Relevant bibliographies by topics / Digoxin

Academic literature on the topic 'Digoxin'

Author: Grafiati
Published: 4 June 2021
Last updated: 30 July 2024

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Journal articles on the topic "Digoxin"

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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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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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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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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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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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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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Dissertations / Theses on the topic "Digoxin"

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Alexandrovich, Susan K. "Characterization of monoclonal antibodies against digoxin /." Online version of thesis, 1987. http://hdl.handle.net/1850/10681.

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Matthewson, Beryl Ellen. "Digoxin-like immunoreactive substances in the neonate." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/28022.

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Digoxin, a steroidal glycoside that inhibits Na⁺/K⁺-ATPase, is the most commonly prescribed cardiac medication in North America. Blood levels of this drug are routinely measured to reduce the risks of toxicity. Reports questioning the specificity of antisera used in radioimmunoassays for serum digoxin measurements began to appear after 1975¹ when plasma from patients with renal failure, not on glycoside therapy, showed false-positive digoxin levels. Since then, digoxin-like immunoreactive substances (DLIS) have been found in sera from patients with hepatic failure, hypertension, pre-eclampsia, in amniotic fluid and cord blood. Some of the highest values for DLIS have been detected in premature infants, where levels have often exceeded the therapeutic range (0.2-2.0 µg/L) for digoxin. Cord blood has been identified as a rich source of DLIS. Dahl et al² were the first to suggest that a circulating saluretic substance "endoxin", may cause hypertension in salt sensitive rats. Gruber et al³ reported on the existence of digoxin-like factor(s) in the plasma of volume-expanded dogs. Plasma from these dogs inhibited Na⁺/K⁺ATPase activity. A number of other studies have supported the concept that such digoxin-like factors may be of etiological significance in hypertension⁴. In view of these observations, a study was undertaken to isolate and fractionate DLIS from mixed cord blood and determine whether or not any of this digoxin-like material possessed Na⁺/K⁺-ATPase inhibitory properties. Cord blood collected in the Grace Hospital Maternity Unit (Vancouver, BC), was pooled and DLIS extracted using C₁₈,R-Sep Paks. Extracts were resolved by high performance liquid chromatography (HPLC) into several fractions containing digoxin equivalent immunoactivity as measured by radioimmunoassay (RIA). A number of steroids and bile acids (dehydroepi-androsterone-sulfate, cortisone, Cortisol, deoxycortisone, ∆⁴androstene-dione, progesterone and glycochenodeoxycholic acid) cross-reacted with digoxin antisera and had HPLC retention times similar to DLIS-containing fractions. The ability of HPLC generated DLIS positive cord blood fractions to inhibit Na⁺/K⁺-ATPase activity was determined in three different assay systems; red cell ⁸⁶Rb uptake canine kidney-Na⁺/K⁺-ATPase and red cell membrane-Na⁺/K⁺-ATPase. At least six fractions contained DLIS and inhibited Na⁺/K⁺-ATPase activity. Inhibition varied with the assay system used but none of the fractions inhibited ⁸⁶Rb uptake by erythocytes. One fraction (which eluted at 29 minutes) contained progesterone; 72% of the inhibitory activity present in this fraction was attributable to this steroid. Another inhibitory fraction co-eluted with dehydroepiandrosterone-sulfate (DHEAS-S). The only fractions found to inhibit both the red cell membrane and canine kidney Na⁺ /K⁺-ATPase enzymes eluted at 7 and 29 minutes. In summary, a number of digoxin-like immunoreactive substances were isolated from cord blood by HPLC fractionation and found to inhibit Na⁺/K⁺-ATPase activity. Inhibition varied with the assay system used. There was no apparent correlation between inhibition and digoxin immunoreactivity. Very large quantities (500 mL) of cord blood were extracted to demonstrate these properties. It remains to be determined whether or not DLIS isolated during the perinatal period is of physiological significance.
Medicine, Faculty of
Pathology and Laboratory Medicine, Department of
Graduate
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Hui, James. "Analysis for digoxin and metabolites in serum and digoxin disposition in the elderly with gastrointestinal disease after two oral dosage forms /." The Ohio State University, 1988. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487587604130428.

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Hallberg, Pär. "Pharmacogenomics of antihypertensive treatment & clinical pharmacological studies of digoxin treatment /." Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-5782.

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Cavet, Megan Elizabeth. "Intestinal secretion of organic solutes." Thesis, University of Newcastle Upon Tyne, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318538.

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Svensson, Åsa. "Applications of a new logic to old drugs: angiogenesis inhibition in neuroblastoma /." Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3458.

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BARROS, Isabel Cristina Medeiros. "Monitoração terapêutica das concentrações plásmaticas da digoxina em pacientes com insuficiência cardíaca." Universidade Federal de Goiás, 2008. http://repositorio.bc.ufg.br/tede/handle/tde/1703.

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Made available in DSpace on 2014-07-29T15:29:05Z (GMT). No. of bitstreams: 1 dissertacao isabel cristina.pdf: 549593 bytes, checksum: ff591d0e143ca66263716f60188e9801 (MD5) Previous issue date: 2008-10-27
It was investigated the clinical, lab and plasma digoxin concentration profiles in 15 cardiac heart failure (CHF) outpatients of the Cardiac Heart Service of the Goias Federal University Clinical Hospital. It was aimed to know plasma digoxin concentration profile in 15 cardiac heart failure (CHF) outpatients by two analytical methods, taking account clinical, laboratorial, habits, anthropometric data and drug usage. Digoxin dosage was developed by LC/MS/MS and immunoassay methods; questionnaire and consults handbooks were performed. Results and Conclusions: 87% of the patients who over 46 years of age (33% above 61), the masculine majority; the IC of Chagas disease origin presented greater occurrence, followed of the hipertensive and idiopatic (59%); IC functional classroom II (53.33%); hypertension and diabetes had been distinguished as co-morbidities (26.67% and 20%); tobaccoism, overweight and obesity degree I had presented low occurrence. No patients presented relevant clinical data suggestive of digitalis intoxication. No observed changes in biochemical and hematological exams. The ejection fractions were good by means 41.7 ± 9%. Some drugs with interaction potential had been associated to the treatment, apparently without alterations. Statistical significative difference between both methods was observed (P < 0.05, ANOVA, Tukey Test). In the immunoassay method, all the patients were inside of the therapeutical range (0, 5-2, 0 ng/mL), whereas for the LC-MS/MS method, 8 patients they would be in subtherapeutical concentrations. However, no patient presented signals or symptoms of poisoning or inefficacy of the digoxin, demonstrating biological variability. The two methods are useful, since that it has a correlation with the clinical and laboratorial state of the patients.
Investigou-se o perfil clínico, laboratorial e as concentrações de digoxina plasmática em 15 pacientes com insuficiência cardíaca (IC) atendidos no Ambulatório de Insuficiência Cardíaca do HC-UFG. Objetivou-se estudar o perfil de concentrações plasmáticas de digoxina em pacientes com IC, utilizando dois métodos analíticos, e descrever a digoxinemia considerando os dados clínicos, laboratoriais, hábitos, IMC e consumo de medicamentos. A metodologia utilizada consistiu de cromatografia líquida de alta eficiência acoplada a espectrometria de massas (LC/MS/MS) e Imunoensaio, aplicação de questionário e consulta a prontuários. Como resultados, observou-se: 87% dos pacientes maiores que 46 anos de idade (33% acima de 61), a maioria masculina, a IC de origem chagásica apresentou maior ocorrência, seguida da hipertensiva e idiopática (59%); IC classe funcional II (53,33%); hipertensão e diabetes destacaram-se como co-morbidades (26,67% e 20%); tabagismo, sobrepeso e obesidade grau I apresentaram baixa ocorrência. Nenhum dos pacientes apresentou dados clínicos relevantes sugestivos de intoxicação digitálica. Não houve alterações em exames bioquímicos e hematológicos. A fração de ejeção média foi 41,7 ± 9%, portanto nenhum paciente apresentou FE como preditor de mau prognóstico. Vários fármacos com potencial de interação estiveram associados ao tratamento, aparentemente sem alterações. Houve diferença significativa (P < 0,05, ANOVA, Teste de Tukey) entre os métodos analíticos. No método de imunoensaio, todos os pacientes estavam dentro da faixa terapêutica (0,5-2,0 ng/mL), enquanto que pelo método LC-MS/MS, 8 pacientes estariam em sub-dosagens. Entretanto, nenhum paciente apresentou sinais ou sintomas de intoxicação ou de ineficácia da digoxina, demonstrando variabilidade biológica. Os dois métodos são úteis, desde que haja uma correlação com o estado clínico e laboratorial dos pacientes.
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Embree, Leanne. "Development of a sensitive, quantitative high-performance liquid chromatographic assay for the measurement of digoxin in patient groups with high levels of digoxin-like immunoreactive substances." Thesis, University of British Columbia, 1989. http://hdl.handle.net/2429/29093.

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Digoxin is the most commonly used digitalis glycoside for the treatment of congestive heart failure and certain disturbances of cardiac rhythm. The low therapeutic index observed for digoxin and the clinical significance of digoxin therapy have necessitated the development of sensitive analytical methods for the quantitation of digoxin in biological samples. Digoxin may be analysed by several methods including immunoassays, chromatographic procedures and various biological and chemical methods. Immunoassays, both radioimmunoassay (RIA) and fluorescence polarization immunoassay (FPIA) procedures, are used in the clinical laboratory because of their speed, precision, sensitivity and relatively low cost. However, reaction of the digoxin antibodies used in the immunoassay methods with digoxin metabolites, endogenous compounds such as digoxin-like immunoreactive substances (DLIS), and other drugs that may be co-administered with digoxin continues to be a major problem. The lack of specificity of the immunoassay methods for digoxin has led to difficulties in interpretation of assay values. Attempts to compensate for this lack of specificity have included the use of chromatographic systems as elaborate sample handling methods prior to immunoassay. However, since an immunoassay was used for detection of digoxin in these techniques, the specificity may still be quest ionable. A sensitive and specific assay for digoxin using physico-chemical methods for measurement is therefore needed. A method was developed using pre-column derivatization of digoxin and its metabolites with 3,5-dinitrobenzoyl chloride followed by HPLC analysis with electrochemical detection. A maximum sensitivity of 0.883 ng of 3,5-dinitrobenzoyl digoxin (0.394 ng digoxin) was observed using dual electrode detection in the redox mode. Although resolution between derivatized digoxin and its metabolites was obtained, the low yield of the digoxin derivative and the formation of metabolites when small (ng) samples were derivatized made this method unsuitable for evaluating patient samples. A high-performance liquid chromatographic (HPLC) assay using post-column derivatization of digoxin, which separated digoxin from its metabolites and some commonly coadministered drugs, was developed. Post-column (PC) derivatization of digoxin with concentrated hydrochloric acid and dehydroascorbic acid, followed by fluorescence detection, allowed for quantitation within the therapeutic range of digoxin. Steroids which have been reported to cross-react with digoxin antisera were assayed using the HPLC-PC method developed in this study. The steroid samples either did not elute from the HPLC system or did not produce a fluorescent product under these conditions. Serum samples from digitalized patients were evaluated using both the HPLC-PC and the FPIA methods. When compared to the HPLC procedure, the FPIA assay results gave, on average, higher digoxin levels. This may have been due to the inclusion of digoxin metabolites or endogenous compounds with the FPIA assay. Serum samples from undigitalized patient groups where high DLIS levels have been reported were also evaluated. These included umbilical cord blood samples and samples from hypertensive patients, renal failure patients and hepatic failure patients. Comparison of the HPLC-PC and FPIA methods demonstrated that the HPLC-PC assay gave fewer false positive results than the FPIA. The HPLC-PC assay developed for analysis of digoxin was unaffected by the presence of digoxin metabolites, numerous steroids, co-administered drugs and endogenous compounds, most of which have been reported to give false positive results with the FPIA.
Pharmaceutical Sciences, Faculty of
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9

Hallberg, Pär. "Pharmacogenomics of Antihypertensive Treatment & Clinical Pharmacological Studies of Digoxin Treatment." Doctoral thesis, Uppsala universitet, Institutionen för medicinska vetenskaper, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-5782.

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In Part I we found that the CYP2C9 genotype appears to influence the diastolic blood pressure response to the angiotensin II-receptor antagonist irbesartan in patients with hypertension and left ventricular hypertrophy. Those with the *1/*2 genotype (slower metabolism) responded better than those with the *1/*1 genotype (normal metabolism), likely due to a slower elimination of the drug. We further found that a +9/-9 exon 1 polymorphism of the B2 bradykinin receptor gene – shown to affect mRNA expression - appears to influence the regression of left ventricular mass during therapy with irbesartan or the beta-blocker atenolol in the same patients. Subjects with the -9/-9 genotype (higher mRNA expression) had a greater regression than carriers of the +9 allele. In Part II we found that women on digoxin therapeutic drug monitoring have higher serum digoxin concentrations (SDCs) as compared to men (1.54±0.04 [nmol/L±SE] vs 1.20±0.05 [nmol/L±SE], p<0.001), which could be of importance since an SDC >1.4 nmol/L has been associated with increased mortality. We further found that coadministration of P-glycoprotein inhibitors with digoxin was common (47%) among the same patients, and that the SDC increased in a stepwise fashion with the number of P-glycoprotein inhibitors (20-60%). Lastly, we found that patients admitted to Swedish coronary care units with atrial fibrillation without heart failure and who had been given digoxin had a higher 1-year mortality than those not given digoxin (RR 1.44 [95% CI 1.29-1.60], adjustment made for potential confounders). In conclusion, Part I represents a further step in the pharmacogenomic prospect of tailoring antihypertensive therapy. Part II indicates that heightened attention to the digoxin-dose is warranted in women, that there is a need for awareness about P-glycoprotein interactions with digoxin, and that long-term therapy with digoxin is an independent risk factor for death among patients with atrial fibrillation without heart failure.
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10

Vetticaden, Santosh John. "Evaluation of Analytical, Pharmacokinetic and Pharmacodynamic Methods for the Study of Digoxin." VCU Scholars Compass, 1985. http://scholarscompass.vcu.edu/etd/5103.

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The primary objective of the research was to investigate the pharmacodynamics of digoxin in dogs. Initially an assay specific for digoxin in the presence of its major metabolites, viz., digoxigenin, digoxigenin mono-digitoxoside, digoxigenin bis-digitoxoside and dihydrodigoxin was developed using HPLC-RIA. Methodology for non-invasive measurement of left ventricular ejection time (LVET) and other systolic time intervals (STI) in beagle dogs were developed. This involved surgery for exteriorization of the carotid artery in the dogs and subsequent measurements of LVET and STI after recovery. STI, heart rate (HR) and digoxin levels were monitored in normal beagle dogs administered 0.05 mg/kg or 0.025 mg/kg i.v., infused uniformly over a 5 min. period. The STI did not lend itself to pharmacodynamic modelling. The LVET, QS2 and P-R interval were found to be inversely, but linearly, related to the heart rate. Therefore, the bradycardic response to digoxin was extensively investigated in beagle dogs. Pharmacodynamic models evaluated for modelling the bradycardic response to digoxin were: the pharmacokinetic model with a direct linear link, the linear model, the physiologic-pharmacokinetic model with direct linear link and the effect compartment model. The physiologic pharmacokinetic model was simulated using SPICE2 which uses network thermodynamics to simulate biological systems. Criteria for the selection of appropriate models were established. Using the established criteria, the effect compartment model was demonstrated to be the best model. The implications and applications of pharmacodynamic models in general and specifically of the pharmacodynamic model for the bradycardic response to the digoxin are discussed.
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Books on the topic "Digoxin"

1

Buchko, Sandra. The effect of nebulized salbutamol on serum digoxin concentration. [Ottawa: Ottawa General Hospital, 1991.

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universitet, Odense, ed. Digoxin interactions: The influence of quinidine and verapamil on the pharmacokinetics and receptor binding of digitalis glycosides. Stockholm: distributed by the Almqvist & Wiksell Periodical Company, 1985.

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Klüppel, Arnulf. Untersuchungen zur dosisunabhängigen Pharmakokinetik von Digoxin. [s.l.]: [s.n.], 1986.

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Bissland, Ted. Death shift: The digoxin murders at "Sick Kids". Toronto: Bantam, 1985.

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Kurup, Ravikumar, and Parameswaran Achutha Kurup. The third element: Actinidic archaea, digoxin, and the biological universe. Hauppauge, N.Y: Nova Science Publishers, 2011.

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Kurup, Ravikumar. Hypothalamic digoxin, cerebral dominance and brain function in health and diseases. New York: Nova Science Publishers, Inc., 2003.

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Joreteg, Torbjörn. Digoxin binding to skeletal muscle: Factors of importance for an activity dependency. [s.l.]: [s.n.], 1985.

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Stenzel, Joachim. Der Einfluss von Nisoldipin auf die Digoxin- und Digitoxinplasmaspiegel und hämodynamische Effekte. [s.l.]: [s.n.], 1987.

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Düsseldorf, Universität, ed. Der Einfluss von Digoxin auf die Kernreihenbildung in den Herzmuskelzellen des Schweines. [s.l.]: [s.n.], 1987.

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Peter, Inge. Dosis-Wirkungsbeziehungen extrakardialer Effekte von Digoxin und Meproscillarin an gesunden Versuchspersonen: (placebokontrollierte Doppelblindstudie). [s.l.]: [s.n.], 1985.

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Book chapters on the topic "Digoxin"

1

Gebran, Nicole. "Digoxin." In Textbook of Clinical Pediatrics, 2605–8. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-02202-9_275.

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Beyer, Karl-Heinz. "Digoxin." In Biotransformation der Arzneimittel, 202–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74386-3_107.

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Vidal, C., and W. R. Külpmann. "Digoxin." In Springer Reference Medizin, 702–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_892.

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Vidal, C., and W. R. Külpmann. "Digoxin." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_892-1.

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Dasgupta, Amitava. "Digoxin." In Handbook of Drug Monitoring Methods, 111–31. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-031-7_6.

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Wilson, John Fawcett. "Digoxin." In The Immunoassay Kit Directory, 1515–32. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-0679-5_15.

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Peter, Helga, and Thomas Penzel. "Digoxin." In Springer Reference Medizin, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2020. http://dx.doi.org/10.1007/978-3-642-54672-3_451-1.

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Chen, Ying, Lan Sun, and Guan-Hua Du. "Digoxin." In Natural Small Molecule Drugs from Plants, 49–58. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-8022-7_8.

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Schneider, Achim, Günther Schlunck, and Viola Sieber. "Digoxin." In Geburtshilfefibel, 257–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-97317-8_54.

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Ahmed, Hesham M., Christopher T. Aquina, Vicente H. Gracias, J. Javier Provencio, Mariano Alberto Pennisi, Giuseppe Bello, Massimo Antonelli, et al. "Digoxin Toxicity." In Encyclopedia of Intensive Care Medicine, 722. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_1486.

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Conference papers on the topic "Digoxin"

1

Karthikeyan, Ganesan. "28 Should we be using digoxin in 2018?" In 2nd Asia Pacific Advanced Heart Failure Forum (APAHFF 2018), 16th November 2018, Hong Kong. BMJ Publishing Group Ltd, British Cardiovascular Society and Asia Pacific Heart Association, 2019. http://dx.doi.org/10.1136/heartasia-2019-apahff.28.

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Powell, C., M. Barrett, K. Flynn, D. Meenaghan, and K. McDonald. "54 A year in the life of digoxin." In Irish Cardiac Society 74th Annual Scientific Meeting & AGM, October 12th–14th 2023, Killashee House Hotel, Kildare, Ireland. BMJ Publishing Group Ltd and British Cardiovascular Society, 2023. http://dx.doi.org/10.1136/heartjnl-2023-ics.54.

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Granell, C. Liñana, L. Belles Medall, O. Pascual Marmaneu, R. Ferrando Piqueres, M. Medoza Aguilera, T. Alvarez Martin, and T. Garcia Martinez. "PKP-008 Implementation of a monitoring protocol for digoxin." In 22nd EAHP Congress 22–24 March 2017 Cannes, France. British Medical Journal Publishing Group, 2017. http://dx.doi.org/10.1136/ejhpharm-2017-000640.436.

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Martínez Simón, JJ, A. Martín Suárez, AM Gómez Pedrero, and M. Pérez Encinas. "5PSQ-023 Adequate digoxin dosage in patients with digitalis toxicity." In 24th EAHP Congress, 27th–29th March 2019, Barcelona, Spain. British Medical Journal Publishing Group, 2019. http://dx.doi.org/10.1136/ejhpharm-2019-eahpconf.456.

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Rodríguez Esquíroz, A., C. Leralta González, M. Jiménez Meseguer, ÁL Salcedo Mingorranz, B. García Díaz, M. Sarobe Carricas, and MF Hurtado Gómez. "5PSQ-010 Digoxin adjustment: comparative analysis of three pharmacokinetic software." In 27th EAHP Congress, Lisbon, Portugal, 22-23-24 March 2023. British Medical Journal Publishing Group, 2023. http://dx.doi.org/10.1136/ejhpharm-2023-eahp.237.

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Schwegman, A., S. Herasevich, Y. Subat, O. Gajic, and C. Bennett. "Digoxin Use in Patients with Sepsis: A Single-Center Retrospective Cohort Study." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6500.

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Magro Vázquez, C., C. González Trigueros, AL Salcedo Mingoarranz, MM Noceda Urarte, M. Herrero Fernández, MT Sarobe Carricas, G. Baldominos Utrilla, and B. García Díaz. "4CPS-103 Pharmacokinetic interaction study of osimertinib and digoxin: a case report." In 27th EAHP Congress, Lisbon, Portugal, 22-23-24 March 2023. British Medical Journal Publishing Group, 2023. http://dx.doi.org/10.1136/ejhpharm-2023-eahp.119.

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Abbasi, A., A. Nikfarjam, and J. Mohammadnejad. "Simulation of digoxin single molecule detection through resonant frequency shift of a CNT." In 2013 First RSI/ISM International Conference on Robotics and Mechatronics (ICRoM 2013). IEEE, 2013. http://dx.doi.org/10.1109/icrom.2013.6510132.

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López-Sepúlveda, R., E. Espínola García, MS Martín Sances, S. Anaya Ordóñez, MA García Lirola, and J. Cabeza Barrera. "PKP-006 Pharmacist’s role in clinical pharmacokinetic monitoring of digoxin: minimising toxic effects." In 22nd EAHP Congress 22–24 March 2017 Cannes, France. British Medical Journal Publishing Group, 2017. http://dx.doi.org/10.1136/ejhpharm-2017-000640.434.

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Pothal, S., N. Tengli, N. Patel, and A. Behera. "Efficacy of Digoxin in isolated Right ventricular Dysfunction due to Chronic Pulmonary Diseases." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.135.

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