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Query: UMLS:C0019158 (hepatitis)
30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Amiodarone, originally developed over 20 years ago, is a potent antiarrhythmic drug with the actions of all antiarrhythmic drug classes. It has been successfully used in the treatment of symptomatic and life-threatening ventricular arrhythmias and symptomatic supraventricular arrhythmias. In patients with left ventricular dysfunction amiodarone does not usually produce any clinically significant cardiodepression and the drug has relatively high antiarrhythmic efficacy. Preliminary studies indicate that amiodarone may have a beneficial effect on mortality and survival in certain groups of patients with ventricular arrhythmias, an action probably related to both its antiarrhythmic and antifibrillatory effects. The adverse effect profile of amiodarone is diverse, involving the cardiac, thyroid, pulmonary, hepatic, gastrointestinal, ocular, neurological and dermatological systems. Interstitial pneumonitis and hepatitis are potentially fatal, but the vast majority of adverse events are less serious, and some may be dose dependent. Pretreatment monitoring, regular assessments and the use of minimum effective doses are, therefore, necessary. Thus, with appropriate monitoring to control its well recognised adverse effects amiodarone has an important place as an effective 'broad spectrum' antiarrhythmic drug which has, so far, been used when other treatments have proved ineffective. More recent preliminary data also suggest that it may also have a beneficial effect in the prevention of sudden death in some patients.
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PMID:Amiodarone. An overview of its pharmacological properties, and review of its therapeutic use in cardiac arrhythmias. 137 62

Amiodarone has been hailed as the most effective single antiarrhythmic drug for treatment of refractory supraventricular and ventricular arrhythmias. However, questions continue to arise about its long-term potential toxicity and true efficacy rates. We, therefore, reviewed our experience with 78 patients, mean age 59 +/- 14 years, with drug refractory tachyarrhythmias treated with amiodarone. Sixty-two patients were treated for recurrent ventricular tachycardia or ventricular fibrillation, 4 for complex ventricular ectopy and 12 for supraventricular tachyarrhythmias. Patients have been treated for a mean of 9.9 months (range, 1 day to 39.1 months); 34(55%) continued to be successfully treated for ventricular tachycardia/ventricular fibrillation, 2 (50%) for complex ventricular ectopy and 5 (42%) for supraventricular tachyarrhythmias. Amiodarone toxicity was frequent, occurring in 57/72 patients (79%) who were treated for more than one week. Adverse effects led to drug discontinuation in 15 (21%), 3 because of pulmonary toxicity (1 in combination with neuropathy and another with drug-induced hepatitis); 2 because of chemical hepatitis; 1, confusion; 6, neuropathy; 2, arrhythmia exacerbation; 2, symptomatic bradycardia; and 1 because of impotence. Of the 62 ventricular tachycardia/ventricular fibrillation patients who were treated with amiodarone, 8 (13%) expired: 4 died suddenly and 4 from documented ventricular tachycardia during treatment. In contrast, of 16 patients who had discontinued amiodarone because of initial adverse effects or drug failure and were treated with alternative antiarrhythmic medications, 5 (31%) died suddenly. In conclusion, amiodarone appears to be fairly effective in high risk patients with refractory cardiac tachyarrhythmias but results in a rather high incidence of adverse effects in long-term follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:High incidence of clinical and subclinical toxicity associated with amiodarone treatment of refractory tachyarrhythmias. 294 Nov 21

Amiodarone is believed to have caused acute hepatitis 24 hours after intravenous administration in two patients in whom no other alternative cause of hepatitis was found.
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PMID:Acute hepatitis after parenteral amiodarone administration. 339 27

Amiodarone has proved very effective in the treatment of otherwise resistant cardiac tachyarrhythmias. The use of amiodarone has, however, been limited due to its serious side-effects. A patient with cholestatic hepatitis due to amiodarone treatment is presented below and a review of the hepatotoxicity of amiodarone is given. It is concluded that solid evidence exists of hepatic injury due to amiodarone treatment, including steatosis, alterations resembling alcoholic hepatitis, cholestatic hepatitis and micronodular cirrhosis of the liver. Patients receiving amiodarone should be regularly screened with respect to hepatic enzyme levels. Therapy should be discontinued on the suspicion of cholestatic injury or hepatomegaly.
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PMID:Hepatotoxicity of amiodarone. 396 37

Amiodarone is a cardiac antiarrhythmic agent now undergoing clinical trials in the United States. Its most important side effect is pulmonary toxicity, which may present radiographically in two forms. One is similar to eosinophilic pneumonia with peripheral alveolar opacities but without any of the laboratory or pathologic findings. A second presentation is as a bilateral interstitial pattern resembling interstitial pulmonary edema. This is often mistaken for heart failure in the clinical and radiographic setting. Amiodarone also causes a phospholipidosis of the liver, which is usually asymptomatic but on occasion may present as hepatitis. On abdominal CT the liver will have an abnormally high attenuation (80-140 HU), which appears to be due to accumulation of an amiodarone metabolite in hepatocytes. This appearance is usually distinguishable from the other causes of increased hepatic attenuation by virtue of other CT criteria and clinical history. However, from a radiographic standpoint alone, the combination of acute congestive heart failure and an abnormally dense liver may result in at least an initial misdiagnosis of advanced primary hemochromatosis.
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PMID:Dense liver in a 72-year-old woman with congestive heart failure. 407 46

Amiodarone was administered to 80 patients with recurrent cardiac tachyarrhythmias previously resistant to drug treatment. Forty nine patients were treated for ventricular tachycardia or fibrillation and 31 for supra-ventricular arrhythmias. The mean (range six days to 51 months), permitting a total of 100 patient years of observation. Adverse reactions were observed in 69 patients. Severe side effects were encountered in 13: four patients developed interstitial pneumonitis, four patients developed incessant ventricular tachycardia, three patients taking amiodarone and digoxin sustained sinus node arrest with depression of escape foci, one patient developed hepatitis, and one patient developed hypercalcaemia with renal failure. Furthermore, a rise in the serum concentration of digoxin and potentiation of warfarin anticoagulation occurred in cases in which these agents were combined with amiodarone. Amiodarone was stopped in 14 patients because of side effects. Although amiodarone is effective in suppressing arrhythmias in most patients in whom extensive use of antiarrhythmic drugs has been unsuccessful, it is associated with diverse and serious toxicity. These observations suggest that at present the use of amiodarone should be reserved for patients with life threatening or seriously disabling arrhythmias in whom longer established drugs have been ineffective or are contraindicated.
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PMID:Adverse reactions during treatment with amiodarone hydrochloride. 640 40

Ninety-six patients with recurrent, drug-refractory tachyarrhythmias were treated with amiodarone for 8.0 +/- 7.5 months (range 1 day to 27 months): 77 for recurrent ventricular tachycardia or ventricular fibrillation (VT/VF), two for complex ventricular ectopy, and 17 for supraventricular tachyarrhythmias. The actuarial incidence of successful amiodarone therapy was 52 +/- 7% at 12 months and 28 +/- 9% at 24 months for patients with VT/VF. Neither patient with complex ventricular ectopy was successfully treated. Among the patients with supraventricular tachyarrhythmias, 64.7% were successfully treated for 7.7 +/- 7.6 months (range 1 to 22 months). Amiodarone toxicity occurred in 66 of 91 patients (72.5%) treated for more than 1 week. Fourteen patients had therapy-limiting toxicity. Of these 14, six had pulmonary toxicity, four had arrhythmia exacerbation, one had hepatitis, one had renal toxicity, one had rash, and one had erythema nodosum. The actuarial incidence of therapy-limiting side effects was 27 +/- 7% at 15 months. We conclude that amiodarone is useful in the treatment of refractory tachyarrhythmias but that the rate of efficacy in VT/VF is lower and the incidence of significant toxicity is higher than has been generally appreciated.
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PMID:Amiodarone: clinical efficacy and toxicity in 96 patients with recurrent, drug-refractory arrhythmias. 685 Oct 57

Amiodarone is an iodinated benzofuran derivative class III antiarrhythmic that is highly effective in suppressing ventricular and supraventricular arrhythmias. It is also associated with an imposing side effect profile, which often limits its use. Numerous adverse effects have been documented including skin discolouration, photosensitivity, hepatitis, thyroid dysfunction, corneal deposits, pulmonary fibrosis, bone marrow suppression and drug interactions. These side effects are thought to be correlated with the total cumulative dose of amiodarone, but idiopathic reactions have been reported. The majority of adverse reactions resolve with discontinuation of the drug; however, rapid progression may occur, which may be fatal. The present report documents a patient who had a combination of serious amiodarone toxicities that, once recognized, were treated and eventually resulted in a good outcome.
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PMID:Amiodarone pulmonary, neuromuscular and ophthalmological toxicity. 1085 6

Acute hepatic failure is a rare and potentially lethal complication of propylthiouracil (PTU) use for hyperthyroidism. We present a 20-year-old woman with Basedow-Graves' disease who developed PTU-induced fulminant hepatitis, which progressed to acute hepatic failure with grade III hepatic encephalopathy. Laboratory evaluation ruled out the most common causes of fulminant hepatitis. We treated her hyperthyroidism with amiodarone (average daily dose, 200 mg) for 3 weeks, achieving rapid and persistent euthyroidism, (triiodothyronine [T(3)] levels ranged between 64 and 109 ng/dL) without side effects. Amiodarone treatment did not abolish the thyroid radioactive iodine uptake (RAIU), allowing for subsequent treatment with radioactive iodine. The clinical course was favorable and the patient achieved full hepatic recovery 3 months after the hepatic failure was detected. After an extensive review of the literature, we believe that this is the first communication of the successful use of amiodarone to control hyperthyroidism in a patient with PTU-induced fulminant hepatitis.
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PMID:Successful treatment of hyperthyroidism with amiodarone in a patient with propylthiouracil-induced acute hepatic failure. 1558 85

Amiodarone is an effective antiarrhythmic agent that is widely used for tachyarrhythmias, especially ventricular tachycardia and supraventricular tachycardia. It has some mild short-term (e.g., skin rashes, gastrointestinal symptoms, and corneal microdeposits) and long-term side effects (thyroid dysfunction, visual disturbances, pulmonary infiltrates, ataxia, and hepatitis). We present two infants who had hyperglycemia following amiodarone infusion during the early postoperative period.
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PMID:Unusual and early hyperglycemia following amiodarone infusion in two infants. 1613 3


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