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Metoclopramide and Dyskinesia MORE @ WWW. PHARMACY For references, go to www RX FOCUS DRUG INTERACTIONS TIMES.COM .PharmacyTimes.com/ publications/issue. Metoclopramide John R. Horn, PharmD, FCCP and Dyskinesia John R. Horn, PharmD, FCCP, and Philip D. Hansten, PharmD etoclopramide has been used for any plasma concentration, a larger percent- many years in the treatment of age of metoclopramide would be expected Philip D. Hansten, Mgastroparesis, nausea and vomit- to collect in the brain in patients with PharmD ing, and gastroesophageal reflux disease reduced P-gp. Increasing plasma or brain (GERD). It acts as an antagonist of the concentrations of metoclopramide would dopamine D2 receptor and muscarinic recep- be expected to increase the risk of metoclo- 1,2 tors and as an agonist of 5-HT4 receptors. pramide side effects. These actions increase gastric tone and emptying as well as increase antroduodenal Potential Pharmacokinetic/ coordination, resulting in some efficacy for Pharmacodynamic Interactions gastroparesis and GERD. Metoclopramide’s Little data are available that examine the clopramide may occur with any inhibitor antiemetic effect is thought to be due to its relationship of metoclopramide concen- of CYP2D6 or P-gp. Concurrent adminis- inhibition of D2 and 5-HT3 receptors in the tration to the incidence of side effects, tration of metoclopramide with CYP2D6 chemoreceptor trigger zone. except that several retrospective analyses inhibitors (eg, amiodarone [Cordarone], have found that higher doses are more diphenhydramine [Benadryl], propafe- Metoclopramide-Induced often associated with tardive dyskinesia. none [Rythmol], quinidine, ritonavir Movement Disorders In a study of 24 healthy subjects, pre- [Norvir], terbinafine [Lamisil], drone- Metoclopramide exerts its pharmacologic treatment with fluoxetine (Prozac) 60 mg darone [Multaq], bupropion [Wellbutrin]) activity both peripherally and centrally. It daily for 8 days resulted in an increase in or P-gp inhibitors (eg, clarithromycin is the ability of metoclopramide to affect metoclopramide maximum plasma con- [Biaxin], cyclosporine [Neoral], verapamil central dopamine and serotonin receptors centration and area under the concentration [Calan], ketoconazole [Nizoral], tacroli- that is thought to account for its movement- time curve of 42% and 89%, respectively. mus [Prograf], itraconazole [Sporanox], related side effects. These can include dys- Metoclopramide’s half-life increased from nelfinavir [Viracept]) should probably be tonia, akathisia, parkinsonism, and tardive 5.5 hours to 8.5 hours.9 avoided pending further data. The poten- dyskinesia. These usually abate with dis- Metoclopramide may have pharmaco- tial for increased side effects during the continuation of metoclopramide but tardive dynamic interactions with other drugs, concurrent administration of CYP1A2 or dyskinesia may be irreversible. The FDA including neuroleptic agents and selec- CYP3A4 inhibitors with metoclopramide continues to receive reports of dyskinesia tive serotonin reuptake inhibitors (SSRIs). is unknown. associated with metoclopramide. Antipsychotic drugs with a high risk of movement disorders include fluphenazine Summary Metoclopramide (Prolixin), trifluoperazine (Stelazine), thio- There is no doubt that metoclopramide Pharmacokinetics thixene (Navane), thioridazine (Mellaril), can occasionally cause severe side effects. Metoclopramide is eliminated by sever- chlorpromazine (Thorazine), haloperidol Because it is eliminated by CYP2D6 and al pathways. About 30% is eliminated (Haldol), perphenazine (Trilafon), risperi- appears to be a substrate for P-gp, there are unchanged in the urine.3 The rest is metabo- done (Risperdal), and loxapine (Loxitane). a large number of potential drugs that can lized, primarily by cytochrome P450 (CYP) These drugs will likely potentiate the inhi- interact with metoclopramide to increase 2D6, with perhaps some contribution from bition of dopamine receptors caused by its plasma concentration or passage into CYP3A4 or CYP1A2.4,5 Metoclopramide metoclopramide. the brain. Some patients, such as those also appears to be a substrate for the Thioridazine, chlorpromazine, perphen- with renal failure or a genetic deficiency in P-glycoprotein (P-gp) transporter. azine, haloperidol, and risperidone have CYP2D6 or P-gp activity, may be particu- Genetic variations in CYP2D6 or P-gp been noted to inhibit CYP2D6 and could larly susceptible to metoclopramide move- may alter the risk of movement disorders in increase the plasma concentration of meto- ment-related adverse events, including patients taking metoclopramide.6-8 Reduced clopramide. Theoretically, SSRIs used those exacerbated by drug interactions. n CYP2D6 activity leads to increased meto- concomitantly with metoclopramide could clopramide plasma concentrations and risk increase the risk of serotonin syndrome. Drs. Horn and Hansten are both professors of toxicity. Reduced P-gp activity increases Additionally, some SSRIs [eg, duloxetine of pharmacy at the University of Washington the brain/plasma concentration ratio of (Cymbalta), fluoxetine, and paroxetine School of Pharmacy. For an electronic version metoclopramide, because P-gp acts as an (Paxil)] are inhibitors of CYP2D6. of this article, including references if any, visit www.hanstenandhorn.com. efflux transporter from brain to blood. For Pharmacokinetic interactions with meto- August 2012 www.PharmacyTimes.com 35.
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