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 digoxin toxicity  



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Author25 Posts
  #1

you are treating a patient with heart failure and have put her on digoxin.which one of the following symptoms indicates there is digoxin toxicity?
1) pleural effusion
2) bradycardia
3) blue nose
4) diminished hearing
5) abdominal distension




  #2

2) bradycardia ??? Sinus bradycardia


  #3

B.
Early sign is bradicardia, severe toxicity--- tachycardia


  #4

Atrial tachycardia with variable block is a classic electrocardiographic finding in digitalis toxicity.

The first-line treatment for life-threatening digitalis toxicity is administration of digoxin-specific antibody fragments.



  #5

AAAAA wrote:
Atrial tachycardia with

variable block is a classic

electrocardiographic finding in

digitalis toxicity.



The first-line treatment for

life-threatening digitalis

toxicity is administration of

digoxin-specific antibody

fragments.





  #6

sweetybokhari wrote:
you are treating a patient with heart failure and have put her on digoxin.which one of the following symptoms indicates there is digoxin toxicity?
1) pleural effusion
2) bradycardia
3) blue nose
4) diminished hearing
5) abdominal distension


The correct answer is 4

A symptom is a phenomenon that is experienced by an individual. Anxiety, lower back pain, and fatigue , diminished hearing are all symptoms. They are sensations only the patient

Bradycardia is a sign and is wrong, tachycardia is the correct sign




  #7

Digoxin toxicity can cause these symptoms: irregular heartbeats, or arrhythmias, that were not present before changes in color vision, such as a yellowish tint to the vision seeing halos around lights tiredness
  • weakness
  • confusion
  • dizziness abnormal dreams or nightmares
  • loss of appetite nausea and vomiting


  •   #8

    Digoxin toxicity can cause these symptoms: irregular heartbeats, or arrhythmias, that were not present before changes in color vision, such as a yellowish tint to the vision
    seeing halos around lights tiredness
  • weakness
  • confusion
  • dizziness abnormal dreams or nightmares
  • loss of appetite nausea and vomiting


  •   #9

    AAAAA............. U still havent given the Reason or reference as to if there is Diminished Hearing.

    however this is wht i have found on Digoxin toxicity
    • Constitutional symptoms (eg, weakness, fatigue)
    • Cardiovascular
      • Palpitations
      • Syncope
      • Dyspnea
    • Central nervous system
      • Confusion and somnolence
      • Dizziness without vertigo
      • Agitation, delirium, and hallucinations
      • Headache
      • Paresthesias and neuropathic pain
      • Seizures (extremely rare)
    • Ocular
      • Disturbances of color vision with a tendency to yellow-green coloring
      • Blurred vision and diplopia
      • Halos and scotomas
      • Photophobia
    • Gastrointestinal
      • Nausea, vomiting, anorexia, and diarrhea
      • Abdominal pain (uncommon)
    Physical: Hemodynamic instability is related directly to the presence of a dysrhythmia or acute congestive heart failure (CHF).
    • Cardiovascular findings on physical examination relate to the severity of CHF, dysrhythmias, or hemodynamic instability.
      • Digoxin toxicity may cause any dysrhythmia. Classically, dysrhythmias that are associated with increased automaticity and decreased AV conduction occur (ie, paroxysmal atrial tachycardia with 2:1 block, accelerated junctional rhythm, or bidirectional ventricular tachycardia [torsade de pointes]).
      • Premature ventricular contractions (PVCs) are the most common dysrhythmia. Bigeminy or trigeminy occurs frequently.
      • Sinus bradycardia and other bradyarrhythmias are very common. Slow atrial fibrillation with very little variation in the ventricular rate (regularization of the R-R interval) may occur.
      • First- and second-degree AV block, complete AV dissociation, and third-degree heart block are also very common.
      • Rapid atrial fibrillation or atrial flutter is rare.
      • Ventricular tachycardia is an especially serious finding.
      • Cardiac arrest from asystole or ventricular fibrillation is usually fatal.
    • Gastrointestinal symptoms are common, but the abdominal examination is usually nonspecific.
    • Neurological findings are related to changes in sensorium or mental status. Lateralizing findings usually indicate another disease process.
    • Visual changes occur, but the pupils are spared, and objective findings are few.
    • Drug-induced fever does not occur.



      #10

    Is bradycardia.


    Edited by paganini on Mar 30, 2007 - 7:30 AM

      #11

    blue nose To make it more interesting let's say! Stop fighting kids........








      #12

    Paganini........ Psycho or not but he did point out a very essential point Bradycardia is not a Symptom its a Sign so this Question does remain a Mystery.


      #13

    I am not judging him from this post, I am old in this forum and I have read many posts here, I just want to save you time by not reading his posts. But if you insist do what you want......


      #14

    I am not judging him for this post, I am old in this forum and I have read many posts here, I just want to save you time by not reading his posts. But if you insist do what you want......


      #15

    Hey NNL just remembered, It causes tinnitus too...in mild and hearing loss in higer doses..so D, looking who's laughing now!

    AAAA was right.









      #16

    As u say Boss



      #17

    Is bradycardia!!!!! Read under clinical manifestation on this article. This is in every book. but I could paste this info rapidly.

    Digitalis (cardiac glycoside) intoxication
    Nuhad Ismail, MD



    UpToDate performs a continuous review of over 375 journals and other resources. Updates are added as important new information is published. The literature review for version 15.1 is current through December 2006; this topic was last changed on March 28, 2006. The next version of UpToDate (15.2) will be released in June 2007.

    INTRODUCTION — Cardiac glycoside poisoning caused by digitalis or other compounds is a potentially life-threatening intoxication. Patients can present with digitalis toxicity as a result of chronic therapy or acute overdose. Reported mortality ranges from 3 to 50 percent; outcomes have clearly improved with the administration of digoxin-specific antibody fragments to patients with severe toxicity [1-4]. (See "Digoxin-specific Fab fragments" below).

    This topic review will discuss the presentation and management of digitalis intoxication. The therapeutic use of digitalis and details regarding arrhythmias from digitalis toxicity and treatment with digoxin-specific antibody fragments are found elsewhere. (See "Method of digitalization", see "Electrophysiology of arrhythmias due to digitalis toxicity" and see "Dosing regimen for digoxin-specific antibody fragments").

    EPIDEMIOLOGY AND ETIOLOGY — In a multicenter trial of 150 severely poisoned patients, 50 percent were receiving long-term digitalis (mostly digoxin) therapy, 10 percent had taken a large accidental overdose, and 40 percent had overdosed with suicidal intent [1]. Cardiac glycoside toxicity can also result from ingestion of certain plants, including yellow oleander (Thevetia peruviana) and foxglove (Digitalis purpurea), and a similar toxidrome has been associated with use of herbal dietary supplements [5-9].

    Cardiac glycoside toxicity can occur in a patient with any condition that either increases total body levels, or modifies cardiac sensitivity to the drug. Renal insufficiency is a major factor promoting cardiac glycoside accumulation. End-stage renal disease, for example, prolongs the half-life of digoxin and reduces its volume of distribution. As a result, there must be reductions both in the loading dose and in the maintenance dose in this setting. (See "Method of digitalization", section on Dose adjustments).

    There are a number of factors that can increase the sensitivity to digoxin and predispose to toxicity despite plasma levels at the upper limits of normal. Included in this group are advanced age, certain cardiac diseases (active ischemia, myocarditis, cardiomyopathy, cardiac amyloidosis, cor pulmonale) and a variety of metabolic factors (including hypokalemia, hypomagnesemia, hypoxemia, hypernatremia, hypercalcemia, and acid-base disturbances) [3,10,11].

    Several advances have considerably lowered the incidence of digitalis overdose in patients receiving chronic therapy. Reasons for this reduction in digoxin toxicity include: A better understanding of pharmacokinetics, leading to more appropriate maintenance dosing, particularly in patients with renal failure. As an example, one study of serum digoxin concentration in 2009 patients receiving chronic therapy noted supratherapeutic values (>2.0 ng/mL) combined with evidence of toxicity in only 4 percent [12]. (See "Method of digitalization"). Improvement in digoxin formulations with more predictable drug bioavailability, combined with the development of radioimmunoassays for plasma digoxin levels [13,14]. Increasing awareness of drugs that can affect digoxin metabolism. (See "Drugs affecting digoxin metabolism" below). The availability of other drugs to treat heart failure and cardiac arrhythmias, thereby eliminating the tendency to push digitalis to higher (and potentially more toxic) levels. The realization that digoxin withdrawal is a viable proposition in elderly patients [15].

    Drugs affecting digoxin metabolism — Drugs that affect digoxin metabolism include quinidine, cyclosporine, verapamil, diltiazem, tetracycline, erythromycin, and rifampin. Paroxetine, and some other selective serotonin reuptake inhibitors (SSRIs), may also predispose to digoxin toxicity [16]. Most of these drugs raise digoxin levels in part by reducing its excretion. Rifampin, on the other hand, is an enzyme inducer that enhances digoxin metabolism. Thus, discontinuing rifampin in a stable patient will slow digoxin metabolism, possibly leading to drug accumulation.

    PHARMACOLOGY AND CELLULAR TOXICITY — During depolarization, sodium and calcium enter into myocardial cells. During repolarization, these ions are extruded from the cell: sodium via membrane-bound Na-K-ATPase, and calcium via a Na-Ca transporter that exchanges intracellular calcium for extracellular sodium. The latter reaction is driven by the transmembrane sodium gradient. (See "Excitation-contraction coupling in myocardium").

    Cardiac glycosides inhibit Na-K-ATPase, resulting in an increase in intracellular sodium [17]. This decreases the transmembrane sodium gradient. The driving force of the Na-Ca transporter is therefore reduced, and calcium therefore accumulates in the cell. The net effect of these reactions is the loss of intracellular potassium and the gain of intracellular sodium and calcium; the latter is largely responsible for the increase in cardiac contractility.

    Conduction, as well as inotropy, is affected by cardiac glycosides. Cardiac glycosides decrease conduction through the SA and AV nodes and increase automaticity of cardiac tissue. The electrophysiologic effects of digitalis toxicity are reviewed separately. (See "Basic approach to arrhythmias due to digitalis toxicity" and see "Electrophysiology of arrhythmias due to digitalis toxicity").

    Kinetics — The two digitalis preparations used in clinical practice today are digoxin and digitoxin. The bioavailability of digoxin is about 80 percent, while that of digitoxin is 100 percent. The plasma half-lives of these drugs are 1.6 and 5 days, respectively.

    The major depot for digitalis in humans is skeletal muscle. As a result, dosage requirements and the likelihood of toxicity are related to muscle, mass rather than total body weight. Approximately one-third of the body stores of digoxin are excreted per day; 30 percent unchanged in the urine, and 3 percent as metabolites in stool. In contrast, only 15 to 20 percent of body digitoxin stores are excreted per day, mostly as inactive metabolites. Less than 10 percent of digitoxin is converted to digoxin.

    CLINICAL MANIFESTATIONS — Patients may present with acute or chronic cardiac glycoside toxicity. The history should determine the change, if any, in cardiac glycoside dosing and the presence or absence of an acute ingestion. Other important points include the addition of medications known to elevate cardiac glycoside levels, including verapamil, diltiazem, erythromycin or tetracycline.

    Symptoms of cardiac glycoside toxicity are mostly nonspecific, and include fatigue, blurred vision, disturbed color perception, anorexia, nausea, vomiting, diarrhea, abdominal pain, headache, dizziness, confusion, delirium, and occasionally hallucinations [18].

    Bradycardia is the most frequently encountered vital sign abnormality in cardiac glycoside toxicity; tachyarrhythmias are less common. Hypotension may complicate severe cardiac glycoside toxicity, but blood pressure is usually preserved due to the positive inotropic effects of the drug. The remainder of the physical examination is usually unremarkable.

    Electrocardiographic changes — At therapeutic levels, digoxin produces characteristic electrocardiographic changes, including prolongation of the PR segment and "scooping" of the ST segments. Cardiac glycoside toxicity may produce myriad ECG changes. The earliest sign of toxicity is ventricular ectopy, usually manifest by premature ventricular contractions. Increased automaticity may produce atrial tachyarrhythmias and AV nodal depression frequently produces a high-degree block. Thus, the combination of increased automaticity with high-degree AV block (such as atrial tachycardia with 4:1 or 6:1 conduction) should suggest digoxin toxicity. Ventricular arrhythmias (both ventricular tachycardia and ventricular fibrillation) may be seen in digoxin toxicity. Two rhythms in particular, accelerated junctional rhythm and bidirectional ventricular tachycardia, are relatively specific for cardiac glycoside toxicity, and their presence should suggest this condition until proven otherwise. Almost any rhythm with the exception of supraventricular tachycardia with 1:1 conduction through the AV node may be associated with cardiac glycoside toxicity.

    Cardiac arrhythmias are responsible for mortality in glycoside toxicity. A more complete discussion of cardiac glycoside-induced arrhythmias appears elsewhere. (See "Basic approach to arrhythmias due to digitalis toxicity" and see "Electrophysiology of arrhythmias due to digitalis toxicity").

    Serum potassium — Serum potassium plays an important role in the diagnosis and management of cardiac glycoside toxicity in both acute and chronic cases.

    In acute cardiac glycoside toxicity, hyperkalemia is an ominous sign and a predictor of morbidity and mortality. Hyperkalemia in cases of acute toxicity reflects the degree of poisoning of the Na-K-ATPase, the transporter that moves potassium out of the extracellular space; the higher the potassium level, the higher the tissue levels of cardiac glycoside and the worse the prognosis. In a classic paper published before the use of digoxin-specific Fab fragments, patients with acute digoxin toxicity and potassium levels less than 5.0 meq/dL had a 0 percent mortality, those with potassium levels between 5.0 and 5.5 had a 50 percent mortality, and those with potassium levels above 5.5 meq/dL had a 100 percent mortality [19]. It is for this reason that a serum potassium level above 5.0 meq/dL in the setting of acute cardiac glycoside toxicity is an absolute indication for digoxin-specific Fab fragments.

    In chronic cardiac glycoside toxicity, hypokalemia potentiates toxicity and should be corrected immediately. Hypokalemia decreases Na-K-ATP-ase activity, thereby exacerbating the principle cellular derangement of cardiac glycoside toxicity. In some cases, a patient with a cardiac glycoside-related arrhythmia will improve dramatically when normokalemia is restored.

    Plasma digoxin levels — Drug action depends on the tissue concentration, which is relatively constant in relation to plasma levels. Thus, plasma levels can be used to monitor both compliance and toxicity. Plasma digoxin levels should be measured at least six hours after the last dose, since this is the time required for attainment of the steady state due to gradual distribution through the extravascular space. Measurements made prior to this time may give values two to three times higher, because equilibration has not occurred.

    The plasma digoxin concentration should be used only as a guide to appropriate therapeutic dosing and as an indicator of toxicity. Several factors (such as hypokalemia) can predispose to toxicity at levels below 2 ng/mL (2.6 nmol/L), which is usually considered the upper limit of normal. On the other hand, some patients are asymptomatic despite clearly elevated levels (above 3 ng/mL or 3.8 nmol/L) [20].

    False positive results — False positive elevations of plasma digoxin can occur in newborns, pregnant women, and patients with chronic renal failure or hepatobiliary disease. This problem is thought to result from increased levels of endogenous digoxin-like substances, including a compound that is similar to ouabain [21,22]. (See "Natriuretic hormones: Atrial peptides and ouabain-like hormone").

    The magnitude of the elevation depends on the assay method used as well as the underlying clinical condition. The highest false values (up to 4 ng/mL or 5.2 nmol/L) are seen in neonates [23] and significant elevations have also been reported in children [24]. Smaller errors of 0.6 to 1.8 ng/mL (0.8 to 2.3 nmol/L) have been described in the third trimester of pregnancy [25], renal failure [26-29], and combined hepatic and renal failure [30,31].

    False negative results — Patients patients who have ingested a non-digoxin cardiac glycoside, including foxglove and oleander, may have trivial digoxin levels in the setting of profound clinical toxicity. This is due to a lack of cross-reactivity between the digoxin assay and the cardiac glycoside in question [5].

    DIFFERENTIAL DIAGNOSIS — The differential diagnosis of bradycardia, the most common abnormality in cardiac glycoside poisoning, includes intrinsic cardiac conduction abnormalities (such as sick sinus syndrome and atrioventricular node dysfunction), other drugs that may produce bradycardia, and electrolyte disorders.

    Calcium channel blocking medications (particularly verapamil and diltiazem) and beta-adrenergic antagonists may also produce profound bradycardias. The treatment of poisonings with these agents differs in many important respects from the treatment of cardiac glycoside poisoning, so an accurate medication history is crucial. In particular, calcium salts should not be given to treat bradycardia of unknown etiology until cardiac glycoside toxicity is excluded. (See "Calcium channel blocker toxicity" and see "Beta blocker toxicity").

    Hyperkalemia may also produce bradycardia. Not infrequently, hyperkalemia and elevated cardiac glycoside levels may coexist, either after acute ingestion or in the setting of chronic renal failure. When both conditions are present, simultaneous treatment is reasonable with the exception that calcium salts should not be given to treat hyperkalemia until cardiac glycoside toxicity is excluded.

    TREATMENT — Moribund patients should be intubated, and hypoxic patients treated with supplemental oxygen, but these occurrences are relatively rare in the setting of cardiac glycoside poisoning. Symptomatic bradycardias should be treated with atropine, although patients with chronic cardiac glycoside poisoning may be refractory to this intervention. Transvenous cardiac pacing may precipitate cardiac arrhythmias and deterioration, and should be avoided [32]. Beta-agonists (such as isoproterenol) should be avoided, if possible, because of the risk of precipitating more severe arrhythmias.

    In any patient with hemodynamic instability, immediate preparation must be made to infuse digoxin-specific Fab fragments, as outlined below.

    Gastrointestinal decontamination — Digitalis is adsorbed effectively by activated charcoal if ingestion has occurred within six to eight hours; repeated doses can be given to adsorb active metabolites as they are excreted by the biliary tract. (See "Decontamination of poisoned adults").

    Management of serum potassium — In the setting of acute toxicity, hyperkalemia may be treated in the usual fashion with the exception that calcium salts should not be administered. Exogenous calcium administration may worsen intracellular hypercalcemia, one of the fundamental derangements of cardiac glycoside toxicity.

    In the setting of chronic toxicity, potassium should be lowered with caution, so as not to exacerbate digoxin toxicity. Hypokalemia and hypomagnesemia should be treated aggressively, as both potentiate cardiac glycoside toxicity [33].

    Digoxin-specific Fab fragments — Digoxin-specific antibody Fab fragments (Digibind®) are purified from sheep. They rapidly bind to intravascular digoxin. Fab fragments then diffuse into the interstitial space where they bind to digoxin in the tissues. As a result, the free digoxin concentration in the interstitial space is markedly reduced, creating a favorable concentration gradient for the efflux of digoxin out of the cells and into the extracellular fluid where it binds to digoxin-specific antibody fragments. Bound digoxin cannot reassociate with the inhibitory site on the alpha-subunit of Na-K-ATPase [17].

    The digoxin/digoxin-specific Fab fragment complex is relatively small (mol wt 50,000 Daltons), and is rapidly excreted by glomerular filtration in patients with normal renal function. The elimination half-life of the fragments is 15 to 20 hours in this setting.

    Fab fragments can also be used successfully removed in patients with renal insufficiency, including those on maintenance dialysis [1,34-36]. In one study, 18 patients had a pretreatment plasma creatinine concentration of more than 5 mg/dL (440 µmol/L), including five who were on dialysis [1]. These patients responded to Fab fragments in a manner similar to patients with normal renal function.

    There is a theoretical concern that digoxin could be released from the complex with recurrence of toxicity when excretion is slowed by renal insufficiency [37]. The absence of this complication in the above study suggests that it is probably uncommon. Nevertheless, some patients may be at risk, particularly those with a large digoxin load and low Fab dose. Late rebound digoxin toxicity might be prevented by plasmapheresis or plasma exchange after therapy, although the appropriate interval between Fab administration and these interventions is unclear [36,38,39].

    Indications — Digoxin-specific Fab fragments are indicated in the following settings: Hemodynamic instability ascribed to cardiac glycoside toxicity. Life-threatening arrhythmias ascribed to cardiac glycoside toxicity. Severe bradycardia. Even when bradycardia is responsive to atropine, digoxin-specific Fab fragments are indicated to prevent recurrent toxicity after the effects of atropine have subsided. A plasma potassium concentration above 5 meq/L in the setting of acute overdose, regardless of clinical status or electrocardiographic findings. Plasma digoxin concentration above 10 ng/mL (13 nmol/L), regardless of clinical status or electrocardiographic findings. Ingestion of >10 mg of digoxin in adults or >4 mg in children. Presence of a digoxin-toxic rhythm in the setting of an elevated digoxin level.

    Response to therapy — A rapid favorable response to digoxin-specific antibody fragments has been widely reported [1,34-36,40-42]. In the largest series of 150 patients with life-threatening digitalis toxicity, 80 percent had resolution of all signs and symptoms, 10 percent improved, and 10 percent showed no response [1]. The median time to initial response was 19 minutes and the time to complete response was 88 minutes (with a range of 30 minutes to 4 hours). Of the patients who experienced cardiac arrest, 54 percent survived hospitalization.

    Several factors can contribute to partial responses or resistance. These include, in descending order of frequency, underlying heart disease that was the true cause of some of the presumed manifestations of digitalis toxicity, too low a dose of Fab, and treatment of patients who were already moribund.

    A dramatic fall in the plasma potassium concentration can occur after fragment therapy, as reversal of Na-K-ATPase inhibition results in the pumping of extracellular potassium into the cells. The time course parallels the antiarrhythmic response; the decline in the plasma potassium concentration begins within one hour and is complete within 4 hours [1]. Thus, monitoring of the plasma potassium concentration should be performed in all patients receiving this therapy.

    Although not a randomized clinical trial, these results are much better than those reported with conventional therapy. In one such study, for example, the mortality rate was 55 percent in patients with a pretreatment plasma potassium concentration above 5 meq/L [43] versus less than 20 percent with the antibody fragments [1].

    Side effects — Despite the general improvement induced by Fab fragments, potentially important side effects can occur. These include exacerbation of congestive heart failure, increased ventricular response in patients with atrial fibrillation, and, as noted above, hypokalemia due to the movement of potassium into the cells [1,44].

    Idiosyncratic allergic manifestations are very rare, occurring in less than 1 percent of cases. Thus, routine allergy testing, which will delay urgently needed therapy, is not required. It may, however, be appropriate in high-risk patients, such as those with a known allergy to sheep proteins, or those previously treated with digoxin-immune Fab.

    Although, not generally an important clinical problem, plasma digoxin measurements are unreliable for one to two weeks after fragment therapy because the fragments interfere with the conventional assay [45,46].

    Dosing regimen — Digoxin-specific Fab fragments are given intravenously over 30 minutes, unless cardiac arrest has occurred, in which case the solution is given as a bolus. A simplified calculation of the amount of digoxin needed to treat a given digoxin level is:

    Vials of Digoxin-specific Fab fragments = [Digoxin level (ng/ml) x Mass (kg)] ÷ 100

    The results should be rounded up. For example, a 70 kg female with a digoxin level of 3.0 and frequent premature ventricular contractions would have a calculated need for (3.0) x (70) / 100 = 2.1 vials of digoxin-specific Fab fragments. This would be rounded up to three (3) vials as the appropriate dose. The derivation of the simplified formula outlined above can be found elsewhere (See "Dosing regimen for digoxin-specific antibody fragments").

    Patients who are intoxicated with non-digoxin cardiac glycosides, which can result from herbal remedies or plant ingestion, may have very low digoxin levels despite profound clinical toxicity [5]. Such patients should initially be treated with 5-10 vials of digoxin-specific Fab fragments, a dose that may be repeated if clinical response is inadequate.

    Extracorporeal techniques — Hemodialysis or hemoperfusion may help control hyperkalemia or volume overload in patients with concurrent renal failure, but such techniques should not be considered in the treatment of digoxin toxicity. Anecdotal reports of success of hemofiltration have not been substantiated [1,47-49]. (See "Enhanced elimination of poisons").


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      #18

    We should ask sweetybokhari if she/he was playing with words, which I don't think. bradycardia although is a sign can also be symptomatic, and I still can't find a source saying that digitalis toxicity causes tinitus.


      #19

    I have tried not to copy and paste thousands of words, make things simple

    I am sorry I may type the wrong answer D



      #20

    I make a formal apology to all in this Forum, I have not copy and paste others articles for 1 year and show off.I just point out my opinion ! OK let's contribute instead of pointing others mistakes





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