Pathogenesis Of Stress Urinary Incontinence Research Articles

Elucidating the causal landscape: Mendelian randomization analysis of lifestyle and physiological factors in stress urinary incontinence.

To explore the potential causal links between obesity, type 2 diabetes (T2D), and lifestyle choices (such as smoking, alcohol and coffee consumption, and vigorous physical activity) on stress urinary incontinence (SUI), this study employs a Mendelian Randomization approach. This research aims to clarify these associations, which have been suggested but not conclusively established in prior observational studies. Genetic instruments associated with the exposures at the genome-wide significance (p < 5 × 10-8) were selected from corresponding genome-wide association studies. Summary-level data for SUI, was obtained from the UK Biobank. A two-sample MR analysis was employed to estimate causal effects, utilizing the inverse-variance weighted (IVW) method as the primary analytical approach. Complementary sensitivity analyses including MR-PRESSO, MR-Egger, and weighted median methods were performed. The horizontal pleiotropy was detected by using MR-Egger intercept and MR-PRESSO methods, and the heterogeneity was assessed using Cochran's Q statistics. Our findings demonstrate a significant causal relationship between higher body mass index (BMI) and the risk of SUI, with increased abdominal adiposity (WHRadjBMI) similarly linked to SUI. Smoking initiation is also causally associated with an elevated risk. However, our analysis did not find definitive causal connections for other factors, including T2D, alcohol consumption, coffee intake, and vigorous physical activity. These findings provide valuable insights for clinical strategies targeting SUI, suggesting a need for heightened awareness and potential intervention in individuals with higher BMI, WHR, and smoking habits. Further research is warranted to explore the complex interplay between genetic predisposition and lifestyle choices in the pathogenesis of SUI.

Morphological examination of pelvic floor muscles in a rat model of vaginal delivery

ObjectiveThis study investigated morphological changes in the composition of the pelvic floor muscles, degree of atrophy, and urethral function in a rat of simulated birth trauma induced by vaginal distension (VD) model.MethodsFemale Sprague–Dawley rats were classified into four groups: a sham group, and 1, 2, and 4 weeks post-VD (1 W, 2 W, and 4 W, respectively) groups. We measured the amplitude of urethral response to electrical stimulation (A-URE) to evaluate urethral function. After measuring the muscle wet weight of the pubococcygeus (Pcm) and iliococcygeus (Icm) muscles, histochemical staining was used to classify muscle fibers into Types I, IIa, and IIb, and the occupancy and cross-sectional area of each muscle fiber were determined.ResultsThere were 24 Sprague–Dawley rats used. A-URE was significantly lower in the 1 W group versus the other groups. Muscle wet weight was significantly lower in the VD groups versus the sham group for Pcm. The cross-sectional area of Type I Pcm and Icm was significantly lower in the VD groups versus the sham group. Type I muscle fiber composition in Pcm was significantly lower in the VD groups versus the sham groupand lowest in the 2 W group. Type I muscle fiber composition in Icm was significantly lower in the 2 and 4 W groups versus the sham group.ConclusionMuscle atrophy and changes in muscle composition in the pelvic floor muscles were observed even after improvements in urethral function. These results may provide insight into the pathogenesis of stress urinary incontinence after VD.

Advances in the molecular pathogenesis and cell therapy of stress urinary incontinence.

Stress urinary incontinence (SUI) is very common in women. It affects patients' mental and physical health, and imposed huge socioeconomic pressure. The therapeutic effect of conservative treatment is limited, and depends heavily on patient persistence and compliance. Surgical treatment often brings procedure-related adverse complications and higher costs for patients. Therefore, it is necessary to better understand the potential molecular mechanisms underlying stress urinary incontinence and develop new treatment methods. Although some progress has been made in the basic research in recent years, the specific molecular pathogenic mechanisms of SUI are still unclear. Here, we reviewed the published studies on the molecular mechanisms associated with nerves, urethral muscles, periurethral connective tissue and hormones in the pathogenesis of SUI. In addition, we provide an update on the recent progresses in research on the use of cell therapy for treating SUI, including research on stem cells therapy, exosome differentiation and gene regulation.

A Comparative Study on the Clinical Efficacy of Simple Transobturator Midurethal Sling and Posterior Pelvic Floor Reconstruction.

Background and Objectives: The purpose of this study was to compare the complications, success rate and satisfaction of pelvic floor reconstruction after transobturator midurethral sling (TOT) and TOT combined with pelvic floor reconstruction in the treatment of female stress urinary incontinence. To explore the pathogenesis of stress urinary incontinence after pelvic floor stress injury and improve the surgical treatment strategy. Materials and Methods: From 15 August 2018 to 24 February 2022, patients diagnosed with stress urinary incontinence (SUI) and secondary prolapse of the anterior pelvis were selected to receive surgically. Participants were followed up and evaluated at 2 months, 6 months and 1 year after treatment. According to the patient's chief complaint, the patient can urinate automatically without incontinence. The number of urinary incontinence and urine leakage was significantly reduced compared with those before operation. Urinary incontinence symptoms did not improve or worsen as ineffective, observing the efficacy and complications. Results: We included 191 patients in the TOT group and 151 patients in the pelvic floor reconstruction group after TOT was combined. The operation time and hospital stay in the TOT group were short, but the TOT group needed a second operation to treat recurrent SUI. Perioperative complications were mostly dysuria, and the incidence of postoperative complications in the group of TOT combined with pelvic floor reconstruction was low. The complete success rate and effective rate of pelvic floor reconstruction after TOT in the merger group were significantly higher than those in the TOT group, and the patient satisfaction and complete success rate were also higher. Conclusions: TOT combined with posterior pelvic floor reconstruction has a definite short-term effect on patients with SUI and anterior pelvic secondary prolapse. The operation design should pay attention to the support of the posterior wall of the perineum to the bladder neck and the middle and proximal end of the urethra.

The Anatomical Pathogenesis of Stress Urinary Incontinence in Women.

Stress urinary incontinence is a common disease in middle-aged and elderly women, which seriously affects the physical and mental health of the patients. For this reason, researchers have carried out a large number of studies on stress urinary incontinence. At present, it is believed that the pathogenesis of the disease is mainly due to changes related to age, childbirth, obesity, constipation and other risk factors that induce changes in the urinary control anatomy, including the anatomical factors of the urethra itself, the anatomical factors around the urethra and the anatomical factors of the pelvic nerve. The combined actions of a variety of factors lead to the occurrence of stress urinary incontinence. This review aims to summarize the anatomical pathogenesis of stress urinary incontinence from the above three perspectives.

Dimethyl fumarate ameliorates stress urinary incontinence by reversing ECM remodeling via the Nrf2-TGF-β1/Smad3 pathway in mice.

Mechanical trauma and oxidative injury are involved in the pathogenesis of stress urinary incontinence (SUI), and oxidative stress (OS) is considered a potential therapeutic target. The antioxidant properties of dimethyl fumarate (DMF), a potent activator of Nrf2, have been highlighted recently. We therefore predicted that DMF might have therapeutic effects on mechanical trauma-induced SUI. The SUI mice model was established by vaginal distension (VD). Leak point pressure (LPP), serum OS biomarkers, cell proliferation and apoptosis, collagen, elastin, matrix metalloproteinases (MMP), Nrf2, the TGF-β1/Smad3 signaling pathway, and the associated tissue growth factors in the anterior vaginal wall were measured in either wild-type or Nrf2-knockout (Nrf2-/-) female C57BL/6 mice. The results showed that DMF improved the VD-induced LPP reduction, alleviated oxidative injury, stimulated cell proliferation and inhibited apoptosis in the anterior vaginal wall tissue of mice. Moreover, DMF treatment reduced the hydrolysis of ECM proteins by MMP2 and MMP9. The above effects may be mediated by a series of tissue growth factors, including α-SMA, PAI-1, and TIMP-2, with the TGF-β1/Smad3 signaling pathway as the core regulatory mechanism. In further study, Nrf2-/- mice were used to replicate the SUI model. And the difference is that DMF failed to reactivate the TGF-β1/Smad3 pathway, nor did it improve LPP. Dimethyl fumarate can ameliorate urethra closure dysfunction in the VD-induced SUI mice model, and the therapeutic effect of DMF is mediated by the Nrf2-dominated antioxidant system and its downstream TGF-β1/Smad3 signaling pathway.

Nampt promotes fibroblast extracellular matrix degradation in stress urinary incontinence by inhibiting autophagy

ABSTRACT Stress urinary incontinence (SUI) is defined as involuntary urinary leakage happening in exertion. Nicotinamide phosphoribosyltransferase (Nampt) is seldom researched in the pathogenesis of SUI. Accordingly, the current study set out to elucidate the role of Nampt in SUI progression. Firstly, we determined Nampt expression patterns in SUI patients and rat models. In addition, fibroblasts were obtained from the anterior vaginal wall tissues of non-SUI patients and subjected to treatment with different concentrations of interleukin-1β (IL-1β), followed by quantification of Nampt expressions in fibroblasts. Subsequently, an appropriate concentration of IL-1β was selected to treat anterior vaginal wall fibroblasts. Nampt was further silenced in IL-1β-treated fibroblasts to assess the role of Nampt in autophagy and extracellular matrix (ECM) degradation. Lastly, functional rescue assays were carried out to inhibit autophagy and evaluate the role of autophagy in the mechanism of Nampt modulating IL-1β-treated fibroblast ECM degradation. It was found that Nampt was highly-expressed in SUI patients and rat models and IL-1β-treated fibroblasts. On the other hand, Nampt silencing was found to suppress ECM degradation and promote SUI fibroblast autophagy. Additionally, inhibition of autophagy attenuated the inhibitory effects of Nampt silencing on SUI fibroblast ECM degradation. Collectively, our findings revealed that Nampt was over-expressed in SUI, whereas Nampt silencing enhanced SUI fibroblast autophagy, and thereby inhibited ECM degradation.

Protective effect and potential mechanism of Schwann cell‐derived exosomes on mechanical damage of rat dorsal root ganglion cells

Pudendal nerve (PN) injury was one of the most important pathogenesis of stress urinary incontinence (SUI). Schwann cell (SC)-derived exosomes could promote axonal regeneration. Wnt protein could significantly promote axonal regeneration and participate in the regulation of proliferation and differentiation of neural stem cells. Therefore, we sought to determine whether SCs-derived exosomes might also protect against damaged dorsal root ganglion cells (DRGs) through the Wnt/β-catenin pathway. The DRGs injury model was fabricated using a four-point bending system. The exosomes were separated from the SCs supernatant. XAV939, which was a small molecule inhibitor, was used to inhibit the Wnt/β-catenin pathway. Next, Cell Counting Kit-8 (CCK8) kit was used to detect cell activity. We evaluated the proliferative activity of DRG cells using the cell cycle and apoptosis detection kit. We assessed the cell apoptotic rates through the Annexin V/PE double staining. Finally, we detect the expression of downstream proteins of Wnt/β-catenin pathway in DRG cells using western blotting. SC-derived exosomes had protective effects on DRGs after mechanical damage, which could promote cell proliferation, transition of the cell cycle to the G2 phase, and inhibit cell apoptosis. Exogenous administration of XAV939 suppressed the promoting effect of SCs -derived exosomes on DRG cells and the expression of downstream proteins of Wnt/β-catenin pathway in DRG cells was also suppressed. These results suggested that SC-derived exosomes have a repairing effect on DRG cells injury caused by cyclic mechanical stretching (CMS) and the Wnt/β-catenin pathway is potentially involved in the process.

Large Animal Models for Investigating Cell Therapies of Stress Urinary Incontinence.

Stress urinary incontinence (SUI) is a significant health concern for patients affected, impacting their quality of life severely. To investigate mechanisms contributing to SUI different animal models were developed. Incontinence was induced under defined conditions to explore the pathomechanisms involved, spontaneous recovery, or efficacy of therapies over time. The animal models were coined to mimic known SUI risk factors such as childbirth or surgical injury. However, animal models neither reflect the human situation completely nor the multiple mechanisms that ultimately contribute to the pathogenesis of SUI. In the past, most SUI animal studies took advantage of rodents or rabbits. Recent models present for instance transgenic rats developing severe obesity, to investigate metabolic interrelations between the disorder and incontinence. Using recombinant gene technologies, such as transgenic, gene knock-out or CRISPR-Cas animals may narrow the gap between the model and the clinical situation of patients. However, to investigate surgical regimens or cell therapies to improve or even cure SUI, large animal models such as pig, goat, dog and others provide several advantages. Among them, standard surgical instruments can be employed for minimally invasive transurethral diagnoses and therapies. We, therefore, focus in this review on large animal models of SUI.

Small extracellular vesicles secreted by vaginal fibroblasts exert inhibitory effect in female stress urinary incontinence through regulating the function of fibroblasts.

Stress urinary incontinence (SUI) is a common condition in women and associated with extra-cellular matrix (ECM) reconstruction, which is mainly regulated by fibroblasts. However, the underlying mechanism remains obscure. Small extracellular vesicles (sEVs) play fundamental biological roles in various cellular functions. Some studies suggested that the sEVs were involved in the metabolism of ECM and the function of fibroblasts. The purpose of our study was to investigate the effect of sEVs secreted by vaginal fibroblasts on the pathogenesis of SUI. We showed that the fibroblasts of female anterior vaginal wall secreted sEVs. Moreover, fibroblasts of females with SUI had significantly elevated secretion of sEVs. The collagen contents, proliferation and migration capacity of fibroblasts were decreased when fibroblasts were co-cultured with fibroblasts-derived sEVs (fibroblast-sEVs) from SUI patients. Proteomic analysis revealed that fibroblast-sEVs contained various differentially expressed proteins including TIMP2, TGF-β and ABCC4, which were involved in signaling pathways of fibroblasts regulation. Therefore, we suggested that fibroblast-sEVs contributed to the pathogenesis of SUI through various proteins including TIMP2, TGF-β and ABCC4.

Gene expression in stress urinary incontinence: a systematic review.

A contribution of genetic factors to the development of stress urinary incontinence (SUI) is broadly acknowledged. This study aimed to: (1) provide insight into the genetic pathogenesis of SUI by gathering and synthesizing the available data from studies evaluating differential gene expression in SUI patients and (2) identify possible novel therapeutic targets and leads. A systematic literature search was conducted through September 2017 for the concepts of genetics and SUI. Gene networking connections and gene-set functional analyses of the identified genes as differentially expressed in SUI were performed using GeneMANIA software. Of 3019 studies, 4 were included in the final analysis. A total of 13 genes were identified as being differentially expressed in SUI patients. Eleven genes were overexpressed: skin-derived antileukoproteinase (SKALP/elafin), collagen type XVII alpha 1 chain (COL17A1), plakophilin 1 (PKP1), keratin 16 (KRT16), decorin (DCN), biglycan (BGN), protein bicaudal D homolog 2 (BICD2), growth factor receptor-bound protein 2 (GRB2), signal transducer and activator of transcription 3 (STAT3), apolipoprotein E (APOE), and Golgi SNAP receptor complex member 1 (GOSR1), while two genes were underexpressed: fibromodulin (FMOD) and glucocerebrosidase (GBA). GeneMANIA revealed that these genes are involved in intermediate filament cytoskeleton and extracellular matrix organization. Many genes are involved in the pathogenesis of SUI. Furthermore, whole-genome studies are warranted to identify these genetic connections. This study lays the groundwork for future research and the development of novel therapies and SUI biomarkers in clinical practice.

Electrical stimulation enhances neuronal cell activity mediated by Schwann cell derived exosomes

Electrical stimulation (ES) therapy has good effects in patients with nervous system injury-related diseases. ES promotes nerve cell regeneration and stimulates Schwann cells to express neurotrophic factors. The incidence of stress urinary incontinence (SUI) among elderly people is increasing. Some studies suggest that damage to the pudendal nerve is closely related to the pathogenesis of SUI. It has also been found that pelvic ES can reduce SUI symptoms in a rat model of SUI caused by pudendal nerve injury. Clinically, pelvic floor electrical stimulation is effective in patients with mild to moderate SUI. These studies indicate that ES may ameliorate damage to the pudendal nerve and thus achieve the goal of SUI treatment, although the mechanism of action of this treatment remains unclear. Therefore, the purpose of the present study was to clarify the relationships among ES, neural cells and Schwann cells at the cellular level. We applied ES to nerve cells at 100 mV/mm or 200 mV/mm for 0, 0.5, 1, or 2 h to investigate changes in nerve cell activity. We then co-cultured the nerve cells with Schwann cells to explore the influence of single-culture and co-culture conditions on the nerve cells. Compared to non-ES, ES of the nerve cells increased their activity. Compared to those in single culture, co-cultured nerve cells exhibited an additional increase in activity. We also found that Schwann cell derived exosomes could promote the activity of nerve cells, with glutamate and calcium ions playing a potential role in this process. These results suggest that the mutual regulation of neural cells and Schwann cells plays an important role in the process by which ES ameliorates neurological function, which may provide a basis for subsequent studies.

Endoplasmic reticulum stress contributes to the pathogenesis of stress urinary incontinence in postmenopausal women.

ObjectiveTo investigate the relationship between endoplasmic reticulum stress (ERS) and the pathogenesis of stress urinary incontinence (SUI) in postmenopausal women.MethodsAnterior vaginal wall tissue was collected from postmenopausal women with SUI and control subjects. Western blotting was performed for glucose-regulated protein (GRP78), inositol-requiring enzyme 1(IRE1), protein kinase-like endoplasmic reticulum kinase (PERK), activating transcription factor 6 (ATF6), C/EBP-homologous protein (CHOP), and B-cell lymphoma 2 (Bcl-2). Additionally, mRNA expression levels of PERK, activating transcription factor 4 (ATF4), and CHOP were examined by real-time polymerase chain reaction.ResultsGRP78 protein and mRNA expression levels were significantly lower in women with SUI, compared with control subjects. PERK and p-PERK expression levels were higher in women with SUI than in control subjects. However, no differences in IRE1 or ATF6 expression levels were observed in either group. Notably, higher CHOP and lower Bcl-2 protein expression levels were detected in women with SUI, compared with control subjects. Furthermore, PERK, ATF4, and CHOP mRNA expression levels were significantly higher in women with SUI than in control subjects.ConclusionsAlterations of ERS markers in SUI suggest that ERS may be involved in the development of SUI in postmenopausal women.

Review of traditional Chinese medicine in treatment of stress urinary incontinence

Stress Urinary Incontinence (SUI) has a higher incidence in middle-aged and elderly women. At present, for mild and moderate SUI patients, the treatment of kegel practice or combined with TCM ,and acupuncture, acupoint application or pelvic floor muscle exercise show benefit effect. This article summarized the etiology and pathogenesis of SUI, TCM therapy, integrated traditional Chinese and Western Medicine, in recent years, in order to provide reference for the treatment of the disease and the further study. Key words: Urinary incontinence, stress; Traditional Chinese medicine therapy; Review

Urethral proteomic analysis in ovariectomized mice administered 17β-oestradiol replacement therapy

The molecular mechanism by which 17β-oestradiol (E2) increases urethral tone is unclear. As human tissue is limited in availability, we explored changes in the urethras of ovariectomized (OVX) mice. Twenty-four virgin female mice were randomised into three groups: mice with a sham operation only (control), OVX mice without E2 replacement (OVX), and OVX mice with E2 replacement (OVX + E2). Two weeks after the ovariectomy, mice received either E2 or placebo for 4 weeks. Leak point pressure (LPP) and maximum urethral closure pressure (MUCP) were assessed in these mice at 6 weeks after OVX, under anaesthesia. After measurements were recorded, the animals were sacrificed and the urethras were removed for proteomic and further analyses. LPP and MUCP values were significantly higher in OVX + E2 group than in OVX group. Fourteen differentially expressed proteins within the urethras of mice from OVX and OVX + E2 groups were identified; six proteins were upregulated and eight proteins were down-regulated. Most E2-induced proteins are involved in proteolysis, development, neurophysiological processes, transcription, and the cell cycle. Expression of survival motor neuron (SMN) protein in the urethra was significantly increased in OVX + E2 group compared to OVX group. OVX can impair urethral tone in female mice. E2 supplementation in OVX mice rescued urethral tone. E2-mediated increase in urethral tone in OVX mice involves overexpression of SMN, decreased proteolysis and promotion of development, neurophysiological processes, and transcription in the urethra. The urethra actively undergoes multiple biological processes in response to OVX and OVX with E2 stimuli.Impact statementEstrogens are known to modulate lower urinary tract trophicity. Although treatments with 17β-oestradiol (E2) result in an increase in urethral tone, the mechanism by which E2 increases urethral tone is still not completely understood.Ovariectomy can impair urethral tone in female mice. E2 supplementation in ovariectomized mice rescued urethral tone. E2-mediated increase in urethral tone in ovariectomized mice involves overexpression of survival motor neuron, decreased proteolysis and promotion of development, neurophysiological processes, and transcription in the urethra.This information will offer clues about pathogenesis of stress urinary incontinence after menopause and will open additional avenues for novel research and potential therapies.

Downregulation of AQP2 in the anterior vaginal wall is associated with the pathogenesis of female stress urinary incontinence.

The pathogenesis of stress urinary incontinence (SUI) is unclear. Aquaporins (AQPs) are a family of transmembrane proteins that transport water and small solutes, including glycerol, across cell membranes. AQPs have been demonstrated to serve a role in skin hydration, cellular proliferation, migration, immunity, wound healing and vascular remodeling in multiple organs. Furthermore, studies have confirmed that abnormal synthesis and degradation of collagens in extracellular matrix (ECM) remodeling contributes to SUI, by altering normal tissue architecture and mechanical properties. The authors previously demonstrated that AQP2 expressed in the human endometrium varies during the menstrual cycle. However, it is unknown whether AQP2 serves a role in the pathogenesis of SUI in the urethral supporting tissue. In the present study, AQP2 location and expression was examined in the anterior vaginal wall, and investigated the association between AQP2 and collagen I/III in female SUI. Western blotting, immunohistochemistry and immunofluorescence were used to measure AQP2 expression levels, and to reveal the location of AQP2 in the anterior vaginal wall, as well as fibroblasts in SUI and non‑SUI. The association between AQP2 and collagen I/III was subsequently investigated by AQP2‑small interfering RNA knockdown and overexpression 2 in fibroblasts. AQP2 expression in the anterior vaginal wall was significantly increased in women without SUI compared with those with SUI (P<0.05). Downregulation of AQP2 significantly decreased the mRNA and protein expression of collagenI/III, while AQP2 overexpression significantly increased the mRNA and protein expression of collagen I/III in fibroblasts (P<0.05). AQP2 was demonstrated to be expressed in the anterior vaginal wall and fibroblasts, and to regulate the expression level of collagen I/III in the anterior vaginal wall and fibroblasts, suggesting that AQP2 is associated with the pathogenesis of female SUI through collagen metabolism during ECM remodeling.

Therapeutic Effect and Mechanism of Electrical Stimulation in Female Stress Urinary Incontinence

To investigate the therapeutic effect and underlying molecular mechanism of electrical stimulation (ES) in a murine stress urinary incontinence (SUI) model. Sixty female C57BL/6 mice were divided into 4 groups: CON group, no intervention; VD group, vaginal distension (VD) with an 8-mm dilator for 1 hour; VD + ES 20 group, 20 Hz ES for 0.5 hour for 7 days after VD; and VD + ES 50 group, 50 Hz ES for 7 days after VD. For functional studies, assessments of urodynamics and sneezing test were performed; then, anterior vaginal wall specimens were collected. Pathological changes were validated by Masson's trichrome and Van Gieson staining, and the expressions of collagen, transforming growth factor (TGF)-β1-Smad2/3 pathway components, and T-type calcium channels were detected by Western blotting and reverse transcription polymerase chain reaction. ES significantly increased maximum bladder capacity, leak point pressure, and sneezing positive rate in SUI mice. The staining results showed that collagen was disorganized in the VD group but became organized after ES, especially at 50 Hz. The same results were found for collagens I and III. The expression of TGF-β1, p-Smad2 and p-Smad3 significantly decreased in the VD group and significantly increased in the VD + ES groups, especially in the VD + ES 50 group. The expression of 2 T-type calcium channel subtypes (Cav 3.1 and Cav 3.2) decreased in the VD group compared with the CON group, but increased in the VD + ES group compared with the VD group. Dysregulation of collagen metabolism is involved in the pathogenesis of SUI. ES can ameliorate the symptoms of SUI by activating collagen regeneration through the TGFβ1-Smad2/3 pathway. T-type calcium channels might be involved in these processes.

Obesity with Comorbid Stress Urinary Incontinence in Women: A Narrative Review to Inform Dietetics Practice

Stress urinary incontinence (SUI) is a common problem among women; clinical treatment guidelines include weight reduction as a strategy for controlling urinary leakage. The purpose of this review was to gather evidence on the association between obesity and SUI and to ascertain whether there are any special considerations for implementing medical nutrition therapy with community-dwelling, obese, adult females with comorbid SUI. Five key findings emerged: epidemiologic studies consistently report statistically significant associations between obesity and SUI, randomized control trials found that weight loss appears to ameliorate SUI symptoms, the SUI–activity link may affect weight management, there is a potential interplay between SUI and the obesity–sleep connection, and dietary components are associated with the exacerbation of urinary symptoms. The pathogenesis of SUI and obesity-related contributions to urinary leakage is included in the introductory discussion. Lastly, insights on special considerations for implementing nutrition interventions with this population are offered.

PD7-01 ONO-8055, A NOVEL AND POTENT PROSTANOID EP2 AND EP3 RECEPTOR DUAL AGONIST, IMPROVES VOIDING DYSFUNCTION IN A MONKEY UNDERACTIVE BLADDER MODEL

INTRODUCTION AND OBJECTIVES: The objective of this study was to clarify the role of static and dynamic MRI in evaluating anatomic abnormalities in patients with stress urinary incontinence (SUI). METHODS: We performed MRI in 30 patients suffering from severe SUI. Static 2mm T2-weighted turbo spin-echo images were used in evaluating of structural derangements of the main supporting structures. Control group included 20 continent patients For detailed assessment of urethral support disorders in women suffering from SUI, we draw two lines through the bladder neck on MRI image along the axis of the proximal urethra and tangentially to the base of the bladder (the neck of the bladder during its dilation) with measuring posterior urethrovesical angle (b). The crossing of these lines with the longitudinal axis of the pubic formed a pubourethral triangle with vertex in the bladder neck. Then we dropped a perpendicular (pubourethral distance, h) from the bladder neck to the pubic side of triangle (a) and measured the area of this pubourethral triangle by the formula S 1⁄4 /2 *a * h (Figure 1). RESULTS: The results showed statistically significant differences in the parameters of area of pubourethral triangles in patients with SUI comparing with controls (152.09 10.62 mm2 vs. 242.71 106.04 mm2 p 1⁄4 0.0301), in the length of the pubic side of the pubourethral triangle (a) (14.14 5.04 mm vs. 20.82 7.69 mm, p 1⁄4 0.0281) and posterior urethrovesical angle (b) (152.09 10.62 vs. 138.8 12.59 , p 1⁄4 0.0167, respectively). These data demonstrate the presence of defect of the front urethral support in women with SUI. CONCLUSIONS: Position of urethrovesical segment plays an important role in the pathogenesis of stress urinary incontinence in women. Presented diagnostic system using pubourethral triangle assessment provides a new approach to the study the mechanisms of SUI development on the basis of anatomical and topographical features of the female urethra. It can serve as the beginning for the development of new methods of pathogenetic treatment of this nosology.

MP17-20 MAGNETIC RESONANCE IMAGING IN PATIENTS WITH STRESS URINARY INCONTINENCE - NEW EVALUATION TOOL

You have accessJournal of UrologyImaging/Radiology: Uroradiology III1 Apr 2015MP17-20 MAGNETIC RESONANCE IMAGING IN PATIENTS WITH STRESS URINARY INCONTINENCE - NEW EVALUATION TOOL George Kasyan, Mariya Barinova, Nataliya Tupikina, Mikhail Gvozdev, Boris Godunov, and Dmitry Pushkar George KasyanGeorge Kasyan More articles by this author , Mariya BarinovaMariya Barinova More articles by this author , Nataliya TupikinaNataliya Tupikina More articles by this author , Mikhail GvozdevMikhail Gvozdev More articles by this author , Boris GodunovBoris Godunov More articles by this author , and Dmitry PushkarDmitry Pushkar More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2015.02.862AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES The objective of this study was to clarify the role of static and dynamic MRI in evaluating anatomic abnormalities in patients with stress urinary incontinence (SUI). METHODS We performed MRI in 30 patients suffering from severe SUI. Static 2mm T2-weighted turbo spin-echo images were used in evaluating of structural derangements of the main supporting structures. Control group included 20 continent patients For detailed assessment of urethral support disorders in women suffering from SUI, we draw two lines through the bladder neck on MRI image - along the axis of the proximal urethra and tangentially to the base of the bladder (the neck of the bladder during its dilation) with measuring posterior urethrovesical angle (β). The crossing of these lines with the longitudinal axis of the pubic formed a pubourethral triangle with vertex in the bladder neck. Then we dropped a perpendicular (pubourethral distance, h) from the bladder neck to the pubic side of triangle (a) and measured the area of this pubourethral triangle by the formula S = ½ ∗a ∗ h (Figure 1). RESULTS The results showed statistically significant differences in the parameters of area of pubourethral triangles in patients with SUI comparing with controls (152.09 ± 10.62 mm2 vs. 242.71 ± 106.04 mm2 p = 0.0301), in the length of the pubic side of the pubourethral triangle (a) (14.14 ± 5.04 mm vs. 20.82 ± 7.69 mm, p = 0.0281) and posterior urethrovesical angle (β) (152.09 ± 10.62° vs. 138.8 ± 12.59°, p = 0.0167, respectively). These data demonstrate the presence of defect of the front urethral support in women with SUI. CONCLUSIONS Position of urethrovesical segment plays an important role in the pathogenesis of stress urinary incontinence in women. Presented diagnostic system using pubourethral triangle assessment provides a new approach to the study the mechanisms of SUI development on the basis of anatomical and topographical features of the female urethra. It can serve as the beginning for the development of new methods of pathogenetic treatment of this nosology. © 2015 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 193Issue 4SApril 2015Page: e184 Advertisement Copyright & Permissions© 2015 by American Urological Association Education and Research, Inc.MetricsAuthor Information George Kasyan More articles by this author Mariya Barinova More articles by this author Nataliya Tupikina More articles by this author Mikhail Gvozdev More articles by this author Boris Godunov More articles by this author Dmitry Pushkar More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...