Clinical Utility and Adverse Effects of Amiodarone

8/20/2019 Clinical Utility and Adverse Effects of Amiodarone

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AACN Advanced Critical Care

Volume 21, Number 4, pp.333–338

© 2010, AACN

Earnest Alexander, PharmD, and

Gregory M. Susla, PharmDDepartment Editors

333

Clinical Utility and Adverse Effectsof Amiodarone Therapy

Melissa Roberts, PharmD

Traditional Vaughan Williams classes I and III antiarrhythmic medications areassociated with a high incidence of proarrhythmias. In 1985, amiodarone

(Pacerone, Cordarone) was introduced to the market as a novel new drug totreat ventricular arrhythmias. Its unique mechanism of action produced desir-able arrhythmia suppression with a significantly lower incidence of torsades depointes than agents that were currently on the market.1 Amiodarone is knownto block 4 major contributors to myocardial conduction. Unlike other agents,amiodarone interferes with multiple ion channels, which makes it a hybrid of allof the Vaughan Williams class antiarrhythmics; more specifically, it blocks potas-sium, sodium, and calcium channels. It also possesses qualities of a -adrenergicblocker. -Blockade decreases the myocardium excitability by prolonging theaction potential and increasing the refractory period. A 15% to 20% decrease

in heart rate as well as a 10% increase in the PR-QT interval is expected withamiodarone use.2

Amiodarone has an extensive side effect profile and requires close monitor-ing. An approved Medication Guide2 was mandated by the Food and DrugAdministration (FDA) in 2005 to be dispensed to all patients starting amio-darone therapy. A few reasons for this new requirement included the high vol-ume of amiodarone prescriptions dispensed in 2004, the off-label use in atrialfibrillation, and the potential for the serious risks associated with amiodaronetherapy to be overlooked.3 This educational handout alerts patients to the mostcommon side effects associated with therapy, describes symptoms that shouldbe immediately brought to a physician’s attention, and explains when and how

amiodarone should be taken.2

Although the FDA only requires outpatient phar-macies to dispense the medication guide with new prescriptions, it is imperativefor patients (even when hospitalized) to have all the necessary information tomake an informed decision before starting therapy.

Labeled IndicationsAmiodarone is approved by the FDA to treat recurrent ventricular fibrillation aswell as recurrent ventricular tachycardia, which results in hemodynamic insta-bility. The package insert states that amiodarone should be used only to treatlife-threatening recurrent ventricular arrhythmias when other medical manage-ment has failed or is intolerable; however, current clinical practice uses amio-

darone frequently for both FDA-approved indications and off-label uses. It isstrongly recommended, but not required, to initiate therapy in a hospital setting

Melissa Roberts (formerly Pierce) is Pharmacy Practice Resident, Memorial Medical Center, 1086

Franklin St, Johnstown, PA 15905 ([email protected]).

DOI: 10.1097/NCI.0b013e3181ef86fe

DrugUpdate


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secondary to its multiple drug interactions,side effect profile, and potential to exacerbatearrhythmias.2

Pharmacokinetics

Amiodarone exhibits slow sporadic oral absorp-tion, and only approximately 50% of the dosereaches systemic circulation. Although peakplasma concentrations are reached within 3 to 7hours, full effects are not usually seen for 1 to 3weeks.2,4 When the drug is taken with food, espe-cially high-fat meals, the rate and extent of oralabsorption increases. Not only can amiodaronereach up to 4 times higher concentrations in theblood, it also reaches peak concentrationsapproximately 40% faster in the presence of food.2 Amiodarone has an extremely long half-life of 20 to 47 days2,5 when administered intra-venously and 15 to 142 days2 when given orally,and it has a strong affinity to accumulate in adi-pose tissue as well as organs with a high bloodsupply (eg, spleen, liver, lung).2,4 For this reason,patients on long-term therapy who stop takingthe drug but require reinitiation may see fulleffects much sooner than would a treatment-naive patient. The same is true for drug interac-

tions. Despite cessation of therapy, druginteractions can persist far beyond discontinua-tion.2 Caution should be exercised when usingamiodarone with other medications that candisplace it from protein binding because it ishighly protein bound (96%).2,5

Amiodarone is metabolized by the liver(predominantly cytochrome P 450 3A4), withsubsequent secretion into the bile.2,5 Less than1% of amiodarone and its metabolites areeliminated through the kidneys. Currently, no

dosage adjustments are recommended foreither renal or hepatic dysfunction; however,amiodarone’s major involvement in the liverlends itself to multiple drug interactions(Table 1).1 One major metabolite results fromhepatic metabolism called desethylamio-darone.2,5 It is unknown whether desethy-lamiodarone demonstrates any antiarrhythmicbenefits in humans, but it has been shown todo so in animal models.2 Caution should beexercised for use with elderly patients, because

clearance may be decreased in this popula-tion as well as in people with severe left- ventricular dysfunction.2

Place in TherapySupraventricular tachycardia following openheart surgery can occur in more than 60% of

patients, depending on the type of procedureperformed.7 Prophylactic treatments with med-ications such as -blockers and antiarrhythmicshave been shown to decrease the incidence of atrial fibrillation and atrial flutter by nearly

half.8 A double-blind, randomized, placebo-con-trolled trial titled PAPABEAR published in2005 evaluated the effectiveness and safety of amiodarone therapy compared with placebo fol-lowing elective coronary artery bypass-grafting sur-gery with or without valve repair.9 Overall,amiodarone reduced the rate of supraventriculartachycardia by approximately 50% (16.1% inthe amiodarone group vs 29.5% in the placebogroup, P .001); however, amiodarone therapywas associated with a statistically significantnumber of cardiac side effects including brady-cardia requiring temporary pacing (5.7% vs2.0%) and QTc prolongation (1.3% vs 0%).Given the increased cost and deleterious out-comes associated with postoperative atrial fibril-lation, careful consideration regarding risk andbenefit should be made when using amiodaronefor cardiac surgery prophylaxis.9

No FDA-approved indication is availableto use amiodarone for pharmacologic car-

dioversion of atrial fibrillation to normalsinus rhythm; however, the most recent Amer-ican College of Cardiology/American HeartAssociation/European Society of Cardiologypractice guidelines recommend both oral andintravenous regimens when medical cardiover-sion is indicated.10 Regardless of the durationof atrial fibrillation (the guidelines use 7 daysas the point of reference for changes in therapychoice), amiodarone is regarded as a class IIarecommendation for cardioversion. If a patient

has been in atrial fibrillation for more than48 hours, anticoagulation is necessary. Cliniciansare highly encouraged to initiate therapy in ahospital setting secondary to the adverseeffects associated with both the medicationitself and the conversion to sinus rhythm. Themost common adverse effects associated withintravenous administration include hypoten-sion (seen in 16% of patients),5,11 bradycardia,and QTc prolongation.10 Amiodarone has a44% success rate in acute cardioversion and

65% efficacy in maintaining sinus rhythm12

;however, as is the case with other antiarrhyth-mics, the longer a patient is in atrial fibrilla-tion, the more difficult it is to convert to sinusrhythm, regardless of the agent used.

Traditional management of atrial fibrilla-tion had been primarily treatment with


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VOLUME 21 • NUMBER 4 • O CTOBER–DECEMBER 2010 Drug Update

Table 1: Clinically Significant Drug Interactions With Amiodaronea

Risk of

Medication Interactionb Clinical Intervention

QTc prolongation

Artemether Category X Use is contraindicated

Dronedarone

Lumefantrine

Nilotinib

Pimozide

Quinine

Tetrabenazine

ThioridazineZiprasidone

Azithromycin Category D

Amiodarone decreases the

metabolism of:

Everolimus Category X Use is contraindicated

Tolvaptan

Colchicine Category D

Cyclosporine

Eplerenone

Fentanyl

Flecainide

Tamoxifen

HMG-CoA reductase No interaction with pravastin and fluvastatin

inhibitors Maximum dose simvastatin 20 mg daily

Maximum dose Lovastain 40 mg daily

Digoxin Starting digoxin : 0.125 mg daily in normal

renal function, 0.125 mg every other day inkidney dysfunction

Already on digoxin : Decrease digoxin dose by 50%

Warfarin Starting warfarin: 2.5 mg daily

Decrease warfarin dose by 25%–40% depending

on amiodarone dose

Other interaction

Silodosin Category X Use is contraindicated

Topotecan

Grapefruit juice

Protease inhibitors

aThese data are from amiodarone [package insert]2 and Sanoski.6 Amiodarone is a CYP 3A4 substrate, strong inhibitor of

CYP 1A2, 2C9, 2D6, and 3A4, and P-Glycoprotein inhibitor.

bDrug interaction categories: D—consider therapy modification, X—contraindicated.


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antiarrhythmic medications until 5 major stud-ies were published comparing rate with rhythmcontrol.13–17 All these trials found similar endpoints that showed that rate control wasequally as effective as rhythm control when

assessing all-cause mortality and was also asso-ciated with fewer side effects. The Atrial Fibril-lation Follow-up Investigation of RhythmManagement trial was the largest of these stud-ies, including 4060 patients with atrial fibrilla-tion.17 The hard end point of all-cause mortalitywas assessed in each group. At the end of the5-year follow-up, death in the rhythm-controlgroup was 23.8% compared with 21.3% in therate-controlled group. In addition, this studyfound that 80% of patients in the rhythmcontrol group versus 73% in the rate-controlgroup required hospitalization. The above find-ings have changed clinical practice, and nowboth methods of treatment are consideredacceptable and should be individualized on thebasis of patient-specific characteristics.17 Amio-darone is considered first-line therapy in theAmerican College of Cardiology/AmericanHeart Association/European Society of Cardiol-ogy practice guidelines for patients with atrial

fibrillation and concomitant heart failure whenrhythm control is chosen.10

Warnings and PrecautionsAlthough amiodarone is a highly used and effec-tive medication, it also possesses many seriousadverse effects that often limit its use (Table 2).This article individually reviews 6 predomi-nant complications of amiodarone therapythat should be monitored on a regular basis.These complications are most commonly asso-

ciated with long-term oral therapy secondaryto the drug’s long half-life and potential toaccumulate over time.2

Pulmonary ToxicityTwo major types of pulmonary toxicity areassociated with amiodarone therapy: hyper-sensitivity pneumonitis and interstitial/alveolarpneumonitis. Hypersensitivity pneumonitis is aT-cell–mediated response that typically occursearly in therapy.2,19 Once this condition devel-

ops, amiodarone should be immediately discon-tinued and steroid therapy initiated. Furthermore,these patients should not receive amiodaroneagain, because it can result in a more fulminatereaction upon secondary exposure.2 Intersti-tial/alveolar pneumonitis is distinguishablefrom the hypersensitivity reaction because it is

not T-cell mediated and typically occurs aftermonths to years of long-term therapy; moreover,the proposed mechanism of lung damage isthought to result from oxygen radical releaseand/or phospholipidosis.2,19,20 Although com-

pletely removing amiodarone therapy is desir-able in interstitial pneumonitis, a dosereduction may also prove beneficial inpatients who have no alternative. Addingsteroids can also help improve symptoms. Inmost cases, this toxicity is reversible over 2 to3 weeks. Patients may be rechallenged at alower dose if the benefits of amiodarone ther-apy are found to outweigh the risks.2 It is of paramount importance to identify and evaluateany signs or symptoms of pulmonary compro-mise (eg, new onset shortness of breath, chestpain, nonproductive cough) immediately.19

ArrhythmiasOne of the major concerns regarding antiar-rhythmics is their potential to act as proar-rhythmics and cause torsades de pointes; this isparticularly true with Vaughan Williams classes Ia,Ic, and III.12 Amiodarone has the unique benefitof rarely being associated with torsades de

pointes,

5

and when it does occur, it is usually inthe presence of predisposing factors such aselectrolyte abnormalities. The unique multi-modal mechanism of action does lend itself tothe development of symptomatic bradycardia,atrioventricular nodal block, and QTc prolon-gation. For these reasons, amiodarone is con-traindicated in sinus node dysfunction, whichcauses sinus bradycardia, second- and third-degree atrioventricular heart block, and brady-cardia, resulting in syncope.2

Liver InjuryAcute liver injury is common among patientsreceiving amiodarone therapy. It is usuallybenign and evidenced only through an increasein liver function tests (alanine transaminase,aspartate aminotransferase, and -glutamyltranspeptidase). Amiodarone therapy does notrequire adjustment until liver function testsreach 3 times the upper limit of normal or if liver function tests double in a patient who had

an elevated baseline before initiating amio-darone. In rare instances, fatal liver diseasehas occurred.2,11

Visual ImpairmentsAmiodarone has been implicated in patientswho develop visual impairments, which range


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VOLUME 21 • NUMBER 4 • O CTOBER–DECEMBER 2010 Drug Update

from blurred vision to permanent blindness. Thevast majority of patients will develop cornealmicrodeposits but, in most cases, will be asymp-tomatic; however, as many as 10% of patientswill experience blurred vision or see halos.2,21,22

In this population, reducing the dose or discon-tinuing therapy can reverse these effects.2 In con-trast, a noncausal relationship has beenidentified between amiodarone therapy andoptic neuritis and/or neuropathy. Peripheralvision deficits and clouded vision should promptimmediate ophthalmic examination.2,22

Thyroid FunctionAmiodarone plays a significant role in thyroidfunction and has the ability to cause bothhypothyroidism and hyperthyroidism. This drugis an iodine-containing compound (approximately

37% iodine by weight), which can result in life-threatening arrhythmias.2,23 Signs of thyrotoxicosisare not always evident; however, new onsetand/or recurrent arrhythmias should promptevaluation of thyroid function.2,18,23 Dose reduc-tion and/or amiodarone discontinuation isnecessary in these patients. Rapid reversal of

Table 2: Adverse Effects of Amiodarone Therapya

Adverse Effect Monitoring Parameter Signs/Symptoms Clinical Intervention

Pulmonary toxicityb Pulmonary function Shortness of breath, Hypersensitivity pneumonitis:

tests wheezing, decreased Discontinue amiodarone and

breath sounds start corticosteroids—Cannot

be rechallenged

Chest radiography Interstitial/alveolar pneumonitis:

Discontinue amiodarone or

decrease the dose and start

corticosteroids—Can be

rechallenged at a lower dose

Bradycardia/ Electrocardiography Chest pain and dizziness Decrease the dose or

Arrhythmiasb discontinue amiodarone

Hepatotoxicityb Liver function tests Decrease the dose or

discontinue amiodarone if

liver function tests 3 times

the upper limit of normal or

double from baseline

Vision Impairment Slit-lamp examination Blurred vision, halos, Symptomatic corneal

decreased peripheral microdeposits

vision Decrease the dose or

discontinue therapy

Optic neuritis

Discontinue therapy immediately

Thyroid dysfunction Thyroid function tests Thyrotoxicosis HyperthyroidismNew onset arrhythmias, Discontinue or reduce dose of

tachycardia amiodarone, give antithyroid

medication

Hypothyroid Hypothyroid

Weight gain, fatigue, Give thyroid supplement

constipation,

depression

Dermatologic Physical examination Light sensitivity Patient education: advise the

Slate-blue discoloration use of sunblock, limit sun

of the skin exposure, wear protective

clothing while in the sun

aThese data are from amiodarone [package insert],

2Sanoski,

6and Newman et al.

18

bBlack box warning.


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amiodarone-induced hyperthyroidism is unlikelysecondary to a stored surplus of active thyroidhormones.2 In contrast, hypothyroidism mayresult from amiodarone’s ability to decrease T3levels and increase T4 levels through direct inhi-

bition of peripheral conversion.2,18 Hypothy-roidism occurs more frequently (in up to 10% of patients) but is less likely to result in fatalarrhythmias; thus, it is regarded as the less dan-gerous of the 2 disorders.2,23

Dermatologic ConditionsLong-term amiodarone therapy, especially atdoses greater than 400 mg/d, is associatedwith 2 common dermatologic conditions.2

Approximately 10% of patients are reportedto experience light sensitivity.2,19 Proper patienteducation can help prevent photosensitivity.Patients should be counseled on using properprecautions while in the sun, such as usingprotective sunblock, wearing light-coloredclothing that covers the skin, and limiting theamount of UV-A/UV-B exposure. Less com-monly, a phenomenon referred to as “blue-man syndrome” can occur from melatoninand lipofuscin deposits in the skin, creating the

appearance of a slate-blue discoloration on theskin that is reversible upon discontinuation of therapy or dose reduction. Reversal is slowand can take years to completely resolve.19,24

ConclusionThe multimodal mechanism of action of amio-darone has enabled its use for the treatment andrecurrence of both ventricular and atrial arrhyth-mias despite its limited original FDA-approvedindications. Proven efficacy through well-

designed clinical trials has helped amiodaronefind its place in therapy; however, the benefitof long-term therapy must be weighed againstthe toxic side effect profile. Careful considera-tion should be given regarding patients’ qualityof life, adverse effects, and long-term outcomes.

REFERENCES

1. Babatin M, Lee SS, Pollak PT. Amiodarone hepatotoxic-ity. Curr Vasc Pharmacol. 2008;6(3):228–236.

2. Amiodarone [package insert]. Princeton, NJ: ZydusPharmaceuticals USA Inc; 2009.

3. Neff M. Practice guideline briefs. Am Fam Physician .2005;71(7):1433–1434.

4. Haffagee CI. Clinical pharmacokinetics of amiodarone.Clin Cardiol. 1987;10(7) (suppl 1):I6–I9.

5. Chow MS. Intravenous amiodarone: pharmacology,pharmacokinetics, and clinical use. Ann Pharmacother.1996;30(6):637–643.

6. Sanoski CA. Atrial and ventricular arrhythmias: evolvingpractices. In: Richardson M, Chant C, Cheng JWM, Chess-man KH, Hume AL, Hutchison LC, eds. Pharmacotherapy Self-Assessment Program: Book 1: Cardiology . 7th ed.

Lenexa, KS: American College of Clinical Pharmacy; 2010:125–152.

7. Creswell LL, Schuessler RB, Rosenbloom M, Cox JL.Hazards of postoperative atrial arrhythmias. Ann Thorac Surg. 1993;56(3):539–549.

8. Crystal E, Garfinkle MS, Connolly SS, Ginger TT, Sleik K,Yusuf SS. Interventions for preventing post-operativeatrial fibrillation in patients undergoing heart surgery.Cochrane Database Syst Rev . 2004;(4):CD003611.

9. Mitchell LB, Exner DV, Wyse DG, et al. Prophylactic oralamiodarone for the prevention of arrhythmias that beginearly after revascularization, valve replacement, or repair:PAPABEAR: a randomized controlled trial. JAMA. 2005;294(24):3093–3100.

10. Fuster V, Rydén LE, Asinger RW, et al. ACC/AHA/ESC guide-

lines for the management of patients with atrial fibrillation:executive summary. J Am Coll Cardiol. 2001;38(4):1231–1266.

11. Cahoon W, Flattery MP, Hess ML. Amiodarone: develop-ment, clinical indications, and safety. Prog Cardiovasc Nurs . 2007;22(3):173–176.

12. Medscape. http://img.medscape.com/fullsize/migrated /577/475/euro577475.tab1.gif. Accessed March 26, 2010.

13. Carlsson J, Miketic S, Windeler J, et al. Randomized trialof rate-control versus rhythm-control in persistent atrialfibrillation: the strategies of treatment of atrial fibrillation(STAF) study. J Am Coll Cardiol . 2003;41:1690–1696.

14. Hagens VE, Ranchor AV, Van Sonderen E, et al. Effect of rateor rhythm control on quality of life in persistent atrial fibrilla-tion. Results from the rate control versus electrical cardiover-sion (RACE) study. J Am Coll Cardiol . 2004;43:241–247.

15. Hohnloser SH, Kuck KH, Lilienthal J. Rhythm or rate con-trol in atrial fibrillation—Pharmacological Interventionin Atrial Fibrillation (PIAF): a randomised trial. Lancet .2000;356:1789–1794.

16. Opolski G, Torbicki A, Kosior DA, et al. Rate control vs rhythmcontrol in patients with nonvalvular persistent atrial fibril-lation: the results of the Polish how to treat chronic atrialfibrillation (HOT CAFE) study. Chest . 2004;126:476–486.

17. Wyse DG, Waldo AL, DiMarco JP, et al. A comparison of rate control and rhythm control in patients with atrialfibrillation. N Engl J Med. 2002;347(23):1825–1833.

18. Newman CM, Price A, Davies DW, Gray TA, Weetman AP.Amiodarone and the thyroid: a practical guide to themanagement of thyroid dysfunction induced by amio-darone therapy. Heart . 1998;79:121–127.

19. Gonzalez P, Otero MJ, Barrueco M, Dominguez-Gil A.Amiodarone-induced skin pigmentation and pulmonaryfibrosis. Hosp Pharm. 2002;37(6):615–618.

20. Martin WJ, Rosenow EC. Amiodarone pulmonary toxicity.Recognition and pathogenesis (part 2). Chest . 1988;93(6):1242–1248.

21. Burns KE, Piliotis E, Garcia BM, Ferguson KA. Amiodaronepulmonary, neuromuscular, and ophthalmological toxic-ity. Can Respir J. 2000;7(2):193–197.

22. Santaella RM, Fraunfelder FW. Ocular adverse effects asso-ciated with systemic medications. Drugs . 2007;67(1):84–85.

23. Martino E, Bartalena L, Bogazzi F, Braverman LE. Theeffects of amiodarone on the thyroid. Endocr Rev . 2001;22(2):240–254.

24. Delage C, Lagacé R, Huard J. Pseudocyanotic pigmenta-tion of the skin induced by amiodarone: a light and elec-tron microscopic study. Can Med Assoc J. 1975;112(10):1205–1208.


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CE Test Questions

Clinical Utility and Adverse Effects of Amiodarone TherapyObjectives:Upon completion of this article, the reader will be able to:

1. Identify FDA-approved indications and current off-label uses of amiodarone.

2. Examine the pharmacokinetics of amiodarone.

3. Review warnings and precautions of amiodarone.

1. Which statement is true?

a. Amiodarone blocks only potassium channels.

b. Amiodarone possesses qualities of a -adrenergic

blocker.

c. Amiodarone blocks only calcium channels.

d. Amiodarone is available only in intravenous form.

2. What percent decrease in heart rate can be expected

with amiodarone?

a. 5%–10%

b. 10%–15%c. 15%–20%

d. 25%

3. Which arrhythmia treatment is FDA approved for

amiodarone?

a. Atrial fibrillation

b. Sinus node dysfunction

c. Recurrent ventricular fibrillation

d. Atrioventricular node dysfunction

4. What type of meal increases oral absorption of

amiodarone?

a. High protein

b. High starch

c. High sugar

d. High fat

5. What is the half-life of oral amiodarone?

a. 5–10 days

b. 20–47 days

c. 15–142 days

d. 50–174 days


a. Amiodarone is highly protein bound.

b. Amiodarone is eliminated via the kidneys.

c. One major metabolite from lung metabolism isdesethylamiodarone.

d. Caution should be exercised in elderly patients because of

increased clearance of the drug.

7. What percent reduction of supraventricular

tachycardia occurred with the use of amiodarone

during the PAPABEAR trial?

a. 10%

b. 20%

c. 35%

d. 50%

8. What are the most common adverse effects of

intravenous administration of amiodarone?

a. Hypotension, bradycardia, and QTc prolongationb. Respiratory distress, tachycardia, and PR prolongation

c. Bundle branch block, hypotension, and blue skin

discoloration

d. Hypertension, ST depression, and tachycardia

9. What are two major types of pulmonary toxicity

associated with amiodarone?

a. Respiratory failure and adult respiratory distress syndrome

b. Hypersensitivity pneumonitis and interstitial pneumonitis

c. Pulmonary edema and pneumonia

d. Pulmonary embolism and alveolitis

10. Amiodarone therapy is contraindicated for use with

which rhythm?

a. Atrial fibrillation

b. Sinus node dysfunction

c. Recurrent ventricular fibrillation

d. Recurrent ventricular tachycardia


a. Fatal liver disease is a common adverse effect of

amiodarone therapy.

b. Hypothyroidism is more dangerous than hyperthyroidism

when associated with amiodarone therapy.

c. Two dermatologic conditions associated with long-term

amiodarone therapy are photosensitivity and “blue mansyndrome.”

d. Reversal of dermatologic symptoms is immediate with

discontinuation of amiodarone therapy.

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Clinical Utility and Adverse Effects of Amiodarone