A Physician-Led Communication Initiative to Inform OAB Patients of Dementia Risk Associated With Anticholinergic Medications.

OBJECTIVES: Anticholinergic medications are a core treatment strategy for overactive bladder (OAB). There is evidence that exposure to anticholinergic medications is associated with an increased risk of developing dementia. We launched an initiative to inform our patients of this risk and give them an opportunity to engage in shared decision-making about their treatment. This quality improvement initiative encompassed 3 aims: (1) to evaluate the feasibility of 2 different routes to deliver the written outreach; (2) to evaluate if and how patients changed their OAB treatment; and (3) to assess satisfaction with the outreach initiative. METHODS: A query was performed via the electronic medical record for all patients who had been prescribed an anticholinergic for treatment of OAB. We sent either electronic messages or traditional mail to patients. We contacted patients by telephone to assess if they received the message, were satisfied with their respective method of communication, and decided for ongoing treatment. Health care provider satisfaction was also measured. RESULTS: Of the 231 patients sent the outreach, 32 were still taking the anticholinergic at the time they received the communication. The majority of patients, 84.38%, were satisfied with the initiative and elected to change therapy after learning about the increased risk of dementia. The physicians also uniformly reported satisfaction with the initiative. CONCLUSIONS: Overall, this outreach initiative resulted in an increase in patient counseling that led to a change in treatment for most patients. This initiative was received favorably by patients and health care providers.

Mechanosensitive Vaginal Epithelial Adenosine Triphosphate Release and Pannexin 1 Channels in Healthy, in Type 1 Diabetic, and in Surgically Castrated Female Mice.

BACKGROUND: Distension of hollow organs is known to release adenosine triphosphate (ATP) from the lining epithelium, which triggers local responses and activates sensory nerves to convey information to the central nervous system. However, little is known regarding participation of ATP and mediators of ATP release, such as Pannexin 1 (Panx1) channels, in mechanisms of vaginal mechanosensory transduction and of changes imposed by diabetes and menopause, conditions associated with vaginal dysfunction and risk for impaired genital arousal. AIM: To investigate if intravaginal mechanical stimulation triggers vaginal ATP release and if (a) this response involves Panx1 channels and (b) this response is altered in animal models of diabetes and menopause. METHODS: Diabetic Akita female mice were used as a type 1 diabetes (T1D) model and surgical castration (ovariectomy [OVX]) as a menopause model. Panx1-null mice were used to evaluate Panx1 participation in mechanosensitive vaginal ATP release. Vaginal washes were collected from anesthetized mice at baseline (non-stimulated) and at 5 minutes after intravaginal stimulation. For the OVX and Sham groups, samples were collected before surgery and at 4, 12, 22, 24, and 28 weeks after surgery. ATP levels in vaginal washes were measured using the luciferin-luciferase assay. Panx1 mRNA levels in vaginal epithelium were quantified by quantitative polymerase chain reaction. OUTCOMES: The main outcome measures are quantification of mechanosensitive vaginal ATP release and evaluation of impact of Panx1 deletion, OVX, and T1D on this response. RESULTS: Intravaginal mechanical stimulation-induced vaginal ATP release was 84% lower in Panx1-null (P < .001) and 76% lower in diabetic (P < .0001) mice compared with controls and was reduced in a progressive and significant manner in OVX mice when compared with Sham. Panx1 mRNA expression in vaginal epithelium was 44% lower in diabetics than that in controls (P < .05) and 40% lower in OVX than that in the Sham (P < .05) group. CLINICAL TRANSLATION: Panx1 downregulation and consequent attenuation of mechanosensitive vaginal responses may be implicated in mechanisms of female genital arousal disorder, thereby providing potential targets for novel therapies to manage this condition. STRENGTHS & LIMITATIONS: Using animal models, we demonstrated Panx1 involvement in mechanosensitive vaginal ATP release and effects of T1D and menopause on this response and on Panx1 expression. A limitation is that sex steroid hormone levels were not measured, precluding correlations and insights into mechanisms that may regulate Panx1 expression in the vaginal epithelium. CONCLUSIONS: Panx1 channel is a component of the vaginal epithelial mechanosensory transduction system that is essential for proper vaginal response to mechanical stimulation and is targeted in T1D and menopause. Harroche J, Urban-Maldonado M, Thi MM, et al. Mechanosensitive Vaginal Epithelial Adenosine Triphosphate Release and Pannexin 1 Channels in Healthy, in Type 1 Diabetic, and in Surgically Castrated Female Mice. J Sex Med 2020;17:870-880.

The Role of Pelvic Floor Muscle Training in the Conservative and Surgical Management of Female Stress Urinary Incontinence: Does the Strength of the Pelvic Floor Muscles Matter?

The purpose of this review is to provide an in-depth overview of the role of pelvic floor muscle (PFM) training in the management of stress urinary incontinence (SUI). The definition, epidemiology, and pathogenesis of SUI are described. We review the anatomy of the PFM and the importance of PFM strength in maintaining urinary continence and establishing normal voiding function. A brief description of the surgical options currently available for SUI and the existing data regarding the role of perioperative PFM training for SUI are included. Critical research questions to better evaluate and assess PFM training during the perioperative period are proposed. Promising novel approaches in the treatment of SUI are also presented. This review is useful for physiatrists, urogynecologists, female urologists, and nurse practitioners who specialize in the management and treatment of women with SUI. LEVEL OF EVIDENCE: IV.