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Lanoxin (Digoxin)

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Lanoxin is an effective medication which is used in treatment of certain types of fast heartbeats such as atrial fibrillation or fluttering arrhythmia and heart failure. It also treats angina. This drug can also be used after heart attack.

Other names for this medication:

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Also known as:  Digoxin.


Lanoxin target is struggle against certain types of fast heartbeats such as atrial fibrillation or fluttering arrhythmia and heart failure. It is also treats angina. This drug can also be used after heart attack. The effectiveness of Lanoxin is in keeping the heart rhythm under control and to make heart work better (regularly and strongly). It is cardiac (or digitalis) glycosides.

Generic name of Lanoxin is Digoxin.

Lanoxin is also known as Digoxin, Digitalis, Digitek, Lanoxicaps.

Brand names of Lanoxin are Lanoxicaps, Lanoxin, Cardoxin, Digitek, Lanoxin Elixir Pediatric.


Take Lanoxin tablets (0.25 mg), capsules and pediatric elixir (liquid) orally.

Elderly people (> 65 years) should take the lowest dose.

Take Lanoxin at the same time once a day with water.

Do not crush or chew it.

If you want to achieve most effective results do not stop taking Lanoxin suddenly.


If you overdose Lanoxin and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Lanoxin overdosage: confusion, irregular heartbeats, nausea, seizures, vomiting, extremely fast or slow heartbeats, hallucinations, tiredness, problems with vision, diarrhea, lack of appetite.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture, light and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

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The most common side effects associated with Lanoxin are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Lanoxin if you are allergic to Lanoxin components.

Do not take Lanoxin if you're pregnant or you plan to have a baby, or you are a nursing mother.

Be careful with Lanoxin if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.

Be careful with Lanoxin in case of taking medicines as a steroid medicine (prednisone (such as Deltasone), methylprednisolone (such as Medrol), prednisolone (such as Prelone, Pediapred), dexamethasone (such as Decadron)); a cancer chemotherapy drug; amphotericin B (such as Fungizone); indomethacin (such as Indocin); rifampin (such as Rifadin, Rimactane); cholestyramine (such as Questran, Prevalite) or colestipol (such as Colestid); a thyroid medication; a beta-blocker (atenolol (such as Tenormin), propranolol (such as Inderal), acebutolol (such as Sectral), metoprolol (such as Lopressor), carteolol (such as Cartrol), labetalol (such as Normodyne, Trandate) or nadolol (such as Corgard)); a diuretic (hydrochlorothiazide (such as HCTZ, HydroDiuril, others), chlorothiazide (such as Diuril), chlorthalidone (such as Hygroton, Thalitone), furosemide (such as Lasix), torsemide (such as Demadex), bumetanide (such as Bumex), ethacrynic acid (such as Edecrin), triamterene (such as Dyrenium, Maxzide, Dyazide), amiloride (such as Midamor), spironolactone (such as Aldactone), eplerenone (such as Inspra)); metoclopramide (such as Reglan); tetracycline (such as Broadspec, Emtet, Panmycin, Sumycin, Tetracap); erythromycin (such as E.E.S., E-Mycin, Eryc, Ery-Tab, PCE) or clarithromycin (such as Biaxin); sulfasalazine (such as Azulfidine); sulfasalazine (such as Azulfidine); another medicines for irregular heartbeats (quinidine (such as Quinidex, Quinora, Cardioquin), amiodarone (such as Cordarone) or propafenone (such as Rythmol)); itraconazole (such as Sporanox); a calcium channel blocker (diltiazem (such as Cardizem, Dilacor XR, Tiazac), amlodipine (such as Norvasc), felodipine (such as Plendil), nifedipine (such as Procardia, Adalat), verapamil (such as Verelan, Calan, Isoptin, Covera-HS)), an antacid or laxative that contains aluminum, magnesium or kaolin-pectin (such as Maalox, Rolaids, Mylanta, Milk of Magnesia).

Be careful with Lanoxin if you have allergies to medicines, foods, or other substances.

Be careful with Lanoxin if you suffer from or have a history of thyroid disease, cancer, kidney disease, heart arrhythmias.

Use Lanoxin with great care in case you want to undergo an operation (dental or any other).

Elderly people (> 65 years) should take the lowest dose.

Avoid alcohol.

Avoid machine driving.

Do not stop taking Lanoxin suddenly.

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Prehospital treatment of new-onset supraventricular arrhythmias can be attempted by physician-staffed mobile intensive care units to decrease the hospitalization rate and expense. Identification of patients suitable for at-home pharmacological treatment may help in the triage of patients with new-onset atrial fibrillation (AF). In the present investigation, the value of several clinical variables to predict the success of pharmacological at-home cardioversion was tested. A total of 924 patients with new onset (less than 24 h) AF, rescued by the Florence Mobile Coronary Care Unit (MCCU), were included in the study. By univariate analysis, female sex, palpitations as symptoms leading to MCCU call and a short delay between symptom onset and MCCU intervention were associated with a favourable outcome of treatment, whilst dyspnoea as the main complaint requiring MCCU intervention and the association of AF with an acute cardiovascular event (angina, acute myocardial infarction or pulmonary oedema) were negatively associated with the success rate of treatment. The cardioversion rate was not significantly different in patients with underlying heart disease or in patients with lone atrial fibrillation. By multivariate analysis, only sex and the drug employed for treatment (positive relation for propafenone and bunaftine, negative for amiodarone, digoxin and verapamil) were significant predictors of the outcome of MCCU intervention. Our results suggest that patients with new-onset (less than 24 h) AF with or without underlying heart disease whose main complaint is palpitation can be successfully cardioverted at home with a class IC drug (propafenone). Patients with acute coronary syndromes or left ventricular failure are good candidates for elective cardioversion after hospitalization.

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Atrial fibrillation is a supraventricular tachyarrhythmia, which is characterised by the presence of fast and uncoordinated atrial activation leading to reduced atrial mechanical function. Risk factors for atrial fibrillation include increasing age, coexisting cardiac and thyroid disease, pyrexial illness, electrolyte imbalance, cancer, and coexisting infection.

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In patients with sarcoidosis there was elevated digoxin synthesis, increased dolichol and glycoconjugate levels and low ubiquinone and elevated free radical levels. There was also an increase in tryptophan catabolites and a reduction in tyrosine catabolites. There was an increase in the cholesterol:phospholipid ratio and a reduction in the glycoconjugate level of red blood cell (RBC) membrane in this group of patients. The same biochemical patterns were obtained in individuals with right hemispheric dominance. In individuals with left hemispheric dominance the patterns were reversed.

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Data regarding clinical outcomes were excerpted from the trial reports by one review author (RS) and checked by the second review author (EO). Data were analyzed according to the standards of the Cochrane Neonatal Review Group.

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We report two cases of fetal supraventricular tachycardia with hydrops fetalis. The transplacental therapy with digoxin, sotalol and amiodarone, using combination of both of this drugs, has given in one case a partial conversion, total in the second case. Ultrasounds allow diagnosis of SVT, evaluate the gravity when it is associated with fetal hydrops secondary to a congestive heart failure, research a cause and follow the evolution during the treatment. The treatment must begin when diagnosis of SVT is done, by digoxin; other drugs as sotalol, amiodarone or flecainide acetate are described and also direct fetal therapy by intramuscular or into the umbilical vein injections.

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This study evaluated the effect of digoxin on cardiac sympathetic activity in patients with congestive heart failure.

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In a total of 2,643 hospitalized patients, 191 (7.2%) ADE were detected. Of these, 38 cases (19.9%) were classified as preventable, of which 21.1% were mild; 60.5% moderate and 18.4% serious or life-threatening. Preventable ADE were frequently associated with anti-infective drugs (22.9%), diuretics (18.8%) and digoxin (16.7%). Inadequate therapy monitoring (28.3%), excessive dosage (21.7%), selection of an inappropriate drug according to patient characteristics and/or to diagnosis (15.0%), lack of prescription of a necessary drug (15.0%) and drug-drug interactions (11.7%) were the most common identified type of errors leading to preventable ADE.

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In order to evaluate a possible interaction between digoxin and nifedipine, we studied steady state digoxin pharmacokinetics before and during oral coadministration of nifedipine in eight healthy subjects. Mean plasma digoxin concentration was 0.68 +/- 0.15 ng/ml during control conditions versus 0.74 +/- 0.13 ng/ml (NS) after two weeks of nifedipine coadministration. Nifedipine caused no significant changes in either renal digoxin clearance (173.6 +/- 25.9 versus 173.1 +/- 33.2 ml/min) or 24-hour urinary recovery of digoxin (164.7 +/- 25.7 versus 183.8 +/- 29.2 micrograms/24 hrs). Our findings support earlier observations that nifedipine coadministration is not associated with any significant alteration of digoxin pharmacokinetics.

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The objective of the present study was to test the hypothesis that brain Na, K-ATPase expression and/or activity is altered following an increase in blood pressure produced by constriction of the abdominal aorta just proximal to the renal arteries. A suprarenal constriction (SRC) was made to conform to the diameter of a 19-gauge (19-G) or 20-gauge (20-G) needle, while in a sham-operated group (Sham) the aorta was exposed surgically but not constricted. Within 1 week of SRC, mean arterial pressure was increased and remained elevated at 4 weeks post surgery. At 1 week, whole-brain Na, K-ATPase mRNA levels were depressed for all isoforms (alpha1 approximately beta1>alpha2>alpha3). No changes were observed in the hypothalamus. At 4 weeks, the mRNA levels of all alpha isoforms were significantly increased in the whole brain and these changes were paralleled by an increase of alpha2 and alpha3 transcript in the hypothalamus. beta1 mRNA expression was increased in the hypothalamus only. The alpha-isoform protein expression generally changed in the same direction as mRNA changes at both 1 and 4 weeks, as did alpha1 enzyme activity at 1 week and the combined alpha2/alpha3 enzyme activities at 4 weeks. Since inhibition of brain Na, K-ATPase increases sympathetic nervous system (SNS) activity and blood pressure, the decreases in brain Na, K-ATPase expression and activity at 1 week post SRC may contribute to the hypertension during its developmental phase, while the increase in the alpha2/alpha3 brain expression and activity at 4 weeks may be a compensatory response to established hypertension.

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Positive- and negative-ion mass spectra of five glycoconjugates were obtained using laser desorption/Fourier transform mass spectrometry. These were the glycoalkaloids alpha-solanine and alpha-tomatine and the steroid glycosides gitoxin, lanatoside A and digitonin. Doping with KCl yielded both potassium- and chloride-attachment ions. Few fragment ions were observed for these species, with the exception of digitonin, although the negative-ion spectra showed relatively more fragmentation than the positive-ion spectra. All major fragments appeared to arise from losses of sugar groups due to cleavages at the glycosidic linkages. This contrasted sharply with the behavior of the malto-oligosaccharides studied in this laboratory.

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Gastric pH appears relevant for absorption of some cardiovascular or infectious disease agents. Antisecretory treatment may significantly modify the absorption of co-administered drugs.

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First-generation calcium antagonists have been used in patients with congestive heart failure with rather disappointing results. Therefore, second-generation dihydropyridine calcium-channel blockers, such as felodipine and lacidipine, have been developed that may be beneficial in congestive heart failure owing to their high vasoselectivity and more favorable neurohumoral modulation. The effects of lacidipine in patients with congestive heart failure, who remain symptomatic despite receiving long-term therapy with angiotensin-converting enzyme inhibitors, digoxin, and diuretics, were investigated during a prospective, double-blind, randomized, placebo-controlled, parallel-group study. Twenty-five patients were randomized to receive either lacidipine (4 mg once daily; 12 patients) or placebo (once daily; 13 patients). After 8 weeks of treatment patients receiving lacidipine showed a significantly higher increase in cardiac output (p < 0.01), and a significantly greater reduction in vascular resistance (p < 0.02) than those patients in the placebo group. No significant changes were observed in filling pressures and heart rate. The arteriovenous oxygen content difference was significantly reduced in the lacidipine group (p < 0.01) without significant changes in arterial oxygenation, suggesting an increase in flow that was not a result of pulmonary shunting. Further peak oxygen consumption during cardiopulmonary exercise testing increased significantly in the lacidipine patients (p < 0.02). These beneficial effects were achieved without significant changes in neurohumoral parameters. Analysis of right and left ventricular ejection fractions revealed no cardiodepressant effects. Lacidipine was well tolerated during the course of the study, and adverse reactions were minor. These data suggest that lacidipine has a promising profile for the treatment of congestive heart failure patients, and that further investigation with second-generation dihydropyridines in the field of congestive heart failure appears warranted.

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Direct block of the cardiac potassium channel human ether-a-go-go-related gene (hERG) by a large, structurally diverse group of therapeutic compounds causes drug-induced QT prolongation and torsades de pointes arrhythmias. In addition, several therapeutic compounds have been identified more recently that prolong the QT interval by inhibition of hERG trafficking to the cell surface. We used a surface expression assay to identify novel compounds that interfere with hERG trafficking and found that cardiac glycosides are potent inhibitors of hERG expression at the cell surface. Further investigation of digitoxin, ouabain, and digoxin revealed that all three cardiac glycosides reduced expression of the fully glycosylated cell surface form of hERG on Western blots, indicating that channel exit from the endoplasmic reticulum is blocked. Likewise, hERG currents were reduced with nanomolar affinity on long-term exposure. hERG trafficking inhibition was initiated by cardiac glycosides through direct block of Na(+)/K(+) pumps and not via off-target interactions with hERG or another closely associated protein in its processing or export pathway. In isolated guinea pig myocytes, long-term exposure to 30 nM of the clinically used drugs digoxin or digitoxin reduced hERG/rapidly activating delayed rectifier K(+) current (I(Kr)) currents by approximately 50%, whereas three other cardiac membrane currents--inward rectifier current, slowly activating delayed rectifier K(+) current, and calcium current--were not affected. Importantly, 100 nM digitoxin prolonged action potential duration on long-term exposure consistent with a reduction in hERG/I(Kr) channel number. Thus, cardiac glycosides are able to delay cardiac repolarization at nanomolar concentrations via hERG trafficking inhibition, and this may contribute to the complex electrocardiographic changes seen with compounds such as digitoxin.

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A neonate with ventricular septal defect and large left-to-right shunt was treated with digitalis and diuretics at the usual starting doses. An intensive phototherapy was also required because of a hyperbilirubinemia due to glucose-6-phosphate dehydrogenase deficiency. Toxic digoxin accumulation (plasma level 14 ng/mL) was diagnosed three days after the initiation of treatment by the presence of sinus bradycardia and bursts of ventricular fibrillation. Intravenous administration of digoxin-specific antibody Fab fragments (Digidot) was effective, with a rapid improvement of the digitalis poisoning.

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The rotavirus outer capsid proteins VP4 and VP7 determine the P- and G-serotypes, respectively, of the virus. Three types of VP4 protein are commonly found in human rotaviruses (P4, P6 and P8) which are encoded by distinct VP4 gene alleles. We developed a non-radioactive Northern hybridization method for the P-genotyping of rotavirus field isolates. Double-stranded RNA was isolated from faecal specimens of rotavirus positive patients. Digoxigenin (DIG)-labelled cDNA probes derived from the VP4 gene of the standard strains RV5 (P4), ST3 (P6) and RV4 (P8) were used to discriminate between the different alleles. Although the P4 probe exhibited cross-reactivity with some P8 samples, the P6 and P8 probes were found to be type-specific. In addition, the probes did not react with standard strains representative of other defined human and animal rotavirus P-types. Use of these probes on viral RNA of faecal origin allowed approximately 70% of samples to be assigned a P-type. This method complements PCR- and EIA-based P-typing methods, is relatively inexpensive and is readily applicable to large numbers of samples, thus proving useful for epidemiological studies.

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Newcomers to the DIG System often inquire about the possibility of performing Northern blot hybridizations with nonradioactive techniques. With the following examples, we would like to share our protocol for performing highly sensitive Northern blots. This procedure strictly adheres to the standard procedures detailed in our manuals and pack inserts, and there are no special "tricks" required. As a target, we have used total human skeletal muscle RNA (Clontech). We selected two probes: beta-actin and a probe comprising the cDNA of the transcription factor CTF1, which expresses a low abundant mRNA. We used in vitro transcribed RNAs exclusively as probes because, during the development of the DIG System, we have found that RNA probes exhibit a 10-100-fold higher sensitivity with RNA targets than do DNA probes. They are also less prone to background problems caused by probe concentrations that are too high. For DNA probes, we recommend an optimal probe concentration of 25 ng/ml. Using a probe concentration that is even slightly too high (e.g., 1.5 fold) will dramatically increase the background. For RNA probes, we recommend an optimal probe concentration of 100 ng/ml, which will not lead to background problems. In the following examples, we describe all experimental details, starting from the gel run for the blot.

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There is increasing evidence that cardiac glycosides act through mechanisms distinct from inhibition of the sodium pump but which may contribute to their cardiac actions. To more fully define differences between agents indicative of multiple sites of action, we studied changes in contractility and action potential (AP) configuration in cat ventricular myocytes produced by six cardiac glycosides (ouabain, ouabagenin, dihydroouabain, actodigin, digoxin, and resibufogenin). AP shortening was observed only with ouabain and actodigin. There was extensive inotropic variability between agents, with some giving full inotropic effects before automaticity occurred whereas others produced minimal inotropy before toxicity. AP shortening was not a result of alterations in calcium current or the inward rectifier potassium current, but correlated with an increase in steady-state outward current (Iss), which was sensitive to KB-R7943, a Na+-Ca2+ exchange (NCX) inhibitor. Interestingly, Iss was observed following exposure to ouabain and dihydroouabain, suggesting that an additional mechanism is operative with dihydroouabain that prevents AP shortening. Further investigation into differences in inotropy between ouabagenin, dihydroouabain and ouabain revealed almost identical responses under AP voltage clamp. Thus all agents appear to act on the sodium pump and thereby secondarily increase the outward reverse mode NCX current, but the extent of AP duration shortening and positive inotropy elicited by each agent is limited by development of their toxic actions. The quantitative differences between cardiac glycosides suggest that mechanisms independent of sodium pump inhibition may result from an altered threshold for calcium overload possibly involving direct or indirect effects on calcium release from the sarcoplasmic reticulum.

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The effects of hydralazine plus isosorbide dinitrate were compared with those of enalapril in 804 men receiving digoxin and diuretic therapy for chronic congestive heart failure (CHF) in the Department of Veterans Affairs Cooperative Vasodilator-Heart Failure Trial (V-HeFT II).

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This case evaluation demonstrated probable pruritus induced by intravenous rifampin. Clinicians should be alerted that intravenous rifampin, as well as orally administered rifampin, has the potential to cause moderate pruritus.

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The concomitant use of herbal medicines and pharmacotherapy is wide spread. We have reviewed the literature to determine the possible interactions between seven popular herbal medicines (ginkgo, St John's wort, ginseng, garlic, echinacea, saw palmetto and kava) and conventional drugs. Literature searches were performed using MEDLINE, Cochrane Library and EMBASE and we identified 128 case reports or case series, and 80 clinical trials. Clinical trials indicate that St John's wort (Hypericum perforatum), via cytochrome P450 (CYP) and/or P-glycoprotein induction, reduces the plasma concentrations (and/or increases the clearance) of alprazolam, amitriptyline, atorvastatin, chlorzoxazone, ciclosporin, debrisoquine, digoxin, erythromycin, fexofenadine, gliclazide, imatinib, indinavir, irinotecan, ivabradine, mephenytoin, methadone, midazolam, nifedipine, omeprazole, oral contraceptives, quazepam, simvastatin, tacrolimus, talinolol, verapamil, voriconazole and warfarin. Case reports or case series suggest interactions of St John's wort with adrenergic vasopressors, anaesthetics, bupropion, buspirone, ciclosporin, eletriptan, loperamide, nefazodone, nevirapine, oral contraceptives, paroxetine, phenprocoumon, prednisone, sertraline, tacrolimus, theophylline, tibolone, tryptophan, venlafaxine and warfarin. Ginkgo (Ginkgo biloba) decreases the plasma concentrations of omeprazole, ritonavir and tolbutamide. Clinical cases indicate interactions of ginkgo with antiepileptics, aspirin (acetylsalicylic acid), diuretics, ibuprofen, risperidone, rofecoxib, trazodone and warfarin. Ginseng (Panax ginseng) may interact with phenelzine and warfarin. Kava (Piper methysticum) increases the clearance of chlorzoxazone (a CYP2E1 substrate) and may interact with alprazolam, levodopa and paroxetine. Garlic (Allium sativum) interacts with chlorpropamide, fluindione, ritonavir and warfarin; it also reduces plasma concentrations of chlorzoxazone (a CYP2E1 probe). Echinacea might affect the clearance of caffeine (a CYP1A2 probe) and midazolam (a CYP3A4 probe). No interactions have been reported for saw palmetto (Serenoa repens). Numerous interactions between herbal medicines and conventional drugs have been documented. While the significance of many interactions is uncertain, several interactions, particularly those with St John's wort, may have serious clinical consequences.

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A patient with renal failure due to myeloma kidney and coincident digitalis intoxication due to prescribed daily digoxin administration was treated with digoxin-specific antibody fragments and plasmapheresis. Rapid response to therapy was noted, removal of digoxin-antidigoxin antibody complexes was confirmed, and prevention of delayed rebound toxicity was documented. We suggest that this is the therapy of choice in similar individuals.

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Prospective evaluation of renal (diuresis, creatinaemia, sodium), metabolic (base excess, anion gap, lactate, bicarbonate) and hepatic (alanine transaminase, aspartate aminotransferase, direct bilirubinaemia) tolerance to PG in (pre)term neonates following intravenous administration of formulations (paracetamol, phenobarbital, digoxin) that contain PG. Observations from 48 h before up to 48 after the last PG administration were described and compared (paired analysis). Clinical characteristics and observations collected following intravenous PG-paracetamol administration were compared with a historical cohort of neonates in whom similar (renal, hepatic) observations during exposure to a mannitol-containing paracetamol formulation were collected.

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Disturbances in colour vision are a well-reported adverse ocular effect to toxic levels of digoxin. We present a case history of a patient with both colour vision changes and transient visual field defects to therapeutic serum levels of digoxin.

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The effect of renal and/or hepatic dysfunction, and of concomitant spironolactone therapy, on seven commercial digoxin assays was evaluated in 45 patients taking both these drugs, and a comparison made with the digoxin concentrations measured using the same assays in 30 patients taking digoxin in the absence of spironolactone. The study showed that increasing renal dysfunction resulted in increasing inaccuracy in assay results with the methods tested. The influence of concomitant spironolactone was to produce a further distortion, which was shown to be additive in patients with impaired renal and/or liver function. The results highlight the unresolved specificity problems which persist in many, if not all, of the immunoassays currently offered to clinical laboratories which, if not recognised, could significantly influence digoxin therapy and patient management.

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During exercise without medication, the heart rate was 85 (SD 8) beats.min-1 at rest, 127(19) at the level of anaerobic threshold, and 175(17) at peak exercise. With digoxin, heart rate was reduced to 75(9) beats.min-1 at rest (control v digoxin, p less than 0.01). However, reduction of heart rate was not seen at anaerobic threshold or at peak exercise. With propranolol, heart rate was 63(7) beats.min-1 at rest, 99(16) at anaerobic threshold, and 138(28) at peak exercise (control v propranolol, all p less than 0.01). Heart rate with verapamil was 70(13) beats.min-1 at rest, 107(30) at anaerobic threshold, and 138(28) at peak exercise (control v verapamil, p less than 0.05 at rest and at anaerobic threshold, p less than 0.01 at peak exercise. Neither digoxin, nor propranolol, nor verapamil changed the oxygen uptake during exercise. Without medication, oxygen pulse was 6.5(2.0) ml.beat-1 at anaerobic threshold and 7.7(2.1) ml.beat-1 at peak exercise. With digoxin, the change of oxygen pulse, versus without medication, was not significant at rest or at anaerobic threshold but was increased at peak exercise, at 8.3(2.1) v 7.7(2.1) ml.beat-1, p less than 0.05. With propranolol, oxygen pulse was increased to 8.2(1.9) ml.beat-1 at anaerobic threshold and 9.2(2.3) ml.beat-1 at peak exercise (control v propranolol, both p less than 0.01). With verapamil, oxygen pulse was increased to 8.7(1.8) ml.beat-1 at anaerobic threshold and 10.0(2.1) ml.beat-1 at peak exercise (control v verapamil, both p less than 0.01).

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This descriptive study was conducted in an emergency department (ED) in Iran. Sixty patients with a new onset AF and rapid ventricular response receiving digoxin or verapamil were included and observed.

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Neurokinin-1 (NK1) receptor antagonists (RAs) are commonly coadministered with serotonin (5-HT3) RAs (e.g. palonosetron (PALO)) to prevent chemotherapy-induced nausea/vomiting. Netupitant/palonosetron (NEPA), an oral fixed combination of netupitant (NETU)-a new NK1 RA-and PALO, is currently under development. In vitro data suggest that NETU inhibits CYP3A4 and is a substrate for and weak inhibitor of P-glycoprotein (P-gp). This review evaluates potential drug-drug interactions between NETU or NEPA and CYP3A4 substrates/inducers/inhibitors or P-gp substrates in healthy subjects. Pharmacokinetic (PK) parameters were evaluated for each drug when NETU was coadministered with PALO (single doses) and when single doses of NETU or NEPA were coadministered with CYP3A4 substrates (erythromycin (ERY), midazolam (MID), dexamethasone (DEX), or oral contraceptives), inhibitors (ketoconazole (KETO)), or inducers (rifampicin (RIF)), or a P-gp substrate (digoxin (DIG)). Results showed no relevant PK interactions between NETU and PALO. Coadministration of NETU increased MID and ERY exposure and significantly increased DEX exposure in a dose-dependent manner; NETU exposure was unaffected. NEPA coadministration had no clinically significant effect on oral contraception, although levonorgestrel exposure increased. NETU exposure increased after coadministration of NEPA with KETO and decreased after coadministration with RIF; PALO exposure was unaffected. NETU coadministration did not influence DIG exposure. In conclusion, there were no clinically relevant interactions between NETU and PALO, or NEPA and oral contraceptives (based on levonorgestrel and ethinylestradiol exposure). Coadministration of NETU or NEPA with CYP3A4 inducers/inhibitors/substrates should be done with caution. Dose reduction is recommended for DEX. Dose adjustments are not needed for NETU coadministration with P-gp substrates.

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Blood pressure (BP) regulation depends on the interaction between multiple environmental and genetic factors. Of these, BP sensitivity to dietary sodium intake has been one that has been investigated in adults but not in children. The aim of the present study was to investigate, prospectively, the BP profile in relation to different genetic and hormonal factors, in the first 3 years of life.

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We studied the effect of varying water and salt intake on the renal excretion of endogenous digoxin-like immunoreactive factors (DLIF). DLIF were measured in human urine and serum by competitive displacement of 125I-labeled digoxin from anti-digoxin antibodies. Diuresis was selectively induced in normal healthy humans by acute water ingestion, and natriuresis was preferentially induced by acute saline ingestion. We found the amount of endogenous immunoreactivity excreted in urine to be correlated with urine flow rate but not with urinary sodium excretion. Urinary excretion of DLIF, normalized to creatinine, was 3.6-fold greater at a urine flow rate of 5.5 mL/min than at 0.5 mL/min. On the other hand, saline intake increased urine flow rate 1.9-fold and increased sodium excretion threefold, but did not affect urinary excretion of DLIF. Fractional excretion of DLIF was linearly related to fractional excretion of water. This study demonstrates that normalization of DLIF values to urinary creatinine does not make DLIF excretion independent of urine flow rate and underscores the need for information on urine flow rate when DLIF measurements in urine are being interpreted.

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lanoxin mg 2015-03-23

We hypothesized that buy lanoxin an unfavorable bias may exist against black patients in the medical management of heart failure.

lanoxin 50 mg 2015-06-21

A foal with vegetative bacterial endocarditis affecting the wall of the left atrium was treated successfully with cefotaxime, erythromycin, and rifampin. Bacterial isolates included Escherichia coli from blood and Rhodococcus equi from a P-type osteomyelitic lesion of the left third metatarsal bone and from synovial fluid from the left metatarsophalangeal joint. Cardiac complications included cardiomegaly and atrial fibrillation, which responded to treatment with digoxin and quinidine sulfate. Cardiac function was considered buy lanoxin normal 18 months after treatment. Bacteriologic cure of osteoarthritis was achieved by use of surgical debridement, lavage, and local and systemic antimicrobial treatment; however, lameness developed 18 months after treatment when training for flat racing was begun. Radiography revealed chronic degenerative joint disease.

lanoxin overdose 2015-06-14

Firstly, we showed buy lanoxin the results of the statistical tests performed on each population to verify their distribution. Analysis by several statistical tests (Passing and Bablok regression, Youden and Bland and Altman diagrams, the Mountain plot and multivariate analysis) showed that all the assays studied were valid in both serum and lithium heparin plasma matrices.

lanoxin yellow tablet 2017-04-26

Digoxin-specific antibodies (Fab) are currently the treatment of choice for digoxin intoxication. These fragments bind to digoxin, leading to Fab-digoxin complexes, and promote the release of receptor-bound digoxin. These complexes are renally excreted. In the case of anuria, they could be dissociated and lead to renewed intoxication. In this case plasma exchanges are proposed. We report the case of an anuric patient with digoxin intoxication, treated with a Fab injection, followed by a plasma exchange 16 hours later, a second Fab injection was given followed by two plasma exchanges, 38 and 86 hours later. The buy lanoxin disappearance of cardiac abnormalities showed the efficiency of the Fab, the drop in serum digoxin concentration and the high digoxin concentration in the exchanged plasma indicate effective elimination. The association of Fab and plasma exchanges could be proposed in the case of digoxin intoxication in the anuric patient.

lanoxin 125 mg 2015-08-08

The buy lanoxin purpose of this study was to document adverse drug reaction (ADR)-related hospitalizations from a nursing facility population.

lanoxin cost 2017-10-22

This report describes the normalization of left ventricular ejection fraction and resolution of signs and symptoms of chronic and severe heart failure in both male and female patients (mean age 54 years) treated with standard medical therapy. These observations were made in 11 patients with idiopathic dilated cardiomyopathy treated in a single cardiology practice, who had evidence of myocardial "viability" (dysfunctional but noncontractile myocardium that has the potential for improvement in function) as assessed by cardiac magnetic resonance imaging, low-dose dobutamine echocardiography, or nuclear imaging. These patients were treated with standard available therapies including beta-blockers, angiotensin-converting enzyme inhibitors, digoxin, and potassium and non-potassium-sparing diuretics buy lanoxin . The average ejection fraction at presentation was 17% +/- 9% which improved to 59% +/- 5%. All patients improved to New York Heart Association functional class I with available therapy. The majority of patients received micronutrient supplementation with coenzyme Q10, vitamin B1, and amino acids, which target the pathways of cardiac metabolism and may aid in the restoration of cardiac function. This case series demonstrates that normalization of cardiac function is possible with standard therapy and the importance of assessing myocardial viability in all patients with heart failure and reduced ejection fraction. Given the unique metabolic needs of the failing heart, the role of micronutrients in combination with standard therapy warrants further investigation.

lanoxin usual dosage 2016-02-14

433 patients aged 29-80 with mild to moderate heart failure entered a multicentre double-blind randomised between-patient comparison of xamoterol 200 mg twice daily, digoxin 0.125 mg twice daily, and placebo. Patients were assessed at baseline and after three months. Of 349 who completed the double-blind phase buy lanoxin , 300 had valid exercise tests. Compared with placebo, xamoterol significantly increased exercise duration and work done on a bicycle ergometer and improved breathlessness and tiredness during daily life as assessed by visual analogue scale and by Likert scale. Digoxin showed no statistically significant advantage over placebo on any of the measures except the Likert scale. Exercise performance and work done were significantly higher with xamoterol than with digoxin.

lanoxin syrup dosage 2015-05-05

The aim of this review is to demonstrate why the management of compliance, although not an explicit feature of the rules of Good Clinical Practice, is essential to the successful conduct of clinical trials and in correct interpretation of the results. Methods to measure compliance in randomized clinical trials are also described. The relevant literature was retrieved by a manual search of the Cumulated Index Medicus 1975-1989 and a MEDLINE computer search of publications in 1990 using the Medical Subject Headings "patient compliance" and "clinical trials". All retrieved articles are discussed. Research into patient compliance has stagnated because of the lack of a "gold" standard of measurement. Nevertheless, management of compliance at the different stages of clinical trials is necessary; at trial design, compliance should be taken into account in sample size calculations; during the conduct of a trial, compliance should be monitored in order to safeguard the power of the study; and in interpretation of trial results, compliance data are helpful both in order to avoid erroneous conclusions and to enrich the value of the buy lanoxin data. Compliance should be measured in all limbs of randomized trials, including the placebo limb, without breaking trial blinding. A classification of compliance behaviour into six types (complier, partial complier, overuser, erratic user, partial dropout and dropout) is proposed, based on the changes in the risk-benefit ratio produced by non-compliance. The use of deuterium oxide, low dose phenobarbitone (2 mg per day), digoxin (2.2 micrograms per day) and the new electronic monitoring devices are suitable methods for measurement in clinical trials.

lanoxin reviews 2015-03-14

Isotopic and colorimetric in situ hybridization techniques were combined to determine if nerve growth factor (NGF) mRNA is colocalized with mRNA for the GABA biosynthetic enzyme glutamic acid decarboxylase (GAD) in adult rat hippocampus. Quantification of neurons labeled with both 35S-labeled GAD67 mRNA and digoxigenin-labeled NGF cRNA determined that of the NGF cRNA-labeled neurons, 97% within regions CA3-CA1, and 88% within the hilus, were also labeled with GAD67 cRNA. Overall, 47% of the total population of GAD67 cRNA labeled cells were NGF cRNA positive. The greater portion of stratum granulosum was lightly labeled by the NGF cRNA alone. The results indicate that, excepting stratum granulosum, buy lanoxin NGF is predominantly synthesized by GABAergic neurons in rat hippocampus.

lanoxin dosage iv 2015-10-26

Reverse transcriptase-polymerase chain reaction (RT-PCR) of mRNA from canine large intestine, skeletal muscle, pancreas, kidney, and spleen and from cultured wild-type and C7 and C11 Madin-Darby canine kidney (MDCK) cells revealed considerable variation in anion exchanger (AE)1 and AE2 mRNA levels between the tissues. Similar high levels of AE2 mRNA were detected in all the MDCK cell populations. AE2 in MDCK cells is probably buy lanoxin the basolateral Cl-/HCO3- exchanger common to the principal and beta-intercalated cells.

lanoxin drug interactions 2017-08-06

Seventy consecutive patients who underwent CABG (group A) were compared to 70 consecutive subsequent patients who underwent CABG + ventral cardiac denervation (group B). Both groups were well-matched for age, gender, disease severity, LV function, Euro scores, Parsonnet scores, preoperative beta-blockers, Ca-channel blockers, digoxin, and angiotensin converting enzyme inhibitors. The same cardioplegia, bypass, and operation techniques were used in all cases. buy lanoxin Denervation before initiating bypass increased operation time by approximately 5 minutes. Heart rate and rhythm were monitored by continuous telemetry until postoperative day 5 and then 4- hourly until discharge.

lanoxin and alcohol 2017-03-04

Compliance with the treatment guidelines remains suboptimal and further patient buy lanoxin education is needed.

lanoxin dosage 2017-09-11

HeLa/pSV-GT expressed significantly high degree of GST-pi mRNA, whereas both HeLa/pSV-neo and HeLa cells had very low expression. Cytotoxicities of HeLa/pSV-GT and HeLa/pSV-neo with 4 anticancer drugs were measured by MTT assay. Drug buy lanoxin concentrations for yielding 50% inhibition (IC50) in HeLa/pSV-GT by adriamycin, mitomycin and cisplatinum were 70.13 microg/mL, 10.95 microg/mL and 16.52 microg/mL, respectively. In contrast, IC50 in HeLa/pSV-neo was 10.34 microg/mL, 7.48 microg/mL and 13.70 microg/mL, respectively. The cytotoxicities of vincristine on both HeLa/pSV-GT and HeLa/pSV-neo were not significantly different.

lanoxin drug card 2017-10-15

Current understanding of the pathophysiology of chronic congestive cardiac failure resulting from dilated cardiomyopathy has shifted management strategy from steps that directly improve myocardial function to those that modulate the neuroendocrine profile and peripheral vascular reactivity. Similar advances in therapeutic applications would Tricor Mg be assisted by controlled studies and full licensing of drugs for use in children. Medical intervention will remain the cornerstone of management until advances in surgical techniques become more widely available.

lanoxin therapeutic dose 2015-04-28

Increased heart rate is a normal physiological adaptation occurring during pregnancy. Some women have severe tachycardia requiring medical attention. Aim Valtrex 3000 Mg of this study is to determine the number of women with benign symptomatic palpitations who receive treatment.

lanoxin dose range 2017-10-30

A double-blind randomised, parallel, placebo-controlled study was performed in patients with congestive heart failure, at 13 centres in 10 countries, to assess the efficacy and safety of lisinopril, a new angiotensin-converting enzyme inhibitor. After a 2-week run-in period, 130 patients receiving digoxin and/or diuretics were randomised to 12 weeks of treatment with lisinopril 5 mg daily (87 patients) or with placebo (43 patients), with an option to increase lisinopril dosage to 10 or 20 mg. Patients treated with lisinopril improved significantly more than placebo-treated patients (p less than 0.05) for all clinical parameters except oedema and paroxysmal nocturnal dyspnoea. Left ventricular ejection fraction rose by 8% in lisinopril patients compared to 2% in the placebo group, while the cardiothoracic ratio and echocardiographic end systolic diameter fell in the lisinopril group (p less than 0.01) but not in the placebo group. Exercise duration was greater in the lisinopril group at all timepoints, and the increase in exercise duration at 12 weeks was greater by more than 2 min in the lisinopril group as compared to the placebo group (p less than 0.01). Changes in clinical and noninvasive parameters such as the New York Heart Association status, were well correlated with changes in exercise duration. Four patients in the lisinopril group and three in the placebo group died in this study, and there were 31 adverse clinical experiences in the 87 lisinopril-treated patients compared to 13 in the 43 placebo-treated patients. We conclude that lisinopril in doses of 2.5-20 mg/day is Lexapro Cost well tolerated and effective in patients with heart failure who are receiving digitalis and diuretics.

lanoxin loading dose 2015-04-20

Patients with congestive heart failure (CHF) can be treated by diuretics, inotropic agents and vasodilators. Increased diuresis lowers left and right ventricular filling pressures but may further reduce cardiac output. Nevertheless, diuretics produce symptomatic improvement in most patients. Digoxin also has beneficial hemodynamic effects in patients with advanced CHF and sinus rhythm, but the frequency and degree of therapeutic response is inferior to that of vasodilators. Among the latter, ACE inhibitors are the most appropriate for long-term administration since they do not lead to Cytoxan Medication development of tolerance and seem to improve long-term prognosis in patients with severe CHF. Newer inotropic agents have marked hemodynamic effects in the short term, but their utility for chronic treatment remains questionable. The optimum choice of drugs in various forms and stages of CHF is discussed.

lanoxin tablet dosage 2015-09-06

Digoxin has a narrow therapeutic margin and potentially life-threatening cardiac adverse effects. Gastrointestinal disorders, neuropsychological disorders and bradycardia are warning signs. Some drug combinations can aggravate the cardiac adverse effects of digoxin, or reduce its efficacy. We reviewed the literature, using the standard Prescrire methodology, in order to examine which drugs are involved in these interactions, and the mechanisms involved. Most relevant data are based on small pharmacokinetic studies or detailed case reports. The adverse effects of digoxin are potentiated by Geodon Iv Dose renal impairment, which may be pre-existing or due to nephrotoxic drugs such as nonsteroidal antiinflammatory drugs (NSAIDs), angiotensin-converting-enzyme (ACE) inhibitors, angiotensin II receptor antagonists and ciclosporin. Some coadministered drugs such as macrolides and cardiovascular drugs (especially amiodarone) can cause digoxin overdose through pharmacokinetic interactions. The mechanism most often implicated is inhibition of P-glycoprotein, of which digoxin is a substrate. Hypercalcaemia and hypokalaemia inducing drugs, heart-rate lowering drugs, and drugs that prolong the QT interval or slow cardiac conduction can potentiate the cardiac adverse effects of digoxin. Plasma concentration of digoxin is not affected. Several drugs, including sucralfate, acarbose, cytotoxic agents, and enzyme inducers, can reduce digoxin plasma concentrations. This effect is attributed to decreased gastrointestinal absorption or increased elimination of digoxin. In practice, patients treated with digoxin, and their caregivers, should be aware that digoxin has a narrow therapeutic margin and frequent and potentially severe adverse effects. Close clinical monitoring is necessary to detect early warning signs (bradycardia and gastrointestinal or neurological disorders). Digoxin assay alone is not always sufficient. Special care is required for patients with renal failure, the elderly and patients receiving potentially interacting drugs.

lanoxin recommended dose 2016-08-30

A group of 25 patients in III-IV haemodynamic period of chronic stagnant circulatory failure (pzns) in clinical conditions for two weeks were administered digoxin and furosemide (DF), then for the following two weeks DF therapy was combined with nifedipine (N), in the following 4 weeks the DFN therapy was combined with captopril (DFNK), in the last two weeks DFN therapy was applied again. The authors used the following doses per 24 h: D--0.29 +/- 0.96 mg, F--13.5 +/- 4.8 mg, N--40.8 +/- 12.8 mg and K 75.0 +/- 28.8 mg. Each cycle of the therapy was followed by a precise clinical evaluation, analysis of the function of the left ventricle by means of two-dimensional echocardiography, the evaluation of the tolerance of physical effort and the evaluation of chest radiograms. Besides, blood was studied for the concentrations of potassium, sodium, chloride, urea, creatinine, uric acid, haematocrit value and pH value. The addition of nifedipine to the classical therapy did not give significant improvement in the clinical condition, haemodynamic parameters and the tolerance of physical effort in patients with pzns. In comparison to DF period, the use of captopryl brought about a statistically significant increase (p less than 0.05) in ejection fraction (EF) from 43.0 +/- 15.3% up to 45.2 +/- 11.7%, in effort power from 36.5 +/- 16.4W up to 47.1 +/- 17.5W, in effort duration from 3.5 +/- 1.6 min. up to 4.5 +/- 1.8 min. and a significant decrease (p less than 0.05) in body weight from 68.1 +/- 13.8 down to 66.9 +/- 13.0 kg and heart volume from 1175.5 +/- 487.3 cm3 down do 1074.6 +/- 380.9 cm3. One could notice, though statistically not significantly (p greater than 0.05) an increase in stroke volume index and cardiae index. Besides, the authors noticed a tendency to an increase Lexapro Regular Dosage in potassium concentration in blood serum. Eliminating captopryl caused fast regression of positive haemodynamic effects, decrease in physical effort tolerance, and clinical condition resumed the condition observed in the period of DFN therapy.

lanoxin y3b pill 2017-10-31

63 consecutive patients with chronic atrial fibrillation accepted for treatment with electrical cardioversion. Before cardioversion all patients were treated with digoxin, verapamil Bactrim 600 Mg , or a combination of both to attain a resting heart rate < or = 100 beats per minute.

lanoxin 250 mg 2017-04-26

Results indicate significant (P < 0.05) reduction in Na+K+-ATPase activity in the Type 1 diabetic patients (0.38 +/- 0.08 vs. 0.59 +/- 0.07 microM Pi/mgprotein/h) compared to the control but with greater reduction in the diabetic subgroup with poor glycemic control (n = 20) and in whom cases of hypercholesterolemia (8.8%), hypertriglyceridemia (2.9%) and elevated LDL-cholesterol (5.9% each) were found. Correlation analyses further revealed significant (P < 0.05) inverse correlations [r = -(0.708-0.797] between all the atherogenic lipid metabolites measured and Na+K+-ATPase in this subgroup contrary to group with good glycemic control or non-diabetic subjects in which significant (P < 0.05) Na+K+-ATPase and HDL-C association were found (r = 0.427 - 0.489). The Na+K+-ATPase from the diabetic patients also exhibited increased sensitivity to digoxin and alterations in Accutane Online Pharmacy kinetic constants Vmax and Km determined by glycemic status of the patients.

lanoxin dosage range 2016-05-17

Despite the absence of cardiac or renal pathologies, edema and mild hyponatremia may often occur in patients affected by chronic obstructive pulmonary disease (COPD). Therefore, it has been suggested that hypoxia may influence the release of different hormones regulating renal sodium handling. To evaluate the effect of hyperoxia and O2 removal on plasma digitalis-like substance (DLS) levels, 9 patients affected by COPD and 7 normal subjects were studied. After 1 h in supine position, O2 was administered for 3 h by a tight-fitting face-mask. Blood samples for plasma DLS were taken at time 0, 60, 180 min and then for 3 h after O2 removal. In normal subjects, plasma DLS did not vary after O2 administration (from basal values of 162.25 +/- 8.59 to 107.75 +/- 6.65 pg/ml at 180 min; NS), and O2 removal (143.7 +/- 16.87 pg/ml after 3 h from O2 removal; NS). On the contrary, in patients affected by COPD, plasma DLS levels increased during O2 administration (from basal values of 138.98 +/- 8.31 to 202.14 +/- 8.21 pg/ml at 180 min; p < 0.05), and returned to baseline levels (142.59 +/- 8.28 pg/ml) 3 h after O2 removal. In the same patients, DLS increase was accompanied by a rise in Na+ excretion (from 0.08 +/- 0.01 at time 0 to 0.16 +/- 0.02 mEq/min after Imitrex Daily Dosage 3 h of O2 administration; p < 0.05). In conclusion, our findings showed an oxygen-related increase in plasma DLS levels and in urinary Na+ excretion in patients affected by COPD. This phenomenon could promote Na+ urinary loss during prolonged O2 therapy in these patients and should be taken into account in their management.

lanoxin overdose effects 2017-11-15

This study evaluated seven clinical questionnaires for the diagnosis of heart failure in the community. Their low sensitivity impairs their usefulness as diagnostic instruments, but their high specificity makes them useful for the identification of patients with fluid retention and/or exercise intolerance from non-cardiac causes.

lanoxin 2 mg 2015-11-19

MPO and NA beta G were not considered very useful as biochemical predictors of muscle damage for these formulations. Histology generally correlated with RbLV values. Compared to saline, RbLV was marked for all formulations within 1-3 days of injection. After day 3, lesions quickly resolved, and no significant differences were found. For these formulations, all CK animal models and RFE were generally predictive of RbLV. A formulation with RtCK > 1000 U/L or RbCK > 3000 U/L, was predicted to be poorly, tolerated.

lanoxin tablets dose 2015-08-10

The potential interaction between nimesulide, a nonsteroidal anti-inflammatory drug, and digoxin was studied in 9 patients [6 males, 3 females; mean age 67 (range 57 to 70) years] with mild heart failure. All patients were receiving maintenance therapy with digoxin (0.25 mg/day, orally) and were treated with oral nimesulide 100mg twice daily for 7 days. Blood samples were collected at 8am and 6pm for 4 days before and throughout the nimesulide treatment period for determination of serum digoxin concentrations. Physical health, electrocardiographic recordings and blood and urine samples were also monitored. Mean serum digoxin concentrations remained within the normal therapeutic range throughout the study despite large interindividual variation. Furthermore, there were no significant differences between the morning and afternoon serum digoxin concentrations and there was no major change in the clinical condition of any patient. These results indicate that short term administration (7 days) of conventional therapeutic doses of nimesulide (100mg twice daily) does not modify the serum digoxin profile in patients with low class heart failure treated with a maintenance dose (0.25 mg/day) of this cardiac glycoside.

lanoxin drug dose 2015-07-19

The mouse hybridoma cell line 40-150 secretes antibodies with high affinity toward the cardiac glycosides digoxin and digitoxin. A spontaneous mutant, 40-150 A2.4, produces an antibody which carries a single residue mutation, Ser----Arg, in its heavy chain (H94) and has an altered specificity. A second-order mutant, 40-150 A2.4 P.10, produces two antibody molecules, one the same as 40-150 A2.4, the other lacking two residues at the N-terminus of its H chain, and having a specificity profile approaching that of 40-150 antibody. The N-terminus and the position H94 are distant from the antigen-binding site of the antibody; thus, the structural basis of the specificity changes was not immediately clear. Approximate structures of the 40-150 antibody and its mutants were constructed in the computer, based on atomic coordinates of the homologous mouse antibody McPC 603. Using the program CONGEN, the torsional space of the polypeptide backbone and side chains around position H94 was uniformly sampled, and the lowest energy conformations were analyzed in detail. The results indicate that when Arg-H94 is substituted for Ser, Arg-H94 can hydrogen bond to side chains of Asp-H101, Arg-L46, and Asp-L55. This results in a change in the surface of the combining site which may account for the affinity changes. Deletion of the two N-terminal residues increases solvent accessibility of Arg-H94. The solvation may cause a hydrogen bond between Arg-H94 and Asp-H101 to be lost, restoring the structure to one similar to that of 40-150.