Hepatotoxicity associated with carvedilol

K O Hagmeyer1, J Stein

  • 1College of Pharmacy, The University of Toledo, OH 43606, USA. Khagmey@utnet.utoledo.edu

Insights

A patient experienced severe itching and elevated liver enzymes while taking carvedilol, a beta-blocker. This adverse reaction may recur with other beta-adrenergic blockers, necessitating careful patient monitoring.

Area of Science:

  • Cardiology
  • Hepatology
  • Pharmacology

Background:

  • Beta-adrenergic blockers are commonly prescribed for cardiovascular conditions.
  • Carvedilol is a non-selective beta-adrenergic blocker with alpha-blocking activity.
  • Adverse drug reactions require thorough investigation and reporting.

Observation:

  • A case of a 40-year-old male patient presenting with severe pruritus and elevated serum transaminases is detailed.
  • The patient was initially treated with carvedilol for cardiomyopathy.
  • Symptoms resolved after carvedilol discontinuation, but recurred upon switching to metoprolol.

Findings:

  • Carvedilol can induce pruritus and hepatotoxicity, indicated by elevated liver function tests.
  • The adverse reaction appears to be rare and potentially class-specific to beta-adrenergic blockers.
  • Discontinuation of the offending drug led to normalization of liver function tests.

Implications:

  • Clinicians should monitor patients on carvedilol for signs of pruritus and liver dysfunction.
  • Hepatotoxicity associated with carvedilol may necessitate a change in medication to a different drug class.
  • This case highlights the importance of considering drug-induced liver injury in patients presenting with unexplained pruritus and elevated transaminases.
Abstract

Related Concept Videos

Adrenergic Antagonists: ɑ and β-Receptor Blockers01:31

Adrenergic Antagonists: ɑ and β-Receptor Blockers

Third-generation β-blockers, such as labetalol and carvedilol, represent a significant advancement in managing cardiovascular conditions. Unlike conventional β-blockers, which can induce peripheral vasoconstriction, third-generation drugs block α1 adrenoceptors. This promotes vasodilation through several mechanisms, such as increased nitric oxide production, inhibition of calcium ion entry, opening of potassium ion channels, and antioxidant action. Labetalol, for instance, is clinically...
Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
Heart Failure Drugs: β-Blockers01:22

Heart Failure Drugs: β-Blockers

β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation, vasodilation, and...
Effect of Hepatic Disease on Pharmacokinetics: Dose Adjustments Due to Hepatic Impairment01:08

Effect of Hepatic Disease on Pharmacokinetics: Dose Adjustments Due to Hepatic Impairment

Hepatic impairment, characterized by decreased liver function, does not uniformly mandate adjustments in drug dosage. Whether dosage modifications are necessary depends on various factors related to the drug's metabolism and elimination pathways. If a drug is primarily excreted via the kidneys and bypasses significant hepatic processing, if it undergoes minimal metabolic transformation in the liver, or if it is volatile and primarily expelled through the lungs, dose adjustments may not be...
Drug Toxicity: Risk factors01:24

Drug Toxicity: Risk factors

Adverse Drug Reactions (ADRs) are potential complications that arise during pharmacotherapy, influenced by multiple risk factors. Age plays a significant role; both neonates and the elderly are at heightened risk due to their respective immature and diminished metabolic and elimination processes. Gender also impacts ADRs, with females experiencing a 1.5 to 1.7-fold greater risk than males, which may be linked to pharmacokinetic, pharmacodynamic, and hormonal differences. Notably, neonates, the...
Drug toxicity: Drug–Drug Interaction01:30

Drug toxicity: Drug–Drug Interaction

Drug–drug interactions can precipitate toxicity through multiple mechanisms. Absorption interactions alter how drugs enter the body, exemplified when ranitidine increases the absorption of basic drugs, while cholestyramine decreases the levels of propranolol. Protein binding interactions occur when drugs share the same binding sites on plasma proteins. Drugs like aspirin and warfarin, when bound in excess, can lead to increased free drug concentrations, enhancing the potential for...