English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Loratadine Terfenadine Sedating antihistamines Torsade de pointes Arrhythmias ECG EEG QTc interval Correspondence to: Dr. John A. Hey, Schering-Plough Research Institute, 2015 Galloping Hill Road, Kenilworth, NJ 070330539 (USA) Sedation limits the antiallergy utility of classical H, antihistamines, while newer antihistamines are nonsedating. Loratadine and terfenadine represent prototypes of a new class of antihistamines that are devoid of central sedative effects [1-3]. By contrast, classical antihistamines such as diphenhydramine and promethazine induce sedation and drowsiness in humans, and exhibit significant anticholiner-gic side effects. Recent reports of serious ventricular arrhythmias associated with the nonsedating antihistamines terfenadine [4] and astemizole [5], led the FDA to require labeling changes to identify risk factors associated with these arrhythmias. In the case of terfenadine, the arrythmogenic cardiac toxicity is associated with high concentrations of the parent drug. Drugs that interfere with firstpass hepatic metabolism, such as the macrolide antibiotics and ketoconazole, can lead to dangerously high plasma levels of terfenadine, which have been shown to elicit torsade de pointes, a ventricular dysfunction that is potentially fatal. Torsade de pointes is a ventricular arrhythmia characterized by a prolongation of the QTc interval and twisting of the ECG wave form [6]. Drug-induced torsade de pointes in humans occurs secondary to a decrease in heart rate and a prolongation of the QTc interval (value > 550 ms) [7]. The mechanism underlying the cardiotoxicity of terfenadine appears to be blockade of rectifying potassium channels [8]. Due to the cardiotoxicity associated with terfenadine, and more recently astemizole, questions have also been raised regarding whether torsade-type arrhythmias can also occur with the newer agents such as loratadine. Although an extensive clinical data base with

Loratadine Produces Antihistamine Activity without Adverse CNS, ECG or Cardiovascular Effects in Guinea Pigs