Cetirizine; Pseudoephedrine (Zyrtec-D) Interactions
- Acetazolamide
Alpha-blockers
- Ammonium Chloride
Antidiabetic Agents
Antipsychotics
Anxiolytics, Sedatives, and Hypnotics
Beta-blockers
- Bretylium
- Buprenorphine
- Butorphanol
- Caffeine
Cardiac glycosides
Central-acting adrenergic agents
- Citric Acid; Sodium Citrate
- Cocaine
- Cyclopropane
- Dronabinol, THC
Ergot Alkaloids
- Ethanol
- Furazolidone
- Green Tea
- Guarana
Halogenated anesthetics
- Linezolid
- Mecamylamine
- Methazolamide
Monoamine oxidase inhibitors (MAOIs)
- Nalbuphine
Nitrates
Opiate agonists
- Pentazocine
- Potassium Citrate
- Procarbazine
- Reserpine
Sedating H1-blockers
- Sodium Acetate
- Sodium Bicarbonate
- Sodium Lactate
- St. John’s Wort, Hypericum perforatum
Sympathomimetics
- Theophylline, Aminophylline
Thyroid hormones
- Tramadol
Tricyclic antidepressants
Cetirizine; Pseudoephedrine (Zyrtec-D) Interactions
NOTE: This monograph discusses the drug interactions of cetirizine and pseudoephedrine combination products for the relief of nasal congestion and allergic rhinitis. Clinicians may wish to consult the individual cetirizine and pseudoephedrine drug monographs for more specific information.
Pseudoephedrine can potentiate the effects and increase the toxicity of other sympathomimetics including cocaine by adding to their sympathomimetic activity. Although no data are available, cetirizine; pseudoephedrine should be used cautiously in patients using significant quantities of amphetamines, cocaine, or other sympathomimetics, including ephedra and other stimulant drugs used as anorexiants.
Dose-related sedation has been noted in patients taking cetirizine; pseudoephedrine. For this reason, the manufacturer recommends to avoid this combination when used concurrently with other CNS depressants such as antipsychotics, anxiolytics, sedatives, and hypnotics (including barbiturates and benzodiazepines), dronabinol, THC, ethanol, buprenorphine, butorphanol, nalbuphine, pentazocine, opiate agonists, tramadol, tricyclic antidepressants, and also other sedating H1-blockers. Pseudoephedrine interacts with many tricyclic antidepressants, resulting in an increased risk for severe headaches or cardiovascular toxicity.
In clinical trials, when low dose theophylline (400 mg daily for 3 days) was combined with cetirizine (20 mg once daily for 3 days) the clearance of cetirizine was decreased by 16%; the clinical significance of this interaction is not known. It is possible that larger doses of theophylline could decrease the clearance of cetirizine even further. Theophylline disposition was not altered by cetirizine. Concurrent administration of caffeine, theophylline or other xanthines with pseudoephedrine can produce excessive stimulatory effects such as nervousness, irritability, insomnia, or tremor. Excessive caffeine ingestion should be avoided while taking pseudoephedrine concurrently. This includes ingestion of foods and beverages that contain high amounts of caffeine such as coffee, teas, green tea, colas, and chocolate and dietary supplements such as guarana.
Cetirizine has not produced a significant prolongation of the QTc interval in single dose studies up to 6 times the therapeutic dose (60 mg), or in combination with erythromycin, azithromycin or ketoconazole. However, in one crossover study, cetirizine (20 mg) and ketoconazole (400 mg per day) were given alone and in combination. After 10 days, the QTc increased by a mean of 9.1 msec with cetirizine and by 8.3 msec with ketoconazole. When cetirizine and ketoconazole were combined, the QTc increased by 17.4 msec, equal to the sum of the individual agents. Thus, it appears there was no significant interaction on QTc with the combined medications.
MAOIs, or drugs that possess MAO-inhibiting activity such as furazolidone, linezolid, or procarbazine, can prolong and intensify the cardiac stimulation and vasopressor effects of pseudoephedrine. Phenelzine and tranylcypromine appear to produce the greatest risk since these two MAOIs also have intrinsic amphetamine-like activity. In the presence of MAOIs, pseudoephedrine and other drugs that cause release of norepinephrine induce severe cardiovascular and cerebrovascular responses. It is unclear if selegiline, an inhibitor of MAO type B, can also predispose to this reaction. Cetirizine; pseudoephedrine is contraindicated for use during or within 14 days following the use of MAOIs or drugs with MAO-inhibiting activity due to the potential for hypertensive crisis.
The cardiovascular effects of sympathomimetic agents may reduce the antihypertensive effects produced by reserpine, alpha-blockers, beta-blockers, central-acting adrenergic agents (e.g., clonidine, guanfacine, guanabenz, methyldopa), and mecamylamine. Blood pressure and heart rates should be monitored closely to confirm that the desired antihypertensive effect is achieved. In addition to the potential loss of antihypertensive activity in the presence of beta-blockade, the alpha-receptor agonist effects of pseudoephedrine may be more pronounced with concurrent beta-blocker therapy. The effect of unopposed alpha vasoconstriction can result in hypertension and/or reflex bradycardia. The effect may be more likely to occur with non-selective beta-blockers like propranolol.
Concomitant use of digoxin or cardiac glycosides with sympathomimetics can cause arrhythmias. Sympathomimetics enhance ectopic pacemaker activity.
Halogenated anesthetics and cyclopropane may sensitize the myocardium to the effects of sympathomimetics, including pseudoephedrine.
Concomitant use of nitrates with sympathomimetics like pseudoephedrine can result in antagonism of the antianginal effects of the nitrate.
Drug interactions with St. John’s wort, Hypericum perforatum are unclear at this time. Some of the components of this herb have been shown to inhibit monoamine oxidase (MAO) in vitro, but in vivo activity is unclear. If St. John’s wort does have MAOI-like activities, it could potentially increase the cardiac stimulation and vasopressor effects of the sympathomimetic. St. John’s wort should be used cautiously with cetirizine; pseudoephedrine.
Administration of bretylium causes an initial surge in catecholamine release from nerve terminals. Prolonged therapy with bretylium prevents release of the neurotransmitter but adrenergic stores of norepinephrine are not depleted. Inhibition of the release of norepinephrine eventually leads to increased receptor sensitivity. Thus, the action of sympathomimetics may be enhanced in patients receiving bretylium either acutely or chronically. Increased sensitivity to sympathomimetics should be expected in patients receiving bretylium.
Some ergot alkaloids, notably ergotamine and, to a lesser extent, ergonovine, may produce peripheral vasoconstriction due to alpha-receptor agonism in the peripheral circulation. Although no data are available, it is possible that concomitant use of pseudoephedrine with ergotamine could cause additive and possibly severe peripheral vasoconstriction. Similar problems have been observed when ergot alkaloids were used in combination with other drugs known to cause peripheral vasoconstriction (e.g., ergonovine with dopamine; ergotamine with propranolol). Hypertension, headache, myocardial ectopy, and seizures have occurred when bromocriptine, an ergot alkaloid derivative, was combined with various sympathomimetics. Pseudoephedrine use should be avoided in patients taking ergot alkaloids, including bromocriptine, whenever possible.
Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Ammonium chloride, by acidifying the urine, increases the elimination of pseudoephedrine while sodium bicarbonate, a urinary alkalinizer, allows for increased tubular reabsorption of pseudoephedrine. While the interaction with ammonium chloride is unlikely to be clinically significant, concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions. Other urinary alkalinizers include sodium citrate, potassium citrate, sodium lactate, and sodium acetate.
Concomitant use of sympathomimetics and thyroid hormones can enhance the effects of either drug on the cardiovascular system. Patients with coronary artery disease have an increased risk of coronary insufficiency from either agent. Combined use of these agents may further increase this risk.
Pseudoephedrine may increase blood sugar via stimulation of beta2-receptors which leads to increased glycogenolysis. A pharmacodynamic interaction with antidiabetic agents may occur. Patients receiving antidiabetic agents should be closely monitored for loss of diabetic control when therapy with sympathomimetic agents is instituted.
Acetazolamide or methazolamide can decrease the excretion and enhance the effects of pseudoephedrine. Carbonic anhydrase inhibitors increase the alkalinity of the urine, thereby increasing the amount of nonionized pseudoephedrine available for renal tubular reabsorption. Use caution if a carbonic anhydrase inhibitor is coadministered; monitor for excessive pseudoephedrine-related adverse effects.
[ Last revised: 9/27/2004 5:24:00 PM ]
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