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The year 2002 saw a warning from the US Food and Drug Administration not to use the diet agent, Lipokinetix, and brought to light a few new agents as potential hepatotoxins. Numerous other reports confirmed the hepatotoxicity of several previously described agents. Refinements in causality assessment remain an important aspect in defining drug-induced liver disease and proposed new upper limits of normal for alanine aminotransferase that are lower than most laboratories currently report may require rethinking our definition of "normal liver function tests." Chronic viral hepatitis B and C remain important risk factors for antiretroviral-induced liver injury in patients co-infected with the human immunodeficiency virus and in patients receiving antituberculosis therapy. Acetaminophen retains its status as the most common cause of acute drug-induced liver failure in the United States and in many other countries. Several papers addressed the issue of accidental versus intentional overdoses, the role of alcohol consumption as a risk factor, and newer aspects of treating and preventing acetaminophen injury to the liver. Finally, the use of potentially hepatotoxic medications in patients with underlying liver disease continues to be a controversial topic and a rational approach to the use of such drugs in this setting is provided.
The year 2002 saw a warning from the US Food and Drug Administration not to use the diet agent, Lipokinetix, and brought to light a few new agents as potential hepatotoxins. Numerous other reports confirmed the hepatotoxicity of several previously described agents. Refinements in causality assessment remain an important aspect in defining drug-induced liver disease and proposed new upper limits of normal for alanine aminotransferase that are lower than most laboratories currently report may require rethinking our definition of "normal liver function tests." Chronic viral hepatitis B and C remain important risk factors for antiretroviral-induced liver injury in patients co-infected with the human immunodeficiency virus and in patients receiving antituberculosis therapy. Acetaminophen retains its status as the most common cause of acute drug-induced liver failure in the United States and in many other countries. Several papers addressed the issue of accidental versus intentional overdoses, the role of alcohol consumption as a risk factor, and newer aspects of treating and preventing acetaminophen injury to the liver. Finally, the use of potentially hepatotoxic medications in patients with underlying liver disease continues to be a controversial topic and a rational approach to the use of such drugs in this setting is provided.
Amiodarone is a highly effective antiarrhythmic agent for the treatment and prevention of atrial and ventricular arrhythmias. Acute liver damage after intravenous amiodarone, possibly induced by the solubilizer polysorbate 80, is rare but potentially harmful. Amiodarone loading should therefore be adapted to the necessity of an immediate effect of the drug, and liver function should be monitored closely in critically ill patients. Oral maintenance therapy with amiodarone is possible, even in patients who developed liver disease during intravenous loading.
Amiodarone is considered a first-choice antiarrhythmic drug in critically ill patients with new-onset atrial fibrillation (AF). However, evidence supporting the use of this potentially toxic drug in critically ill patients is scarce. Magnesium sulphate (MgSO4) has shown to be effective for both rate and rhythm control, to act synergistically with antiarrhythmic drugs, and to prevent proarrhythmia. Treatment with MgSO4 may reduce the need for antiarrhythmic drugs such as amiodarone in critically ill patients with new-onset atrial fibrillation. The efficacy of a new institutional protocol was evaluated. Patients were treated with a new institutional protocol for new-onset atrial fibrillation in critically ill patients. An MgSO4 bolus (0.037 g/kg body weight in 15 minutes) was followed by continuous infusion (0.025 g/kg body weight/h). Intravenous amiodarone (loading dose 300 mg, followed by continuous infusion of 1200 mg/24 h) was given to those not responding to MgSO4 within 1 hour. Clinical response was defined as conversion to sinus rhythm or decrease in heart rate <110 beats/min. Sixteen of the 29 patients responded to MgSO4 monotherapy, whereas the addition of amiodarone was needed in 13 patients. Median (range) time until conversion to sinus rhythm after MgSO4 was 2 (1-45) hours. Median (range) conversion time in patients requiring amiodarone was 4 (2-78) hours, and median (range) conversion time in all patients was 3 (1-78) hours. The 24-hour conversion rate was 90%. Relapse atrial fibrillation was seen in 7 patients. The magnesium-amiodarone step-up scheme reduces the need for amiodarone, effectively converts new-onset atrial fibrillation into a sinus rhythm within 24 hours, and seems to be safe in critically ill patients.
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