Dicyclomine (Bentyl) Interactions
- Amantadine
- Amoxapine
Antacids
Antimuscarinics
Anxiolytics, Sedatives, and Hypnotics
- Bupropion
- Cisapride
- Clozapine
- Cyclobenzaprine
- Digoxin
- Disopyramide
- Erythromycin
- Ethanol
- Ketoconazole
- Levodopa
- Maprotiline
- Memantine
- Metoclopramide
- Olanzapine
Opiate agonists
- Orphenadrine
Parasympathomimetics
Phenothiazines
- Procainamide
- Quinidine
Sedating H1-blockers
- Tegaserod
- Topiramate
Tricyclic antidepressants
Dicyclomine (Bentyl) Interactions
Additive anticholinergic effects may be seen when dicyclomine is used concomitantly with other antimuscarinics. Other commonly used drugs with moderate to significant anticholinergic effects include amantadine, amoxapine, bupropion, clozapine, cyclobenzaprine, disopyramide, maprotiline, olanzapine, orphenadrine, the sedating H1-blockers, most phenothiazines, procainamide, quinidine, and most tricyclic antidepressants. Clinicians should note that antimuscarinic effects might be seen not only on GI smooth muscle, but also on bladder function, the eye, and temperature regulation. With many of the listed agents, additive drowsiness may also occur when combined with dicyclomine.
Opiate agonists should be used cautiously with antimuscarinics, such as dicyclomine, since additive depressive effects on GI motility or bladder function may been seen. Pharmacology texts report that meperidine exerts less pronounced effects on GI smooth muscle than other opiate agonists.
Dicyclomine can cause drowsiness, so it should be used cautiously in patients receiving CNS depressants like ethanol or anxiolytics, sedatives, and hypnotics.
Ketoconazole requires an acidic pH for oral absorption. Medications that increase gastric pH or decrease acid output can cause a notable decrease in the bioavailability of ketoconazole. Medications that have this effect include antimuscarinics. Antimuscarinics have a prolonged duration of action, and staggering their time of administration with ketoconazole by several hours may not prevent the drug interaction. An alternative imidazole antifungal should be considered if antimuscarinic medications are required.
Oral formulations of digoxin can produce higher serum concentrations when administered concurrently with antimuscarinics (e.g., propantheline) because of decreased GI motility induced by the antimuscarinic agent. This interaction has mostly occurred in the literature with slowly-dissolving, large-particle formulations of digoxin tablets; the manufacture of oral digoxin products today, utilizing liquid formulations and/or smaller particle sizes, theoretically reduces the potential for absorption interactions. However, there is wide variability expected in individual responses to many digoxin-drug interactions. Other pharmacodynamic and pharmacokinetic systemic interactions are possible between digoxin and select antimuscarinic agents. Anticholinergics, because of their ability to cause tachycardia, can also antagonize the beneficial actions of digoxin in atrial fibrillation/flutter. Routine therapeutic monitoring should be continued when an antimuscarinic agent is prescribed with digoxin until the effects of combined use are known.
Due to antimuscarinic properties that may slow GI motility, use dicyclomine with caution in patients receiving cisapride, erythromycin (when erythromycin is being administered to enhance GI motility), metoclopramide, or tegaserod. Avoid chronic administration of antimuscarinics along with prokinetic agents under most circumstances. The clinical significance of these potential interactions is uncertain.
The muscarinic actions of parasympathomimetics, including both direct cholinergic receptor agonists and cholinesterase inhibitors, can antagonize the antimuscarinic actions of dicyclomine and vice-versa.
The doses of antimuscarinics and levodopa may need to be adjusted when the drugs are given simultaneously. Through central antimuscarinic actions, anticholinergics can potentiate the dopaminergic effects of levodopa. While some patients may benefit from this interaction, clinicians should be ready to decrease doses of levodopa if an antimuscarinic is added. Antimuscarinic properties, by slowing GI transit, may also decrease levodopa bioavailability; however, this mechanism appears to be of modest clinical significance.
Concomitant administration of amantadine, benztropine, or trihexyphenidyl with levodopa can enhance the therapeutic effects of levodopa. Combining these drugs may be therapeutic in patients with parkinsonism and may allow for reduced dosages of levodopa.
Antacids may inhibit the oral absorption of dicyclomine and other antimuscarinics. Simultaneous oral administration of dicylcomine with an antacid should be avoided when feasible; separate dosing by at least 2 hours to limit an interaction.
Through an additive effect, the use of topiramate (a weak carbonic anhydrase inhibitor) with agents that may increase the risk for heat-related disorders, such as antimuscarinics, may lead to oligohidrosis, hyperthermia and/or heat stroke.
The adverse effects of antimuscarinics, such as dry mouth, urinary hesitancy or blurred vision may be enhanced with use of memantine; dosage adjustments of the anticholinergic drug may be required when memantine is coadministered.
[ Last revised: 4/6/2006 1:48:00 PM ]
References
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