent or Turbidimetric Assay." Archives of Pathology & Laboratory Medicine 131, no. 4 (2007): 619–21. http://dx.doi.org/10.5858/2007-131-619-ioaaai.

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Abstract Context.—Ginsengs are widely used by the general population. These herbs interfere with serum digoxin measurement using the fluorescence polarization immunoassay. Objective.—To assess potential interference of different ginsengs (Asian, American, and Indian, also known as Ashwagandha) in vitro and in vivo in a mouse model by using a new enzyme-linked chemiluminescent immunosorbent digoxin assay and an existing turbidimetric assay. Comparisons were made with the fluorescence polarization immunoassay. Design.—Aliquots of drug-free serum pools were supplemented with ginseng and apparent

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20

Hursting, M. J., V. A. Raisys, K. E. Opheim, J. L. Bell, G. B. Trobaugh, and T. W. Smith. "Determination of free digoxin concentrations in serum for monitoring Fab treatment of digoxin overdose." Clinical Chemistry 33, no. 9 (1987): 1652–55. http://dx.doi.org/10.1093/clinchem/33.9.1652.

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Abstract A rapid method for assessing the free digoxin concentration in the serum of digoxin-overdosed patients receiving treatment with digoxin-specific Fab fragments has been developed. For this method, a protein-free ultrafiltrate is prepared from the patient's serum, and the digoxin in the ultrafiltrate (free digoxin) is measured by fluorescence polarization immunoassay. Both the inaccuracies associated with measurements of total digoxin by immunoassay in the presence of Fab and the long turnaround time associated with measurements of free digoxin by equilibrium dialysis were avoided. Good

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21

Skogen, W. F., M. R. Rea, and R. Valdes. "Endogenous digoxin-like immunoreactive factors eliminated from serum samples by hydrophobic silica-gel extraction and enzyme immunoassay." Clinical Chemistry 33, no. 3 (1987): 401–4. http://dx.doi.org/10.1093/clinchem/33.3.401.

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Abstract Elimination of endogenous digoxin-like immunoreactive factors (DLIF) that interfere with accurate measurement of digoxin requires use of a highly specific anti-digoxin antibody, or that DLIF be separated from digoxin before immunoassay. Several commercial digoxin-assay kits include a step for separating serum proteins and other substances from digoxin before immunoassay. We tested six different immunoassay methods (some having pretreatment steps) for their ability to detect DLIF in serum from patients in renal failure, pregnant women, and neonates, all of whom were not taking digoxin.

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Suharyani, Ine. "EVALUASI PENGGUNAAN KOMBINASI OBAT DIGOKSIN DAN FUROSEMID." Jurnal Kesehatan 6, no. 2 (2020): 700–707. http://dx.doi.org/10.38165/jk.v6i2.150.

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Gagal jantung merupakan kondisi ketika otot jantung sangat lemah sehingga tidak bisa memompa cukup darah keseluruh tubuh dengan tekanan yang tepat. Penelitian ini bertujuan untuk mengetahui ketepatan penggunaan kombinasi digoksin dan furosemid berdasarkan aspek klinis serta pengeluaran kalium dalam tubuh. Penelitian ini dilakukan dengan metode retrospektif yaitu menggunakan data yang telah lalu yang diperoleh dari bagian rekam medik. Data yang diambil adalah resep penggunaan obat kombinasi digoksin dan furosemid yang ada di poli klinik jantung pada periode Oktober – Desember 2014. Hasil peneli

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Aruna, Augustine S., and Sandra G. Jue. "Digoxin Immune Fab Administration following an Unexplained Increase in Serum Digoxin Concentration." Journal of Pharmacy Technology 10, no. 6 (1994): 246–49. http://dx.doi.org/10.1177/875512259401000604.

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Objective: To report a case of digoxin immune Fab (DIF) administration following an unexplained increase in serum digoxin concentration in an asymptomatic patient with chronic renal failure. Case Summary: A 70-year-old man presented to the hospital with congestive heart failure, atrial fibrillation, chronic renal failure, and suspected digoxin toxicity. By day 3, he developed a more stable cardiac rhythm with nodal beats. His last known digoxin dose was 12 hours prior to admission. No explanation for an elevated serum digoxin concentration 48 hours after admission could be found. Despite absen

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North, Donald S., Allan L. Mattern, and Wesley W. Hiser. "The Influence of Diltiazem Hydrochloride on Trough Serum Digoxin Concentrations." Drug Intelligence & Clinical Pharmacy 20, no. 6 (1986): 500–503. http://dx.doi.org/10.1177/106002808602000615.

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A significant drug interaction between verapamil and digoxin, resulting in elevated serum digoxin concentrations, has been well documented in the medical literature. However, a similar interaction between digoxin and the calcium channel blockers nifedipine and diltiazem has not been conclusively established. This study investigated the influence of diltiazem hydrochloride on trough serum concentrations of concurrently administered digoxin in eight healthy volunteers. During the control phase of the study, volunteers were administered digoxin 0.25 mg/d for 13 days, and subsequently judged to be

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Syahputra, Rony Abdi, Urip Harahap, Aminah Dalimunthe, M. Pandapotan Nasution, and Denny Satria. "Drug therapy monitoring (TDM) of Digoxin: safety and efficacy review." Pharmacia 69, no. 2 (2022): 261–64. http://dx.doi.org/10.3897/pharmacia.69.e81467.

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Digoxin was developed as a novel medication for the treatment of heart failure and atrial fibrillation (AF) 200 years ago. This investigation began with a PubMed and Google Scholar search for various papers using the terms digoxin safety and efficacy, digoxin in heart failure, and digoxin in atrial fibrillation. Digoxin should be administered at a dose of 0.5–0.7 ng/mL in individuals with heart failure and reduced ejection fraction. Digoxin should be administered to decrease hospital readmissions, although SDC, creatinine, and potassium levels should be continuously maintained to limit the ris

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Syahputra, Rony Abdi, Urip Harahap, Aminah Dalimunthe, M. Pandapotan Nasution, and Denny Satria. "Drug therapy monitoring (TDM) of Digoxin: safety and efficacy review." Pharmacia 69, no. (2) (2022): 261–64. https://doi.org/10.3897/pharmacia.69.e81467.

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Digoxin was developed as a novel medication for the treatment of heart failure and atrial fibrillation (AF) 200 years ago. This investigation began with a PubMed and Google Scholar search for various papers using the terms digoxin safety and efficacy, digoxin in heart failure, and digoxin in atrial fibrillation. Digoxin should be administered at a dose of 0.5–0.7 ng/mL in individuals with heart failure and reduced ejection fraction. Digoxin should be administered to decrease hospital readmissions, although SDC, creatinine, and potassium levels should be continuously maintained to limit the ris

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Atkins, Clarke E., Patti S. Snyder, Bruce W. Keene, John E. Rush, and Steven Eicker. "Efficacy of digoxin for treatment of cats with dilated cardiomyopathy." Journal of the American Veterinary Medical Association 196, no. 9 (1990): 1463–69. http://dx.doi.org/10.2460/javma.1990.196.09.1463.

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Summary The role of digoxin in treatment of cats with dilated cardiomyopathy and other forms of myocardial failure is unclear. We evaluated the chronotropic and inotropic effects of digoxin by comparing baseline, noninvasive indices of cardiac performance with those obtained after 9 ± 1.3 (mean ± SEM) days of digoxin treatment in 6 cats with heart failure attributable to dilated cardiomyopathy. Two-dimensionally directed, M-mode echocardiography and electrocardiography were used to determine left ventricular shortening fraction, preejection period (PEP), ejection time (LVET), PEP to LVET ratio

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Stone, J. A., and S. J. Soldin. "An update on digoxin." Clinical Chemistry 35, no. 7 (1989): 1326–31. http://dx.doi.org/10.1093/clinchem/35.7.1326.

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Abstract This review deals briefly with recent developments in the therapeutic drug monitoring of digoxin. Strategies for decreasing the interference by digoxin metabolites, digoxin-like factors, and spironolactone metabolites in immunoassays of digoxin are discussed. Other issues addressed include the development of alternative methods of analysis, such as receptor assays and "high-pressure" liquid chromatography; digoxin-like factors in hypertension; drug-drug interactions; redistribution of digoxin stores in the body; and forensic considerations.

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Crome, P., B. Curl, D. Holt, G. N. Volans, P. N. Bennett, and D. S. Cole. "Digoxin and Cimetidine: Investigation of the Potential for a Drug Interaction." Human Toxicology 4, no. 4 (1985): 391–99. http://dx.doi.org/10.1177/096032718500400405.

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1 The potential for a pharmacokinetic interaction between digoxin and cimetidine was investigated in a series of studies. 2 In a single-dose cross-over study in healthy volunteer subjects cimetidine increased the area under the plasma digoxin concentration curve and the peak plasma digoxin concentration. 3 In a repeated-dose study in healthy volunteer subjects taking digoxin 0.25 mg daily, co-administration of cimetidine resulted in an average increase in plasma digoxin concentration of 0.15 ng/ml. 4 In a repeated-dose study in healthy volunteer subjects taking digoxin 0.5 mg daily, co-adminis

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Patel, Riya, Prancy Patel, Nisarg Patel, Jatin Gangwani, and Dhaval Patel. "Case report on the interaction between furosemide and digoxin that caused digoxin toxicity." Journal of Drug Delivery and Therapeutics 12, no. 5-S (2022): 9–12. http://dx.doi.org/10.22270/jddt.v12i5-s.5717.

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Toxicity from digitalis is a typical clinical issue. In this case, the interaction of digoxin and furosemide is becoming more widely recognised as a major cause of digitalis toxicity. We present an abnormal ECG that demonstrates digoxin-induced cardiotoxicity. We report a case of a Digoxin toxicity in a 79-year-old male patient admitted with complains of nausea, increase frequency of micturition, decrease appetite, increase nocturia, shortness of breathing. The patient is taking furosemide and digoxin as past medication for Heart block and Chronic kidney disease treatment. In patient, Serum di

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Stenzel, R., and B. Reckmann. "Cross-Reactivity of Anti-Digoxin Antibodies with Digitoxin Depends on Tracer Structure." Clinical Chemistry 38, no. 11 (1992): 2228–32. http://dx.doi.org/10.1093/clinchem/38.11.2228.

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Abstract The most common methods for measuring digoxin concentrations in serum are immunoassays. The prerequisite for exact determination of the digoxin value is an antibody that specifically binds digoxin. Because digitoxin differs from digoxin only in the C-12 hydroxy group, it is difficult to obtain anti-digoxin antibodies that do not cross-react with this compound. During the development of a fluorescence polarization immunoassay (FPIA) for digoxin, we investigated digoxin tracers with different structures. We found that in FPIA the digitoxin cross-reactivity of an antibody could be reduce

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Ravis, W. R., W. M. Pedersoli, and J. D. Turco. "Pharmacokinetics and interactions of digoxin with phenobarbital in dogs." American Journal of Veterinary Research 48, no. 8 (1987): 1244–49. https://doi.org/10.2460/ajvr.1987.48.08.1244.

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SUMMARY In one experiment, 5 dogs were administered digoxin (0.022 mg/kg of body weight, iv), were rested for 2 weeks, were then given phenobarbital (13.2 mg/kg orally) for 14 days, and then were given digoxin again (0.022 mg/kg, iv). Comparing prephenobarbital (control) digoxin half-lives of 42.4 ± 8.8 hours and postphenobarbital digoxin half-lives of 18.0 ± 2.2 hours, the half-life was significantly (P < 0.05) decreased after phenobarbital administration. Clearance was increased by 84%, and the volume of distribution given was decreased by 34%. In a second experiment, 5 dogs were given di

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Soldin, S. J. "Digoxin--issues and controversies." Clinical Chemistry 32, no. 1 (1986): 5–12. http://dx.doi.org/10.1093/clinchem/32.1.5.

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Abstract This review deals briefly with the clinical pharmacology of digoxin and reviews in some depth the problems inherent in methods of digoxin measurement. Digoxin-like factors (materials that cross react in digoxin immunoassays) are discussed, and some current evidence suggesting the existence of a new hormone, endoxin (endogenous digoxin), is summarized.

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Morton, Mark R., and James W. Cooper. "Erythromycin-Induced Digoxin Toxicity." DICP 23, no. 9 (1989): 668–70. http://dx.doi.org/10.1177/106002808902300908.

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The potential interaction between certain antibiotics and digoxin has been discussed in the literature; however, few cases of actual erythromycin-induced digoxin toxicity have been reported. We present a case in which an 86-year-old woman who was taking digoxin 0.25 mg/d developed probable digoxin toxicity after the administration of erythromycin for the treatment of otitis media and streptococcal pharyngitis. Her digoxin concentration increased from a trough of 1.9 to 5.1 nmol/L six days after the erythromycin was started. Digoxin was discontinued and restarted approximately six weeks later w

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Chillet, P., J. M. Korach, D. Petitpas, et al. "Digoxin Poisoning and Anuric Acute Renal Failure: Efficiency of the Treatment Associating Digoxin-Specific Antibodies (Fab) and Plasma Exchanges." International Journal of Artificial Organs 25, no. 6 (2002): 538–41. http://dx.doi.org/10.1177/039139880202500608.

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Digoxin-specific antibodies (Fab) are currently the treatment of choice for digoxin intoxication. These fragments bind to digoxin, leading to Fab-digoxin complexes, and promote the release of receptor-bound digoxin. These complexes are renally excreted. In the case of anuria, they could be dissociated and lead to renewed intoxication. In this case plasma exchanges are proposed. We report the case of an anuric patient with digoxin intoxication, treated with a Fab injection, followed by a plasma exchange 16 hours later, a second Fab injection was given followed by two plasma exchanges, 38 and 86

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Guerriero, Stephanie E., Eli Ehrenpreis, and Kathryn L. Gallagher. "Two Cases of Clarithromycin‐Induced Digoxin Toxicity." Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy 17, no. 5 (1997): 1035–37. http://dx.doi.org/10.1002/j.1875-9114.1997.tb03796.x.

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Two patients experienced clarithromycin‐induced digoxin toxicity. Both had stable renal function within normal limits and had been maintained on a consistent dosage of digoxin. No changes in drug therapy had been made except for the addition of clarithromycin. Administration of clarithromycin to patients receiving long‐term digoxin therapy may induce digoxin toxicity. When concomitant therapy is employed, patients should be closely monitored for clinical signs and symptoms of digoxin toxicity, and digoxin concentrations should be measured to avoid it.

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Pudek, M. R., D. W. Seccombe, B. E. Jacobson, and K. Humphries. "Effect of assay conditions on cross reactivity of digoxin-like immunoreactive substance(s) with radioimmunoassay kits." Clinical Chemistry 31, no. 11 (1985): 1806–10. http://dx.doi.org/10.1093/clinchem/31.11.1806.

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Abstract One or more digoxin-like immunoreactive substances (DLIS), most frequently present in serum of premature and full-term neonates. cross react to various extents with different digoxin immunoassay kit reagents. Mostly, this variation is attributed to the relative cross reactivity of DLIS with the antiserum in each kit. However, modification of standard assay procedures for digoxin can also greatly alter the relative cross reactivity of DLIS. Using sequential RIA kit methods for digoxin by 20 to 60% relative to the standard equilibrium RIA mode. Cross reactivity was decreased still more

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Treacy, Oliver. "Digoxin: Review of Current Laboratory Practice and Considerations." Clinical Biochemist Reviews 43, no. 1 (2023): 11–16. http://dx.doi.org/10.33176/aacb-22-00002.

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Digoxin is a drug used for its effects on the heart, particularly its effect on rate and strength of contraction. Levels are particularly useful in clinical practice owing to its narrow therapeutic index, with toxicity and therapeutic levels being relatively close. Clinically, digoxin toxicity can be acute or chronic, and can manifest with signs and symptoms related to the gastrointestinal system, nervous system, and cardiovascular system. Given digoxin toxicity can lead to fatal dysrhythmias, accurate and reproducible analysis by the laboratory is essential in the treatment of patients with s

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Shereen, Shaima, Mohammed Fareedullah, and Raqshan Jabeen. "A case report on digoxin toxicity." International Journal of Basic & Clinical Pharmacology 13, no. 3 (2024): 389–91. http://dx.doi.org/10.18203/2319-2003.ijbcp20240998.

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Digoxin is an inotropic drug that is commonly prescribed in patient with heart related diseases. The effective dose of digoxin is 0.8-2.0 ng/ml beyond which digoxin causes toxic effects like visual dysfunction, irregular heartbeat, and cardiovascular collapse. Digoxin toxicity is caused due to increased automaticity and inotropy due to intracellular calcium and decreased dromotropy due to poisoning of sodium potassium transporter and AV nodal blockade. Digoxin toxicity should be assessed by continuous hemodynamic and cardiac monitoring including 12-lead electrocardiogram. There should be timel

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Christenson, R. H., S. D. Studenberg, S. Beck-Davis, and F. A. Sedor. "Digoxin-like immunoreactivity eliminated from serum by centrifugal ultrafiltration before fluorescence polarization immunoassay of digoxin." Clinical Chemistry 33, no. 4 (1987): 606–8. http://dx.doi.org/10.1093/clinchem/33.4.606.

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Abstract Digoxin determined in the Abbott "TDx" by fluorescence polarization immunoassay by the manufacturer's recommended method involving precipitation of protein with 5-sulfosalicylic acid (SSA) is subject to interference from endogenous compounds having digoxin-like immunoreactivity. Guided by the work of Graves et al. (Clin Chem 1986;32:1506-9), we eliminated interference caused by digoxin-like immunoreactivity by substituting ultrafiltration for precipitation with SSA to remove protein. Using the manufacturer's method, we quantified digoxin in serum from 53 patients in three clinically d

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Datta, P., L. Xu, S. Malik, et al. "Effect of antibody specificity on results of selected digoxin immunoassays among various clinical groups." Clinical Chemistry 42, no. 3 (1996): 373–79. http://dx.doi.org/10.1093/clinchem/42.3.373.

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Abstract We examined the specificity of three automated digoxin immunoassays (Abbott TDxFLx Digoxin II assay, Baxter-Dade Stratus II Digoxin assay, and Ciba Corning ACS Digoxin assay) applied without modification to (a) sera from 229 digoxin-free patients in 12 cohorts associated with nonspecific or endogenous digoxin-like immunoreactive factor (DLIF) interference, and (b) drug-free serum supplemented with the major metabolites and analogs of digoxin. We observed three patterns of apparent digoxin results among the DLIF samples: one common to kidney and liver failure patients, where TDx and St

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Nawarskas, James J., David M. McCarthy, and Sarah A. Spinier. "Digoxin Toxicity Secondary to Clarithromycin Therapy." Annals of Pharmacotherapy 31, no. 7-8 (1997): 864–66. http://dx.doi.org/10.1177/106002809703100711.

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OBJECTIVE: To report a case of digoxin toxicity thought to be secondary to clarithromycin therapy. CASE SUMMARY: A 78-year-old white woman with congestive heart failure taking digoxin 0.25 mg po qd presented to our hospital with nausea, vomiting, and diarrhea. She had taken clarithromycin 500 mg po bid for 3 days, and a serum digoxin concentration obtained the day of admission was 4.4 μg/L. An electrocardiogram (ECG) done on admission revealed ST segment changes consistent with digoxin effect and later asymptomatic, nonsustained ventricular tachycardia (NSVT). Clarithromycin was discontinued a

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Dasgupta, Amitava, Amanda Peterson, Alice Wells, and Jeffrey K. Actor. "Effect of Indian Ayurvedic Medicine Ashwagandha on Measurement of Serum Digoxin and 11 Commonly Monitored Drugs Using Immunoassays: Study of Protein Binding and Interaction With Digibind." Archives of Pathology & Laboratory Medicine 131, no. 8 (2007): 1298–303. http://dx.doi.org/10.5858/2007-131-1298-eoiama.

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Abstract Context.—Ashwagandha, a popular Ayurvedic medicine, is now available in the United States. Alkaloids found in this herb have structural similarity with digoxin. Objective.—To study potential interference of Ashwagandha with serum digoxin measurement by immunoassays. Potential interference was also investigated with immunoassays for 11 other commonly monitored drugs. In addition, interaction of components of Ashwagandha with the Fab fragment of antidigoxin antibody (Digibind) was investigated. Design.—Two different brands of liquid extract and 1 dry powdered form of Ashwagandha were us

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Penkauskaitė, Justina, Romaldas Mačiulaitis, Birutė Varanavičienė, Irena Milvidaitė, and Birutė Tarutienė. "Evaluation of needs for therapeutic monitoring of digoxin in a tertiary hospital." Medicina 45, no. 1 (2009): 46. http://dx.doi.org/10.3390/medicina45010007.

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Objectives. To collect the data about the consumption of digoxin, evaluate the tendencies towards usage of this drug during 2004–2007, and to find departments, which cover the main part of digoxin consumption in a tertiary hospital. To evaluate the intensity of serum digoxin concentration measurements during 2005–2007. Material and methods. Our study was carried out in a tertiary hospital with 2600 beds and 63 departments. Consumption of digoxin is expressed in defined daily doses per 100 occupied beds daily during 2004–2007. All serum concentration measurements in 2005–2007 were evaluated. Re

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Gheshlaghi, Farzad, Anselm Wong, Gholamali Dorooshi, et al. "Ten Years of Experience in Treating Patients With Digoxin Toxicity Without Using Digoxin Fab Antibody." International Journal of Medical Toxicology and Forensic Medicine 11, no. 1 (2021): 31239.1–31239.10. http://dx.doi.org/10.32598/ijmtfm.v11i1.31239.

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Background: Digoxin is extensively prescribed for cardiac diseases, so its chronic or acute toxicity commonly occur. Although digoxin specific antibodies (anti-digoxin Fab) are recommended to be used in patients with cardiac symptoms of digoxin toxicity, there is ongoing controversy about the effectiveness and dose of anti-digoxin Fab. Because our department lacks access to anti-digoxin Fab and the high cost of the antidote, we evaluated 10 years of experience in treating patients with digoxin toxicity without using digoxin Fab antibodies considering outcomes. Methods: A retrospective study wa

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Ferrari, Samira Jorge, Reinaldo Bulgarelli Bestetti, Augusto Cardinalli-Neto, and Talita Bottan Bortoluzzi. "Digoxin serum levels in patients with Chagas' cardiomyopathy and heart failure." Revista da Sociedade Brasileira de Medicina Tropical 43, no. 5 (2010): 496–99. http://dx.doi.org/10.1590/s0037-86822010000500004.

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INTRODUCTION: The purpose of this study was to determine digoxin serum concentrations in patients with Chagas' cardiomyopathy with chronic heart failure, because little is known concerning this laboratory test in patients with this condition. METHODS: This study focuses on 29 (29%) out of 101 patients with chronic heart failure secondary to Chagas' cardiomyopathy receiving digoxin therapy. Digoxin was measured by the immune-enzymatic method. RESULTS: New York Heart Association Functional Class III/IV was noted in 13 (45%) patients. The mean potassium serum level was 4.3± 0.5mEq/L, mean creatin

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Tanaka, Hideko, Kana Matsumoto, Kazuyuki Ueno, et al. "Effect of Clarithromycin on Steady-State Digoxin Concentrations." Annals of Pharmacotherapy 37, no. 2 (2003): 178–81. http://dx.doi.org/10.1177/106002800303700202.

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OBJECTIVE: To evaluate the magnitude and dose-relatedness of the effect of clarithromycin on the pharmacokinetics of digoxin, and to compare the effects of clarithromycin with those of P-glycoprotein inhibitors. METHODS: Eight Japanese inpatients with congestive heart failure participated in this study. Each patient received oral digoxin therapy for at least 7 days and were coadministered oral clarithromycin to prevent or treat pneumonia. To evaluate the effects of clarithromycin on the pharmacokinetics of digoxin, digoxin concentrations were compared before and after coadministration of clari

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Singkham, Noppaket, Yuttana Wongsalap, Duangkamon Poolpun, Sirichok Phetnoo, and Chuthalak Somkhon. "Utilization of Digoxin among Hospitalized Older Patients with Heart Failure and Atrial Fibrillation in Thailand: Prevalence, Associated Factors, and Clinical Outcomes." Annals of Geriatric Medicine and Research 25, no. 4 (2021): 260–68. http://dx.doi.org/10.4235/agmr.21.0098.

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BackgroundDigoxin is used to control heart rate in patients with heart failure (HF) and atrial fibrillation (AF). However, its use is often limited in older patients, as they are prone to digoxin toxicity. This study aimed to determine the prevalence of digoxin use, investigate the factors associated with digoxin use, and explore the association between digoxin use and clinical outcomes in older Thai patients with HF and AF.MethodsThis cross-sectional study used data obtained from an electronic medical records database. We performed logistic regression analysis to determine the prevalence of d

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Fraser, Gilles L., David E. Wennberg, John D. Dickens, and Costas T. Lambrew. "Changing Physician Behavior in Ordering Digoxin Assays." Annals of Pharmacotherapy 30, no. 5 (1996): 449–54. http://dx.doi.org/10.1177/106002809603000502.

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OBJECTIVE: TO assess the ability to modify physicians' use of serum digoxin assays in a sustained fashion through (1) an educational intervention by a clinical pharmacist, and (2) changes in the computerized medical information system. DESIGN: A before/after methodology was used to compare test use by hospital staff physicians in two phases. Phase 1 was an educational intervention conducted by a clinical pharmacist with an 8-month follow-up. Phase 2 was a medical information system intervention with a 12-month follow-up. PATIENTS: Adult inpatients from July 1990 through December 1993 who recei

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Mayan, Haim, Einat Bloom, and Amnon Hoffman. "Use of Digoxin Monitoring in a Hospital Setting as an Essential Tool in Optimizing Therapy." Journal of Pharmacy Technology 18, no. 3 (2002): 133–37. http://dx.doi.org/10.1177/875512250201800304.

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Objective To determine what triggers the use of digoxin therapeutic drug monitoring (TDM) that adheres to established indications and the change in digoxin dosage after the result of monitoring is obtained. Methods This prospective study included 86 patients admitted to 6 medicine wards and 2 intensive cardiac care unit wards in a tertiary-care center. Data on patients' demographics, drug therapy, serum chemistry values, indications for digoxin therapy, indications for ordering the drug assay, timing of the blood sample relative to administration of the last dose, and physicians' decisions aft

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