Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The majority of sudden cardiac deaths in children occur in patients with prior arrhythmias and an abnormal heart. Amiodarone was given to 39 young patients (35 with an abnormal heart) with arrhythmias unresponsive to conventional treatment. Their age ranged from 6 weeks to 30 years with nine patients younger than 2 years of age. Atrial flutter was present in 16 patients, ventricular tachycardia in 14 patients and supraventricular tachycardia in 9 patients. The most common diagnosis (14 patients) was postoperative repair of congenital heart disease. The dose ranged from 2.5 to 21.6 mg/kg per day (mean 8.2). Elimination of arrhythmia (on 24 hour electrocardiography) occurred in 15 of 16 patients with atrial flutter, 11 of 14 with ventricular tachycardia and 5 of 9 with supraventricular tachycardia. Symptomatic side effects were: rash (three patients), headache (two patients), nausea (one patient) and peripheral neuropathy (one patient); seven patients had asymptomatic corneal microdeposits which normalized in all after the drug was discontinued. No side effects occurred in patients younger than 10 years of age. The following changed with treatment (p less than 0.05): heart rate decreased (three patients with atrial flutter and sick sinus syndrome required pacemaker implantation for bradycardia) and QTc increased; thyroxine (T4) and serum reverse triiodothyronine (T3) increased. During follow-up study (range 6 months to 3 years), 21 of the 39 patients continued to take amiodarone with complete control of arrhythmias, 9 were no longer taking the drug and 9 died (7 nonsudden and 2 sudden deaths). Amiodarone is an extremely effective treatment for infants and children with tachyarrhythmias resistant to conventional treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Amiodarone treatment of critical arrhythmias in children and young adults. 638 28

Amiodarone was administered to 154 patients who had sustained, symptomatic ventricular tachycardia (VT) (n = 118) or a cardiac arrest (n = 36) and who were refractory to conventional antiarrhythmic drugs. The loading dose was 800 mg/day for 6 weeks and the maintenance dose was 600 mg/day. Sixty-nine percent of patients continued treatment with amiodarone and had no recurrence of symptomatic VT or ventricular fibrillation (VF) over a follow-up of 6 to 52 months (mean +/- standard deviation 14.2 +/- 8.2). Six percent of the patients had a nonfatal recurrence of VT and were successfully managed by continuing amiodarone at a higher dose or by the addition of a conventional antiarrhythmic drug. One or more adverse drug reactions occurred in 51% of patients. Adverse effects forced a reduction in the dose of amiodarone in 41% and discontinuation of amiodarone in 10% of patients. The most common symptomatic adverse reactions were tremor or ataxia (35%), nausea and anorexia (8%), visual halos or blurring (6%), thyroid function abnormalities (6%) and pulmonary interstitial infiltrates (5%). Although large-dose amiodarone is highly effective in the long-term treatment of VT or VF refractory to conventional antiarrhythmic drugs, it causes significant toxicity in approximately 50% of patients. However, when the dose is adjusted based on clinical response or the development of adverse effects, 75% of patients with VT or VF can be successfully managed with amiodarone.
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PMID:Long-term efficacy and toxicity of high-dose amiodarone therapy for ventricular tachycardia or ventricular fibrillation. 663 51

A clinical investigation was carried out in 13 patients in order to answer the question of a possible interaction between amiodarone (A) and digoxin (D) and to study the extent to which plasma digoxin levels (PDL) may be influenced by A. Combined therapy with A + D was instituted in patients with supraventricular tachyarrhythmia where treatment with D alone was insufficient. All patients had normal renal function. Amiodarone was added to the treatment regimen of patients receiving D at doses ranging from 0.125 to 0.5 mg daily on a long term basis. The initial dosage of A was 1200 mg daily for 5 days to achieve saturation, followed by a maintenance dose of 200-400 mg daily. 3 PDL were measured before therapy with A was added and during combined A and D treatment at weeks 1, 2 and 3 and 3 months after the addition of A. In 11 patients a significant increase in PDL occurred as early as the 1st and 2nd weeks following the addition of A. In one patient PDL was elevated only after 3 months and in one other patient it remained unchanged. In 4 patients the PDL increase was associated with nausea. No other subjective or objective symptoms of digitalis intoxication were observed. This investigation has demonstrated a clinically relevant interaction between A and D. Regular monitoring of PDL is recommended during the first 3 weeks of combined treatment with A + D, and the D doses should be adjusted accordingly.
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PMID:[Interaction of amiodarone and digoxin]. 665 16

In a group of 95 patients having cardiac operations with extracorporeal circulation, intravenous (IV) amiodarone, administered in doses of 2.5 to 5 mg/kg, was used in the treatment of various perioperative arrhythmias. Conversion to sinus rhythm was achieved in 55 (61%) of 90 patients with supraventricular arrhythmias, the other patients showing a satisfactory slowing of their heart rate. Total suppression and control was obtained in 18 patients with persistent ventricular extrasystoles associated with various supraventricular arrhythmias. Amiodarone was administered in five patients with life-threatening ventricular arrhythmias resistant to other antiarrhythmic agents: Suppression was obtained in one of two patients with recurrent ventricular tachycardias and control was achieved in three patients with repetitive ventricular tachycardia and ventricular fibrillation, allowing the effective use of intra-aortic balloon counterpulsation (IABP) needed for hemodynamic support. Seven patients experienced minor side effects such as nausea or flushing. No complete atrioventricular (AV) block was noted. Significant hypotension occurred at the end of the IV injection in 17 (18%) patients. In all but five patients, hypotenion was transient, without clinical complications. In the five others, adrenergic drugs in four cases and IABP in one case were necessary. Those five patients had marked cardiomegaly with poor myocardial contractility. IV bolus injection of amiodarone seems prohibited in such patients; constant infusion would be preferable.
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PMID:Intravenous amiodarone in the treatment of various arrhythmias following cardiac operations. 745 41

Amiodarone chlorhydrate is a diiodated benzofuran derivative, and it is used to treat cardiac rhythm abnormalities. Hepatotoxicity is a relatively uncommon side effect of amiodarone, and symptomatic hepatic dysfunction occurs in fewer than 1% of the patients taking amiodarone. Cirrhosis is a rare complication that's been confirmed in 12 cases. Peripheral neuropathy occurs in 10% of patients taking aminodarone. We report here on an unusual case of amiodarone-induced hepatotoxicity and peripheral neurotoxicity. A 75 year old man with normal liver function was given amiodarone for treating his atrial fibrillation and heart failure. He developed nausea, vomiting, muscle weakness and wasting after 17.8 months therapy with amiodarone (400 mg orally once per day). Liver biopsy showed the presence of foam cells in the hepatic sinusoids and Mallory bodies in the periportal hepatocytes on light microscopy. Sural nerve biopsy showed demyelination, and nerve conduction studies showed mixed sensorimotor polyneuropathy. These observations show the necessity of monitoring the hepatic function and conducting neurologic examination of the patients treated with amiodarone.
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PMID:Amiodarone-induced hepatitis and polyneuropathy. 1793 44

Amiodarone is a di-iodated benzofuran derivative that is commonly used to treat patients with various cardiac arrhythmias. It is associated with side effects that involve the liver, thyroid, and other organs. Approximately 1-3% of patients treated with amiodarone suffer from symptomatic liver disease. Thyroid dysfunction occurs in 10% of patients treated with amiodarone. A 65-year-old woman with coronary heart disease and atrial fibrillation was administered with amiodarone. She developed nausea, vomiting, dyspepsia, and sweating within 9 months of amiodarone administration (200 mg orally once a day). Results of the laboratory finding showed increased hepatic enzymes, and low thyroid hormone levels. A liver biopsy showed irregular arrangement of hepatocytes and diffuse micro- and macrovesicular fatty changes. Electron microscopy findings showed pleomorphic mitochondria with crystalloid inclusions and membrane-bound lysosomal structures. The liver and thyroid functions returned to normal, after the amiodarone was stopped. We describe an unusual case in which amiodarone induced hepatitis and hypothyroidism simultaneously. Physicians should take a close look to the adverse event when using amiodarone which can cause adverse effects in multiple organs.
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PMID:[A case of simultaneously occurred amiodarone-induced hepatitis and hypothyroidism]. 2395 62

A 55-year-old male presented with history of nausea, vomiting, palpitation paresthesis and profuse sweating in emergency department 2h after ingestion of "Bachnaag" (Aconite) root. Examination revealed shock with irregular pulses. Initial ECG showed frequent multifocal ventricular ectopics (VE), which later turned to short runs of ventricular tachycardia (VT). Immediate gastric lavage was done and activated charcoal given. Patient was treated with fluid resuscitation without any improvement in blood pressure. Patient was started on nor-adrenaline infusion with gradual recovery from hypotension over a period of 6h, but support was continued for 48h. Amiodarone was started to control ventricular excitability, which persisted over 72h with gradual decrease in frequency of VT and VE. Patient was discharged with normal sinus rhythm on oral amiodarone on 5th day of hospitalization. On follow-up after 2 weeks patient was totally asymptomatic and amiodarone was stopped.
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PMID:Aconite poisoning with arrhythmia and shock. 2775 Dec 90

Amiodarone is a lipophilic structure with a half-life of 25-100 days. Long-term oral amiodarone is associated with photosensitivity, thyroid dysfunction, and pulmonary and hepatic toxicity. Intravenous amiodarone can lead to sweating, heating sensation, nausea, phlebitis at the injection site, and rarely acute hepatitis. This is a compelling case of a 60-year-old male who developed acute liver injury 24-36 h after starting amiodarone. All the possible causes of acute liver injury were ruled out, and his liver enzymes improved after discontinuing amiodarone.
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PMID:Amiodarone-Induced Acute Liver Injury. 3223 7