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Journal articles on the topic 'Digoxin'

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Author: Grafiati

Published: 4 June 2021

Last updated: 30 July 2024

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1

Wang, Kai-di, Xiang Ding, Nan Jiang, Chao Zeng, Jing Wu, Xian-yi Cai, Aubryanna Hettinghouse, et al. "Digoxin targets low density lipoprotein receptor-related protein 4 and protects against osteoarthritis." Annals of the Rheumatic Diseases 81, no. 4 (December 1, 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 effects of digoxin using a surgically-induced OA model; A propensity-score matched cohort study using The Health Improvement Network to examine the relationship between digoxin use and the risk of joint OA-associated replacement among patients with atrial fibrillation; identification and characterisation of the binding of digoxin to low-density lipoprotein receptor-related protein 4 (LRP4); various assays, including use of CRISPR-Cas9 genome editing to delete LRP4 in human chondrocytes, for examining the dependence on LRP4 of digoxin regulation of chondrocytes.ResultsSerial screenings led to the identification of ouabain and digoxin as stimulators of chondrocyte differentiation and anabolism. Ouabain and digoxin protected against OA and relieved OA-associated pain. The cohort study of 56 794 patients revealed that digoxin use was associated with reduced risk of OA-associated joint replacement. LRP4 was isolated as a novel target of digoxin, and deletion of LRP4 abolished digoxin’s regulations of chondrocytes.ConclusionsThese findings not only provide new insights into the understanding of digoxin’s chondroprotective action and underlying mechanisms, but also present new evidence for repurposing digoxin for OA.

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2

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 (September 10, 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 AUC and Cmax for digoxin increased by 14% and 32%, respectively (p<0.05), with no change in Tmax. The 24‐hour urinary digoxin excretion and 24‐hour renal digoxin clearance increased by 45% and 26%, respectively (p<0.05), with no change in creatinine clearance. Carvedilol appears to increase digoxin's oral bioavailability as well as renal elimination. The absolute change in digoxin pharmacokinetics was small and not clinically significant. The significance of the interaction in other patient populations remains to be studied.

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Scalese, Michael J., and Dominick J. Salvatore. "Role of Digoxin in Atrial Fibrillation." Journal of Pharmacy Practice 30, no. 4 (April 10, 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. Despite digoxin’s extensive history, recent literature has cast doubt on the efficacy and safety of this medication in the population with AF. Large amounts of data suggest digoxin offers no benefit on mortality and may increase the risk of mortality though this was not consistent in all evaluations. While robust, the majority of the available studies are not randomized which limits the ability to draw firm conclusions. The potential risk of mortality must be weighed against the expected benefits of digoxin use to make individualized patient care decisions. Clinicians should refrain from utilizing digoxin monotherapy for rate control in AF when other options are viable.

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4

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 (May 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 classified into: PPI only, digoxin only, or both PPI and digoxin. Record linkage provided 60-day follow-up data on all-cause, gastrointestinal and arrythmia-related hospitalisations or deaths. Univariate and multivariable Cox proportional hazards models were run applying inverse probability of treatment weighting for age, sex, SIMD, ethnicity, and background conditions to address confounding by indication. Results: The cohort comprised 200,769 (92%) patients who commenced on a PPI only, 3,358 (1.5%) on digoxin only, and 14,126 (6.5%) on both. The 53-day crude incidence of all-cause hospitalisation or death was 7.7%, 11.0% and 16.3% respectively. Compared with PPI only, the risk was higher for those taking a PPI plus digoxin (adjusted HR 1.93, 95% CI 1.81;2.07) but not digoxin only. This was explained by gastrointestinal conditions which were the most frequent cause of hospitalisation and death. Arrythmia-related hospitalisations/deaths were more likely among those taking digoxin even if not also taking a PPI. Conclusions: Concomitant use of a PPI and digoxin significantly increases the risk of early clinically significant gastrointestinal complications.

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5

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 (June 16, 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-like antitumor agents. In addition, the docking scores for digoxin and its derivatives were found to correlate with their cytotoxicity, indicating a potential use of these values in the prediction of the cancer cell cytotoxicity of other cardiac glycosides. Moreover, in these docking studies, digoxin was found to bind to FIH-1 and NF-κB but not HDAC, IAP, and PI3K, suggesting that this cardiac glycoside directly targets FIH-1, Na+/K+-ATPase, and NF-κB to mediate its antitumor potential. Differentially, digoxigenin, the aglycon of digoxin, binds to HDAC and PI3K, but not FIH-1, IAP, Na+/K+-ATPase, and NF-κB, indicating that this compound may target tumor autophagy and metabolism to mediate its antitumor propensity.

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6

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 (December 28, 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 untuk mengetahui estimasi kadar digoxin dalam darah pada pasien gagal jantung dan perhitungan penyesuaian dosis secara pendekatan farmakokinetika agar kadar obat dalam darah sesuai kisaran terapetik. Metode penelitian ini adalah observasional kuantitatif yang dilakukan secara prospektif. Pengambilan sampel menggunakan metode total sampling. Hasil penelitian ini menunjukkan bahwa jumlah pasien yang berada dalam kisaran terapeutik (0,50 – 0,90 ng/ml) sebanyak 4 pasien (13,33%) dan jumlah pasien yang berada diluar kisaran terapeutik (>1,00 ng/ml) sebanyak 26 pasien (86,67%). Penyesuaian dosis digoxin dilakukan kepada 26 pasien (86,67%) secara individual dengan interval pemberian tiap 24 jam agar dapat mencapai Css sesuai kisaran terapetik. Berdasarkan hasil penelitian tersebut dapat disimpulkan bahwa pasien gagal jantung yang memiliki estimasi kadar obat dalam darah tidak sesuai kisaran terapetik perlu adanya penyesuaian dosis untuk meningkatkan outcome clinic dan mencegah kejadian toksisitas pada pasien.

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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 (March 31, 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 potenciais fatores de risco associados à mortalidade. Dos 65 prontuários analisados a sobrevida foi menor nos pacientes que utilizavam a dosagem de 0,125mg (p=0,093). A taxa de mortalidade foi de 35,9% e as chances de óbitos aumentaram nos indivíduos com idade acima de 76 anos (p=0,010; ORaj: 4,021), que possuíam outras doenças cardíacas (p=0,004; ORaj: 5,943) e com maior tempo de uso da digoxina (p=0,047; ORaj: 1,164).Descritores: Digoxina, Mortalidade, Idoso. Mortality of digoxin-treated elderly cardiac subjectsAbstract: This study aimed to describe the mortality and survival rates of elderly with heart failure who used digoxin, as well as to identify the risk factors associated with mortality. Records of elderly patients (≥60 years old) treated at the heart failure outpatient cardiology clinic were screened and selected for this retrospective study. Sociodemographic and clinical variables were measured. Survival was verified by Kaplan-Meier curves and log-rank test. Adjusted multiple logistic regression was used to assess potential risk factors associated with mortality. Of the 65 medical records analyzed, survival was lower in patients using 0.125 mg (p=0.093). The mortality rate was 35.9% and the chances of death increased in individuals over the age of 76 years (p=0.010; ORaj: 4.021), who had other heart disease (p=0.004; ORaj: 5.943) and with longer use of digoxin (p=0.047; ORaj: 1.164).Descriptors: Digoxin, Mortality, Aged. Mortalidad de ancianos cardiacos tratados con digoxinaResumen: El objetivo es describir las tasas de mortalidad y supervivencia de personas mayores con insuficiencia cardíaca que usaban digoxina, así como identificar los factores de riesgo asociados con la mortalidad. Los registros de pacientes ancianos (≥60 años de edad) tratados en la clínica ambulatoria de cardiología con insuficiencia cardíaca se examinaron para este estudio retrospectivo. Se midieron variables sociodemográficas y clínicas. La supervivencia se verificó mediante curvas de Kaplan-Meier y prueba de log-rank. Se utilizó la regresión logística múltiple ajustada para evaluar los posibles factores de riesgo asociados con la mortalidad. De los 65 registros médicos analizados, la supervivencia fue menor en los pacientes que utilizaron 0.125 mg (p=0.093). La tasa de mortalidad fue de 35.9% y las posibilidades de muerte aumentaron en personas mayores de 76 años (p=0.010; ORaj: 4.021), que tenían otras enfermedades cardíacas (p=0.004; ORaj: 5.943) y con uso más prolongado de digoxina (p=0.047; ORaj: 1.164).Descriptores: Digoxina, Mortalidad, Anciano.

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8

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 (December 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 areas under the curve for digoxin immune Fab were 213–1026 μg·h/mL, and total body clearances were 2.3–7.1 mL/min. The total digoxin concentrations peaked at 14–33 times the pre-Fab digoxin concentrations 5–30 hours after digoxin immune Fab administration. In comparing these data with data available from patients with normal renal function, the half-life of digoxin immune Fab and total digoxin was longer, the peak total digoxin concentration occurred later, the ratio of the peak total digoxin concentration to pre-Fab digoxin concentration was larger, and the rebound in free digoxin occurred later in patients with renal impairment. The Fab dose should not be reduced in patients with renal impairment; however, post-Fab monitoring should be extended to compensate for the prolonged half-life of Fab and later rebound of free digoxin.

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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 (April 27, 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 concentrations, signs and symptoms of digoxin toxicity, electrocardiograms, and co-morbidities. Reviewers performing chart review and electrocardiogram analysis were blinded to digoxin levels. Descriptive statistical methods were used and comparisons were made between patients with and without toxic serum digoxin concentrations (>2 ng/ml).ResultsThere were 87 patients who met study criteria (male 46%, mean age 8.4 years). CHD was present in 67.8% and electrocardiograms were performed in 72.4% of the patients. The most common indication for digoxin toxicity was heart failure symptoms (61.5%). Toxic serum digoxin concentrations were present in 6.9% of patients (mean 2.6 ng/ml). Symptoms associated with digoxin toxicity occurred in 48.4%, with nausea/vomiting as the most common symptom (36.4%), followed by tachycardia (29.5%). Compared with those without toxic serum digoxin concentrations, significantly more patients with toxic serum digoxin concentrations were female (p=0.02). The presence of electrocardiogram abnormalities and/or signs and symptoms of digoxin toxicity was not significantly different between patients with and without serum digoxin concentrations (p>0.05).ConclusionSerum digoxin concentrations in children are not strongly associated with signs and symptoms of digoxin toxicity.

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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 (August 1, 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. Design.—The effects of hawthorn extract on serum digoxin measurements using Digoxin III (Abbott Laboratories, Abbott Park, Illinois) and the Tina-Quant digoxin assay (Roche Diagnostics, Indianapolis, Indiana) were investigated using 2 different brands of extract. To study the pharmacodynamic interaction between hawthorn and digoxin, we used an isolated adult rat cardiomyocyte system, measuring calcium transients by real-time fluorescence spectrophotometry. Results.—Hawthorn interfered only with the Digoxin III immunoassay but had no effect on the Tina-Quant assay. Both hawthorn extracts increased intracellular calcium levels, but the lack of additive response with digoxin suggests both may bind to the same site of Na, K adenosine triphosphatase. Conclusion.—Because of interference of hawthorn with a digoxin immunoassay and pharmacodynamic interaction with digoxin, a patient receiving digoxin should avoid hawthorn.

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

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Bizjak, Eric D., and Vincent F. Mauro. "Digoxin–Macrolide Drug Interaction." Annals of Pharmacotherapy 31, no. 9 (September 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 be of clinical significance. Addendum Following acceptance of this manuscript, two additional reports of a digoxin–clarithromycin drug interaction have been published. Nawarskas et al.28 described clarithromycin-induced digoxin toxicity (digoxin-induced ST segment changes, non-sustained ventricular tachycardia, and a digoxin concentration of 4.4 ng/mL) due to 3 days of clarithromycin 500 mg bid in a 78-year-old woman stabilized on oral digoxin 0.25 mg/d. Laberge and Martineau29 observed a clinical presentation suggestive of digoxin toxicity and an elevated digoxin concentration of 3.9 ng/mL in a 78-year-old man stabilized on digoxin 0.25 mg/d who had received 4 days of clarithromycin 250 mg bid.

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Suharyani, Ine. "EVALUASI PENGGUNAAN KOMBINASI OBAT DIGOKSIN DAN FUROSEMID." Jurnal Kesehatan 6, no. 2 (April 20, 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 penelitian memperlihatkan bahwa 39 resep kombinasi digoksin dan furosemid yang menunjukkan bahwa terdapat 100 % obat berinteraksi, 100 % durasi pemberian obat sesuai dengan literatur, serta 100% penggunaan dosis sesuai dengan literatur. Hasil pemeriksaan laboratorium kadar elektrolit natrium dalam serum adalah 136 – 145 mEq/l, kadar kalium dalam serum adalah 4,4 – 4,5 mEq/l, serta kadar klorida dalam serum adalah 100 – 110 mEq/l yang menunjukkan hasil pemeriksaan laboratorium kadar elektrolit dalam tubuh keadaan normal.Kata kunci : gagal jantung, skrining, digoksin, furosemid ABSTRACTHeart failure is a condition when the heart muscle becomes so weak that it can’t pump enough blood throughout the body at the right pressure. The aim of this research to determine the right of combination of digoksin and furosemide seen from clinical aspects as well as the expenditure of potassium in the body. This research is descriptive method. Data collected used retrospective method used the data in the medical record. Prescription drug use a combination of digoxin and furosemide from October to December 2014. The results are 39 recipes combination of digoxin and furosemide which indicate that the drug interacts are 100%, 100% of the right duration of drug delivery, and 100% are the right dose. Results of electrolyte level in serum sodium is 136-145 mEq / L, potassium is 4.4 to 4.5 mEq / l and chloride is 100-110 mEq / l which shows the electrolytes level in the body at the normal state.Keywords: Heart failure, screening, digoxin, furosemide

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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 (March 1, 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 progressively to near 4.0 micrograms/L over the next several hours and thereafter decreased slowly to 1.0 microgram/L over the next 11 days, despite no digoxin being administered. The unexpectedly high digoxin raised questions about the accuracy of the digoxin measurement, particularly about the possible influence of the digoxin-like immunoreactive factor. Analytical approaches to distinguishing true digoxin from this factor and other artifacts of digoxin measurement were applied to this patient, with unanticipated results.

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Alderman, Christopher P., and Peter D. Allcroft. "Digoxin–Itraconazole Interaction: Possible Mechanisms." Annals of Pharmacotherapy 31, no. 4 (April 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 itraconazole or a metabolite of this compound may have resulted in decreased tubular secretion of digoxin, accounting for decreased urinary digoxin clearance. Conclusions Monitoring of serum digoxin concentrations should be performed if patients taking digoxin are treated with itraconazole. Further investigation is necessary to elucidate the nature of the interaction between digoxin and itraconazole.

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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 (April 1, 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 digoxin concentrations were measured using enzyme-linked chemiluminescent immunosorbent digoxin assay, turbidimetric assay, and fluorescence polarization immunoassay digoxin assays. Mice were fed with different ginseng preparations and apparent digoxin concentrations were measured 1 and 3 hours later. In a separate experiment, aliquots of serum digoxin pools were further supplemented with ginsengs and the serum digoxin concentrations were measured again. Results.—A significant apparent digoxin concentration was observed both in vitro and in vivo using the fluorescence polarization immunoassay, but no apparent digoxin concentration was observed using enzyme-linked chemiluminescent immunosorbent digoxin assay and turbidimetric assay. No interference was observed with enzyme-linked chemiluminescent immunosorbent digoxin assay and turbidimetric assay when digoxin serum pools were further supplemented with various ginsengs. Conclusions.—It was concluded that both enzyme-linked chemiluminescent immunosorbent and turbidimetric digoxin assays are free from ginseng interferences.

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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 (May 1, 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, velocity of circumferential fiber shortening, electromechanical systole, heart rate, and PR interval. Treatment consisted of administration of furosemide (mean dosage, 2.4 mg/kg of body weight/day), digoxin in tablet form (approximately 0.01 mg/kg, q 48 h), aspirin (80 mg, q 48 h), and a commercial low-salt diet. In addition, 2 cats were administered short-term, low-dose fluids IV, and 2 were given taurine supplementation at rates of 500 and 1,000 mg/day. Other off-loading or inotropic agents were not administered. Therapeutic or toxic serum digoxin concentration was achieved in all cats. Significant (P < 0.05) improvement was detected in mean values for shortening fraction, PEP, PEP to LVET ratio, and velocity of circumferential fiber shortening. Mean electromechanical systole and LVET did not change significantly. Improvement, as assessed by indices of cardiac function, was documented in 4 of the 6 cats treated with digoxin, including the 2 cats given taurine supplementation. In the cats given taurine, positive inotropic effect was observed prior to the time when taurine-induced improvement in ventricular function is detectable. Because increase in preload or decrease in afterload was not observed or was not likely, improved ventricular function was thought to be related to digoxin's positive inotropic effect. Digitalization did not significantly decrease mean heart rate, but was associated with a significant (P < 0.05) mean PR interval prolongation of 28 ms.

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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 (September 1, 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 correlation was observed between measurements of free digoxin by this ultrafiltration technique and by equilibrium dialysis. The ultrafiltration method was used to evaluate the concentrations of free digoxin in a digoxin-overdosed patient treated with Fab at our hospital. In retrospect, the results suggest that her hospital stay could have been shortened by a timely appreciation of her increased concentration of free digoxin. Using the ultrafiltration method, one can determine free digoxin concentrations quickly, conveniently, and accurately in the clinical laboratory. This procedure therefore should be a valuable aid in monitoring the efficacy and adequacy of Fab treatment.

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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 (March 1, 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. Extracting digoxin on a column of derivatized silicagel eliminated detectable DLIF from serum as measured by enzyme immunoassay (EMIT; Syva Co.), but recovery of added digoxin was quantitative. In contrast, protein precipitation with 5-sulfosalicylic acid left significant amounts of DLIF in samples, most probably because the procedure (TDx assay; Abbott Labs.) disrupted protein-DLIF binding. A glass-bead radioimmunoassay (Immophase; Corning Medical) had the most digoxin-specific antisera. By preparative silica-gel-chromatography of serum we could eliminate or significantly minimize inaccurate digoxin measurements attributable to endogenous DLIF.

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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 (November 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 absence of other signs of digoxin toxicity, DIF 80 mg iv was administered, and was immediately followed by 40 mg. Discussion: This case illustrates that elevated digoxin concentrations may be observed in patients with renal failure. These may not be true high concentrations because of the following potential factors: (1) the presence of digoxin-like factors, (2) increased biotransformation of digoxin, and (3) accumulation of metabolites that interfere with the assay. Digoxin metabolites are known to cross-react with the antibodies in commonly used digoxin immunoassays, and may be inappropriately interpreted to signal digoxin toxicity. Both the accuracy and reliability of digoxin immunoassay techniques have been questioned or challenged over the years. It is difficult to determine whether a reported toxic serum digoxin concentration represents the true concentration or cross-reactivity between digoxin metabolites and antibodies used in most digoxin immunoassays. Data Sources: Data collection sources included retrospective review of patient medical records, personal contact with one of the physicians involved in rendering patient care for interpretation of the electrocardiogram changes, clinical symptoms and rationale for DIF administration, and contact with the immunoassay technologist, who indicated that the fluorescence polarization immunoassay technique was used for analysis of digoxin concentrations. The medical literature then was reviewed. Conclusions: DIF should be reserved for use in symptomatic patients. Elevated digoxin concentrations must be evaluated for various factors that can cause falsely elevated values. Clinical signs and symptoms are critical in making the decision to use Fab. Antidotal measures should be based on correlation of patient symptoms with serum digoxin concentrations.

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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 (June 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 at steady state by serial determinations of digoxin serum concentrations. Twenty-four hour urine collections were done for creatinine clearance and urinary digoxin clearance determinations. Phase II of the study involved the addition of diltiazem hydrochloride 30 mg qid to the on-going, daily regimen of digoxin. After 14 days of concomitant therapy, steady-state trough digoxin concentrations were again determined, as well as creatinine clearances and urinary digoxin clearances. This investigation demonstrates that concomitant administration of diltiazem hydrochloride with digoxin results in significantly elevated steady-state trough digoxin concentrations (0.32 ± 0.07 ng/ml increasing to 0.48 ± 0.06 ng/ml, p<0.01). Urinary digoxin clearance decreased from 223.5 ± 35.7 ml/min to 153.4 ± 17.5 ml/min (p<0.05). Creatinine clearances were unaltered. A review of the current literature on this topic is included.

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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 (April 5, 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 risk of toxicity. Digoxin may be used in conjunction with diuretics, spironolactone, ACE inhibitors, or beta-blockers. It is preferable to take digoxin on a regular basis. Digoxin should not be used in the pre-excitation syndrome because it can result in the rapid development of accessory route conductors, which can finally result in ventricular fibrillation. Due to the narrow therapeutic index of digoxin, it requires appropriate treatment and continuous monitoring.

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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 (July 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-administration of cimetidine resulted in an average increase in plasma digoxin concentration of 0.19 ng/ml. 5 In a repeated-dose study in patients receiving long-term digoxin therapy for atrial fibrillation co-administration of cimetidine had no significant effect on plasma digoxin concentrations. 6 We have shown that co-administration of cimetidine and digoxin in volunteer subjects causes a statistically significant but small increase in plasma digoxin concentration but no such increase was found in patients. We conclude that it is doubtful that this interaction is of any clinical significance.

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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 (October 15, 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 digoxin level is high due to hypokalemia because of digoxin and furosemide drug interaction. The Electrocardiogram interpretation shows sinus bradycardia, ST segment depression, and T wave inversion which mainly due to digoxin toxicity. So for the management digoxin is omitted from the current treatment. The patient needs to be constantly monitored since digitalis poisoning is deadly. A digoxin-binding antibody is the only treatment for digoxin overdose that can reverse its effects by its antidote but it’s not available. So, the most successful course of treatment is symptomatic or efficient methods of extracorporeal drug removal. Keywords: Digoxin toxicity, furosemide, hypokalemia, cardiotoxicity, complete heart block, ST segment depression.

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Stone, J. A., and S. J. Soldin. "An update on digoxin." Clinical Chemistry 35, no. 7 (July 1, 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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Stenzel, R., and B. Reckmann. "Cross-Reactivity of Anti-Digoxin Antibodies with Digitoxin Depends on Tracer Structure." Clinical Chemistry 38, no. 11 (November 1, 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 reduced by varying the structure of the tracer molecule.

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&NA;. "Digoxin." Reactions Weekly &NA;, no. 1379 (November 2011): 15. http://dx.doi.org/10.2165/00128415-201113790-00053.

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&NA;. "Digoxin." Reactions Weekly &NA;, no. 1381 (December 2011): 12. http://dx.doi.org/10.2165/00128415-201113810-00037.

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&NA;. "Digoxin." Reactions Weekly &NA;, no. 1388 (February 2012): 13–14. http://dx.doi.org/10.2165/00128415-201213880-00051.

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&NA;. "Digoxin." Reactions Weekly &NA;, no. 1393 (March 2012): 18. http://dx.doi.org/10.2165/00128415-201213930-00060.

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&NA;. "Digoxin." Reactions Weekly &NA;, no. 768 (September 1999): 7. http://dx.doi.org/10.2165/00128415-199907680-00022.

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&NA;. "Digoxin." Reactions Weekly &NA;, no. 1127 (November 2006): 11. http://dx.doi.org/10.2165/00128415-200611270-00033.

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&NA;. "Digoxin." Reactions Weekly &NA;, no. 1156 (June 2007): 12–13. http://dx.doi.org/10.2165/00128415-200711560-00037.

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&NA;. "Digoxin." Reactions Weekly &NA;, no. 1158 (June 2007): 12–13. http://dx.doi.org/10.2165/00128415-200711580-00030.

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&NA;. "Digoxin." Reactions Weekly &NA;, no. 541 (March 1995): 5. http://dx.doi.org/10.2165/00128415-199505410-00017.

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&NA;. "Digoxin." Reactions Weekly &NA;, no. 542 (March 1995): 6. http://dx.doi.org/10.2165/00128415-199505420-00023.

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&NA;. "Digoxin." Reactions Weekly &NA;, no. 556 (June 1995): 7. http://dx.doi.org/10.2165/00128415-199505560-00024.

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&NA;. "Digoxin." Reactions Weekly &NA;, no. 558 (July 1995): 7. http://dx.doi.org/10.2165/00128415-199505580-00018.

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&NA;. "Digoxin." Reactions Weekly &NA;, no. 608 (July 1996): 7. http://dx.doi.org/10.2165/00128415-199606080-00018.

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&NA;. "Digoxin." Reactions Weekly &NA;, no. 430 (December 1992): 8. http://dx.doi.org/10.2165/00128415-199204300-00043.

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&NA;. "Digoxin." Reactions Weekly &NA;, no. 442 (March 1993): 7. http://dx.doi.org/10.2165/00128415-199304420-00032.

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&NA;. "Digoxin." Reactions Weekly &NA;, no. 448 (April 1993): 8. http://dx.doi.org/10.2165/00128415-199304480-00033.

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&NA;. "Digoxin." Reactions Weekly &NA;, no. 461 (July 1993): 7. http://dx.doi.org/10.2165/00128415-199304610-00038.

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&NA;. "Digoxin." Reactions Weekly &NA;, no. 466 (August 1993): 6. http://dx.doi.org/10.2165/00128415-199304660-00022.

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&NA;. "Digoxin." Reactions Weekly &NA;, no. 624 (October 1996): 8. http://dx.doi.org/10.2165/00128415-199606240-00019.

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&NA;. "Digoxin." Reactions Weekly &NA;, no. 775 (October 1999): 9. http://dx.doi.org/10.2165/00128415-199907750-00024.

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&NA;. "Digoxin." Reactions Weekly &NA;, no. 1398 (April 2012): 15–16. http://dx.doi.org/10.2165/00128415-201213980-00053.

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&NA;. "Digoxin." Reactions Weekly &NA;, no. 1404 (June 2012): 16–17. http://dx.doi.org/10.2165/00128415-201214040-00048.

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&NA;. "Digoxin." Reactions Weekly &NA;, no. 1404 (June 2012): 17. http://dx.doi.org/10.2165/00128415-201214040-00051.

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&NA;. "Digoxin." Reactions Weekly &NA;, no. 1408 (June 2012): 15. http://dx.doi.org/10.2165/00128415-201214080-00048.

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