The aim of this study was to evaluate if levels of gonadotropic and sex steroidal hormones influence the efficacy of mirabegron in the treatment of overactive bladder.
We included 58 female participants who received treatment with mirabegron 50 mg once daily and provided a blood sample for hormone profiling before treatment was initiated. Serum hormone concentrations for estradiol, progesterone, testosterone, FSH, LH, TSH, and T4 were analyzed. Urinary Distress Inventory (UDI), (overactive bladder domain: UDIOAB), and the short form Pelvic Floor Impact Questionnaire (PFIQ-7) were used to assess subjective outcomes.
There were significant overall improvements in UDI, UDIOAB, and the PFIQ from baseline to the 2 months of follow-up (P = 0.001, 0.001, and 0.008, respectively). The magnitude of the mean difference of improvements was similar between pre- and postmenopausal women. Estrogen levels were nonsignificantly lower in participants who experienced an improvement in UDI and UDIOAB at 2 months of follow-up as compared with those that did not (P = 0.7). There were no other clinically relevant differences in hormone levels in relation to improvements in UDI, UDIOAB, or PFIQ. In logistic regression analysis there were no associations between UDIOAB outcomes and age, previous use of anticholinergic drugs, parity, menopause, and local estrogen treatment.
Estradiol, gonadotropic hormones, thyroid hormones, and testosterone levels did not influence the clinical effects of mirabegron in women with overactive bladder. Menopause status should not be a determinant for mirabegron treatment.
1Department of Women's and Children's Health, Karolinska Institutet, Solna, Sweden
2Department of Clinical Sciences, Karolinska Institutet, Danderyd Hospital, Danderyd, Sweden
3Stockholm Urogynecological Clinic, Stockholm, Sweden
4Aarhus Institute of Advanced Studies, Aarhus University, Aarhus, Denmark
5Department of Statistics and Quantitative Methods, University of Milano-Bicocca, Milano, Italy.
Address correspondence to: Daniel Altman, MD, PhD, Stockholm Urogynecological Clinic, Kommendörsgatan 5, 114 48 Stockholm, Sweden. E-mail: firstname.lastname@example.org
Received 27 January, 2016
Revised 10 May, 2016
Accepted 10 May, 2016
Funding/support: The study was funded through a grant from Karolinska Institutet and the Stockholm County Council.
Financial disclosure/conflicts of interest: D.A. has participated in research projects funded by Astellas, and Merck with grants paid to the institution where he was employed. He has received fees for lecturing, advisory, or consulting assignments from Astellas, Pfizer, Gynecare, and Gedeon Richter. He is funded by a grant from Karolinska Institutet. H.K.K. has participated in research projects funded by Astellas with grants paid to the institution where she was employed. She is funded by a grant from Stockholm County Council. C.E. has received fees for lecturing from Astellas and Allergan. K.-E.A. has participated in research projects funded by Astellas and has received fees for lecturing and advisory board assignments from Allergan, Astellas, and Ferring.