Vaginal Hormone Therapy for Conditions of the Lower Urinary Tract.

PURPOSE OF REVIEW: Up to half of postmenopausal women experience genitourinary symptoms secondary to hormone deficiency, and there is little consensus on the use of vaginal hormone therapy (VHT) for lower urinary tract symptoms (LUTS) in these patients. This is a review of the scientific literature in the last decade evaluating the use of VHT for disorders of the lower urinary tract including overactive bladder (OAB), stress urinary incontinence (SUI), recurrent urinary tract infections (UTI), and interstitial cystitis/bladder pain syndrome (ICS/BPS). RECENT FINDINGS: Vaginal estrogen therapy improves OAB symptoms in postmenopausal women, but results are mixed when VHT is used in combination with other treatments. There is inconclusive or limited data for the use of VHT to treat SUI and IC/BPS. Vaginal estrogen and prasterone (DHEA) therapies have demonstrated efficacy as treatment modalities for patients who experience recurrent UTIs. VHT preparations show efficacy for the treatment of certain LUTS and can be considered in carefully selected patients when clinically indicated.

The exstrophy experience: A national survey assessing urinary continence, bladder management, and oncologic outcomes in adults.

INTRODUCTION AND OBJECTIVE: The bladder exstrophy-epispadias complex (BEEC) is a rare spectrum of congenital genitourinary malformations with an incidence of 1:10,000 to 1:50,000. Advances in reconstructive surgical techniques have improved clinical outcomes, but there is a paucity in data about disease sequela in adulthood. This is the largest survey to date in the United States exploring the urinary continence, bladder management, and oncologic outcomes in adults with BEEC. METHODS: Respondents were over the age of 18 with a diagnosis of bladder exstrophy, cloacal exstrophy, or epispadias. They were treated at the authors' institution, included in the Association for the Bladder Exstrophy Community (A-BE-C) mailing list, and/or engaged in A-BE-C social media. A survey was created using uniquely designed questions and questionnaires. Survey responses between May 2020 and July 2020 were processed using Research Electronic Data Capture (REDCap). Quantitative and qualitative statistics were used to analyze the data with significance at p < 0.05. RESULTS: A total of 165 patients completed the survey. The median age was 31.5 years (IQR 25.9-45.9). Many patients considered themselves continent of urine, with a median satisfaction score of 74 (IQR 50-97) on a scale from 0 (consider themselves to be completely incontinent) to 100 (consider themselves to be completely continent). There was less leakage among those with a continent urinary diversion compared to those who void or catheterize per urethra (p = 0.003). Patients with intestinal-urinary tract reconstruction, such as augmentation cystoplasty or neobladder creation, were more likely to perform bladder irrigations (p = 0.03). Patients with continent channels were more likely to report UTI than all other forms of bladder management (89.0% vs. 66.2%, p = 0.003). Three (1.9%) patients were diagnosed with bladder cancer. A small portion of patients (27.2%) were given bladder cancer surveillance recommendations by a physician. DISCUSSION: Most patients achieved a satisfactory level of urinary continence, with the highest continence rates in those with a continent urinary diversion. Those with intestinal-urinary tract reconstruction were more likely to perform bladder irrigations, perhaps to avoid complications from intestinal mucous production. The rates of self-reported UTI and were higher in patients with continent channels, but recurrent UTIs were not affected by the type of genitourinary reconstruction. Bladder cancer exists in this population, highlighting the need for long-term follow-up. CONCLUSION: Most BEEC patients achieve a satisfactory level of urinary continence, with the best outcomes in those with a continent urinary diversion. This population requires long-term follow-up with a transitional urologist to ensure adequate oncologic care.

Reno-appendiceal fistula in autosomal dominant polycystic kidney disease.

We present a very rare Case of a 53-year-old female with autosomal dominant polycystic kidney disease (ADPKD) who was incidentally found to have a reno-appendiceal fistula while undergoing open bilateral nephrectomy. The mid-portion of the appendix was fistulized to a cyst in the lower pole of the right kidney. The etiology was likely due to chronic inflammation. An appendectomy was performed along with the planned right nephrectomy to ensure complete removal of the fistulous tract.

Maternal diabetes triggers DNA damage and DNA damage response in neurulation stage embryos through oxidative stress.

DNA damage and DNA damage response (DDR) in neurulation stage embryos under maternal diabetes conditions are not well understood. The purpose of this study was to investigate whether maternal diabetes and high glucose in vitro induce DNA damage and DDR in the developing embryo through oxidative stress. In vivo experiments were conducted by mating superoxide dismutase 1 (SOD1) transgenic male mice with wild-type (WT) female mice with or without diabetes. Embryonic day 8.75 (E8.75) embryos were tested for the DNA damage markers, phosphorylated histone H2A.X (p-H2A.X) and DDR signaling intermediates, including phosphorylated checkpoint 1 (p-Chk1), phosphorylated checkpoint 2 (p-Chk2), and p53. Levels of the same DNA damage markers and DDR signaling intermediates were also determined in the mouse C17.2 neural stem cell line. Maternal diabetes and high glucose in vitro significantly increased the levels of p-H2A.X. Levels of p-Chk1, p-Chk2, and p53, were elevated under both maternal diabetic and high glucose conditions. SOD1 overexpression blocked maternal diabetes-induced DNA damage and DDR in vivo. Tempol, a SOD1 mimetic, diminished high glucose-induced DNA damage and DDR in vitro. In conclusion, maternal diabetes and high glucose in vitro induce DNA damage and activates DDR through oxidative stress, which may contribute to the pathogenesis of diabetes-associated embryopathy.