Drug Interactions between iobenguane I 123 and Triavil

MONITOR: Coadministration of a phenothiazine with a tricyclic antidepressant (TCA) may result in elevated plasma concentrations of one or both drugs as well as additive adverse effects. Most phenothiazines and TCAs have been found to undergo metabolism by CYP450 2D6, thus competitive inhibition of the enzyme may occur when more than one of these agents are administered. Although these drugs have been used together clinically, the possibility of increased risk of serious adverse effects such as central nervous system depression, tardive dyskinesia, hypotension, and prolongation of the QT interval should be considered, as many of these agents alone can and have produced these effects. In addition, excessive anticholinergic effects may occur in combination use, which can result in paralytic ileus, hyperthermia, heat stroke, and the anticholinergic intoxication syndrome. Peripheral symptoms of anticholinergic intoxication commonly include mydriasis, blurred vision, flushed face, fever, dry skin and mucous membranes, tachycardia, urinary retention, and constipation. Central symptoms may include memory loss, disorientation, incoherence, hallucinations, psychosis, delirium, hyperactivity, twitching or jerking movements, stereotypy, and seizures.

MANAGEMENT: Concurrent use of phenothiazines and TCAs should be approached with caution, particularly in the elderly and those with underlying organic brain disease, who tend to be more sensitive to the central anticholinergic effects of these drugs and in whom toxicity symptoms may be easily overlooked. Patients should be advised to notify their physician promptly if they experience potential symptoms of anticholinergic intoxication (e.g., abdominal pain, fever, heat intolerance, blurred vision, confusion, hallucinations) or cardiovascular toxicity (e.g., dizziness, palpitations, arrhythmias, syncope). Ambulatory patients should be counseled to avoid activities requiring mental alertness until they know how these agents affect them. A dosage reduction in one or both drugs may be necessary if excessive adverse effects develop.

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GENERALLY AVOID: Coadministration with drugs that block norepinephrine uptake or deplete norepinephrine stores may decrease iobenguane I-123 uptake in neuroendocrine tumors and lead to false-negative imaging results. Since iobenguane I-123 is subject to the same uptake and accumulation pathways as norepinephrine, drugs that alter norepinephrine disposition in adrenergic nerve terminals and presynaptic storage vesicles will likewise affect iobenguane. These drugs include antihypertensive agents that deplete norepinephrine stores or inhibit reuptake (e.g., guanethidine, reserpine, labetalol); antidepressants that inhibit norepinephrine transporter function (e.g., tricyclic antidepressants, selective serotonin reuptake inhibitors); sympathomimetic amines (e.g., phenylephrine, phenylpropanolamine, pseudoephedrine, ephedrine); central nervous stimulants (e.g., amphetamines); phenothiazines; and cocaine. Clinical studies have not determined which specific drugs may cause false-negative imaging results and whether all drugs in a specific pharmacologic class have the same potential to produce negative imaging results. Increasing the dose of iobenguane I-123 will not overcome any potential effect of these drugs.

MANAGEMENT: When medically feasible, any drug that blocks norepinephrine uptake or deplete norepinephrine stores should be discontinued for at least five biological half-lives before iobenguane I-123 administration. Patients should be monitored for the occurrence of clinically significant withdrawal symptoms, especially patients with elevated levels of circulating catecholamines and their metabolites.

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GENERALLY AVOID: Coadministration with drugs that block norepinephrine uptake or deplete norepinephrine stores may decrease iobenguane I-123 uptake in neuroendocrine tumors and lead to false-negative imaging results. Since iobenguane I-123 is subject to the same uptake and accumulation pathways as norepinephrine, drugs that alter norepinephrine disposition in adrenergic nerve terminals and presynaptic storage vesicles will likewise affect iobenguane. These drugs include antihypertensive agents that deplete norepinephrine stores or inhibit reuptake (e.g., guanethidine, reserpine, labetalol); antidepressants that inhibit norepinephrine transporter function (e.g., tricyclic antidepressants, selective serotonin reuptake inhibitors); sympathomimetic amines (e.g., phenylephrine, phenylpropanolamine, pseudoephedrine, ephedrine); central nervous stimulants (e.g., amphetamines); phenothiazines; and cocaine. Clinical studies have not determined which specific drugs may cause false-negative imaging results and whether all drugs in a specific pharmacologic class have the same potential to produce negative imaging results. Increasing the dose of iobenguane I-123 will not overcome any potential effect of these drugs.

MANAGEMENT: When medically feasible, any drug that blocks norepinephrine uptake or deplete norepinephrine stores should be discontinued for at least five biological half-lives before iobenguane I-123 administration. Patients should be monitored for the occurrence of clinically significant withdrawal symptoms, especially patients with elevated levels of circulating catecholamines and their metabolites.

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