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Biomedical subjects

L Ereshefsky

Publications and source records attributed to L Ereshefsky.

61 records · Page 4Linked to original sources
PubMedDate not supplied

Antidepressant properties of trazodone.

The chemistry, pharmacokinetics, biochemistry and pharmacology, clinical trials, adverse effects, FDA-approved indications, and availability and cost of trazodone hydrochloride, a triazolopyridine antidepressant, are reviewed. Trazodone is nearly completely absorbed after oral administration; although food delays absorption and reduces peak serum concentration, total area under the plasma concentration-time curve is not altered. Trazodone has biphasic elimination, with a redistribution half-life of about one hour and an elimination half-life of 10-12 hours. Trazodone is nearly completely metabolized hepatically by hydroxylation and oxidation to metabolites that are probably inactive. Trazodone is less potent but more selective than conventional tricyclic antidepressants; at low doses, trazodone acts as a serotonin antagonist, while at high doses it acts as a serotonin agonist. Trazodone has been compared with imipramine, amitriptyline, desipramine, and placebo in controlled clinical trials and found to be an effective antidepressant. Trazodone causes significantly fewer anticholinergic side effects than does imipramine. Trazodone has few cardiovascular side effects. In patients ingesting toxic amounts of trazodone, no deaths have been reported unless other drugs were present or ingested concomitantly. The usual adult daily dose of trazodone hydrochloride is 150-400 mg given in two divided doses. Trazodone is an effective antidepressant with a low incidence of serious adverse effects. It may be particularly useful in certain depressed patients who are intolerant of anticholinergic effects of other antidepressants, have cardiac conduction disturbances, or who do not respond to treatment with tricyclic antidepressants and in whom electroshock therapy is contraindicted.

Animals↗
PubMedDate not supplied

Neuroleptic malignant syndrome associated with clozapine monotherapy.

Neuroleptic malignant syndrome is thought to be a result of dopamine receptor blockade in the striatum. Clozapine has only weak affinity for dopamine type 1 and 2 receptors, and therefore it was thought this drug would not precipitate the syndrome. However, six cases of the syndrome have been reported in patients receiving clozapine monotherapy. A review of the pathoetiology of symptoms occurring in the syndrome is included.

Adult↗