Atenolol is a cardioselective beta-blocker that is widely used in the treatment of hypertension and angina pectoris. Atenolol has been linked to rare cases of drug induced liver injury.
Atenolol (a ten' oh lol) is considered a “selective” beta-adrenergic receptor blocker in that it has potent activity against beta-1 adrenergic receptors which are found in cardiac muscle, but has little or no activity against beta-2 adrenergic receptors found on bronchial and vascular smooth muscle. Atenolol was approved for use in the United States in 1981 and is still widely used in the therapy of hypertension and angina pectoris. Atenolol is also used to reduce the risk of cardiovascular mortality in patients with coronary artery disease. Atenolol is available in 25, 50 and 100 mg tablets in generic forms as well as under the trade name of Tenormin. It is also available in fixed combinations with a diuretic such as chlorthalidone (Tenoretic and others). Parenteral formulations for intravenous use are also available. The usual oral dose of atenolol in adults is 25 to 50 mg once daily initially, with subsequent adjustment based upon clinical response and tolerance, but rarely beyond 100 mg daily. Common side effects include bradycardia, hypotension, fatigue, dizziness, depression, memory loss and impotence. At high doses, atenolol is less cardioselective and can cause bronchospasm. As with all beta-blockers, sudden withdrawal can trigger rebound hypertension.
Atenolol therapy has been associated with mild-to-moderate elevations of serum aminotransferase levels in 1% to 2% of patients. These elevations, however, are usually asymptomatic and transient and resolve even with continuation of therapy. A few instances of clinically apparent, acute liver injury attributable to atenolol have been reported. In view of its wide scale use, atenolol induced liver injury is exceedingly rare. The onset of injury has been within 1 to 4 weeks and pattern of liver enzyme elevations has been hepatocellular or mixed. Symptoms of hypersensitivity (rash, fever, eosinophilia) are uncommon as is autoantibody formation. Most cases are self-limiting and resolve rapidly once atenolol is stopped; however, fatal instances have been reported.
Mechanism of Injury
The mechanism of drug induced liver injury from atenolol is not known. The agent has little hepatic metabolism and is excreted largely unchanged in the urine.
Outcome and Management
The severity of liver injury due to atenolol ranges from mild serum aminotransferase elevations to acute hepatitis with jaundice. In large case series of acute liver failure due to medications, atenolol has been listed as a rare cause. Rechallenge has not been reported, but should be avoided. There is little information about cross reactivity among the beta-blockers to hepatic injury. Switching to another beta-blocker after atenolol related acute liver injury should be done with caution and prospective monitoring.
|Medication:||Atenolol (25 mg daily)|
|Severity:||3+ (jaundice, hospitalization)|
|Latency:||4 weeks to onset of symptoms and jaundice|
|Other medications:||Vitamins, glucosamine, chondroitin, omega-3-fatty acids|
|Weeks After Starting||Weeks After Stopping||ALT (U/L)||Alk P (U/L)||Bilirubin (mg/dL)||Other|
|Atenolol stopped after 5 weeks of therapy (25 mg daily)|
|DRUG||CAS REGISTRY NUMBER||MOLECULAR FORMULA||STRUCTURE|