Mirabegron is a medication that can be used for overactive bladder. It is a medication that I am seeing used periodically in clinical practice. Here are a few mirabegron clinical pearls that I think are valuable to remember.
The mechanism of action is critical to remember. It is a selective beta-3 agonist. You are likely very familiar with some of the effects of beta-1 (heart) activity and beta-2 (lungs) activity on the body. Beta-blockers can oppose these receptors to varying degrees. In most situations, as we raise the dosing of a medication we can expect that we may lose selectivity. Because of this, hypertension and tachycardia are possible adverse effects and something you should monitor for in patients starting on or increasing the dose of mirabegron.
Drug interactions are important to remember with mirabegron. CYP2D6 is a common metabolic pathway and mirabegron can inhibit this pathway. Drugs like bupropion, paroxetine, amphetamines, and aripiprazole are examples of medications that can have their concentrations increased. Drugs like codeine and tamoxifen that require CYP2D6 for activation may have their actions reduced.
One of the big advantages, particularly in elderly patients, is that mirabegron is less likely to cause anticholinergic adverse effects like dry eyes, dry mouth, confusion, urinary retention, fall risk etc. that urinary anticholinergic like oxybutynin, tolterodine, and others are going to cause.
Don’t be afraid to reassess chronic use. If this medication isn’t working and helping our patients, there likely isn’t a good reason for continuing to take the medication. I reassess this medication similar to the way I reassess urinary anticholinergic. I try to ensure that we are helping the patient if we are going to risk the occurrence of adverse effects.
I discuss the pharmacology of mirabegron further on this episode of the Real Life Pharmacology podcast.
What other mirabegron clinical pearls would you add to this list?