Hepatic toxicity after acebutolol therapy

Article Abstract:

Beta receptor-blocking agents are commonly used to treat high blood pressure (hypertension) and angina (severe chest pain caused by an insufficient blood supply to the heart), and have been associated with increased blood levels of the enzymes transaminase and alkaline phosphatase, and with hepatitis (inflammation of the liver). Six cases are described of patients who developed liver toxicity after taking the beta receptor-blocking agent acebutolol. The liver toxicity was characterized by increased levels of transaminase and alkaline phosphatase, reflecting cell damage, or increased levels of bilirubin, reflecting abnormalities of the gallbladder. The mechanism underlying the disease process has not been established, but may be related to an increased sensitivity reaction. Hypersensitivity-type reactions are characterized by the development of a high fever and recurrence of the toxic reaction upon exposure to the irritating substance. All six patients developed liver toxicity within 31 days of exposure to acebutolol, four patients had a high fever, and two patients experienced a recurrence of liver toxicity after being re-exposed to the drug. It is recommended that physicians be aware of the potential toxic effects of acebutolol to the liver, and serious adverse drug reactions should be reported to the manufacturer or Food and Drug Administration. (Consumer Summary produced by Reliance Medical Information, Inc.)

Evaluation, Causes of, Delayed hypersensitivity, Drug allergy, Drug hypersensitivity, Gallbladder, Acebutolol

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Labetalol hepatotoxicity

Article Abstract:

Liver damage is not frequently associated with antihypertensives, medications used to lower blood pressure. A fatal case of liver cell (hepatocellular) necrosis in a patient treated with the antihypertensive agent labetalol was reported to the Food and Drug Administration (FDA). This single case report prompted the FDA to examine all reports of liver toxicity in which use of the labetalol was mentioned. There were eleven reports that were identified as possible labetalol-induced hepatocellular toxicity. In five cases the results of microscopic liver examinations were available and demonstrated severe hepatocellular necrosis. Clinical improvement occurred in 9 of the 11 patients when labetalol use was discontinued. Since this is a serious condition physicians should monitor baseline liver function tests in all patients before initiating labetalol treatment. Patients should be informed of the signs and symptoms of liver involvement and be urged to seek medical attention immediately. Furthermore, liver function should be monitored during the course of therapy and laboratory evidence of liver injury or the presence of jaundice should result in prompt discontinuation of labetalol therapy, which should not be reinstituted. (Consumer Summary produced by Reliance Medical Information, Inc.)

Reports, Complications and side effects, United States. Food and Drug Administration, Necrosis, Labetalol

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Beta-blockers and sudden cardiac death

Article Abstract:

Physicians underestimate the usefulness of beta-blocking medication in the prevention and treatment of heart disease and sudden cardiac death. Researchers reviewed the current literature to evaluate the use of beta-blocking drugs in treating high blood pressure and in managing patients with heart attacks. One study reported that 30% fewer male patients with high blood pressure died from heart attacks when taking beta-blocking drugs. Other studies have shown a 20%-40% reduction in death rates in patients given beta-blocking drugs after a heart attack, including diabetic patients. Beta-blockers shown to reduce the risk of death from heart attack are timolol, propranolol and metaprolol. Other studies have shown that beta-blockers also may play a role in preventing the formation of plaque deposits on vessel walls. Physicians are sometimes hesitant to prescribe beta-blockers because of side-effects, but the benefits far outweigh possible negative effects in patients at risk of sudden cardiac death.

Prevention, Coronary heart disease, Cardiac arrest

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