TY - JOUR
T1 - Respiratory dysfunction following initiation of mirabegron
T2 - A case report
AU - Malsin, Elizabeth S.
AU - Coleman, John M.
AU - Wolfe, Lisa F.
AU - Lam, Anna P.
N1 - Funding Information:
Dr. Malsin is funded in part via NIH institutional T32 –HL076139.
Funding Information:
Dr. Malsin is funded in part via NIH institutional T32 –HL076139 .
Publisher Copyright:
© 2019 The Authors
PY - 2019
Y1 - 2019
N2 - Background: Mirabegron, a β3 adrenergic receptor agonist, is FDA approved for treatment of overactive bladder. Approved in 2012 in the US, there have been no reports of any effects of mirabegron on pulmonary function. Case presentation: We report the case of a 65 year old male with a history of Parkinson's disease, OSA, and aspiration pneumonia presenting with subacute worsening dyspnea and found to have worsening restrictive ventilatory defect with a pattern consistent with neuromuscular weakness. After recalling that initiation of mirabegron correlated with onset of his worsening symptoms, the patient decided to perform a trial period off the drug. He subsequently reported prompt improvement in his respiratory symptoms, which was confirmed objectively by pulmonary function tests. In this case, mirabegron was temporally associated with subacute worsening of the patient's pulmonary restrictive physiology, with subsequent resolution after discontinuation of the medication. Conclusions: The mechanism of this adverse effect is unknown, but we speculate that this effect may be potentially mediated by the effect of β3 adrenergic receptor agonism on skeletal muscle, in this case in a patient with pre-existing neuromuscular disease. Careful assessment of patients who develop shortness of breath while on mirabegron should include an assessment for restrictive lung disease secondary neuromuscular dysfunction. Additional study is needed of the effects of β3 agonism on skeletal muscle.
AB - Background: Mirabegron, a β3 adrenergic receptor agonist, is FDA approved for treatment of overactive bladder. Approved in 2012 in the US, there have been no reports of any effects of mirabegron on pulmonary function. Case presentation: We report the case of a 65 year old male with a history of Parkinson's disease, OSA, and aspiration pneumonia presenting with subacute worsening dyspnea and found to have worsening restrictive ventilatory defect with a pattern consistent with neuromuscular weakness. After recalling that initiation of mirabegron correlated with onset of his worsening symptoms, the patient decided to perform a trial period off the drug. He subsequently reported prompt improvement in his respiratory symptoms, which was confirmed objectively by pulmonary function tests. In this case, mirabegron was temporally associated with subacute worsening of the patient's pulmonary restrictive physiology, with subsequent resolution after discontinuation of the medication. Conclusions: The mechanism of this adverse effect is unknown, but we speculate that this effect may be potentially mediated by the effect of β3 adrenergic receptor agonism on skeletal muscle, in this case in a patient with pre-existing neuromuscular disease. Careful assessment of patients who develop shortness of breath while on mirabegron should include an assessment for restrictive lung disease secondary neuromuscular dysfunction. Additional study is needed of the effects of β3 agonism on skeletal muscle.
KW - Adverse medication effect
KW - Neuromuscular lung disease
KW - β3 receptor agonist therapy
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U2 - 10.1016/j.rmcr.2019.02.012
DO - 10.1016/j.rmcr.2019.02.012
M3 - Article
C2 - 30886821
AN - SCOPUS:85062083830
SN - 2213-0071
VL - 26
SP - 304
EP - 306
JO - Respiratory Medicine CME
JF - Respiratory Medicine CME
ER -