Search

Background: This is the first report of a newly identified cause of recurrent stress urinary incontinence (SUI) after midurethral tape insertion.Patients and Methods: This article reports a series of cases with primary or secondary tape failure including clinical presentation and findings, the results of pelvic floor (PF) ultrasound, and the (surgical) correction of malpositioned vaginal tapes.Results: A vaginal tape for treating SUI must be accurately placed under the mid-third of the urethra and at a distance of 3-5 mm from the urethra. Alignment parallel to the urethra in the urethrovaginal septum is also essential for adequate function. A tethered tape refers to the adhesion of a tape edge to the anterior vaginal wall either during primary wound closure or due to secondary ingrowths and is typically associated with recurrent SUI during activities or changes in posture. Less common is SUI through an increase in pressure from cranially, which occurs when coughing or laughing. "Vaginal polyps" may point to imminent vaginal erosion of the tape. In the sagittal plane, the PF examination will identify an oblique orientation of the tape at rest, an abnormal closeness of the tape to the transducer, and changes in tape shape upon manipulation of the vaginal probe. Once the diagnosis has been established, a tethered tape is easy to correct by realignment or tightening to accomplish correct positioning parallel to the urethra. This measure restores tape function and continence.Conclusion: Primary or secondary failure of a tension-free vaginal tape may be caused by a tethered tape. This complication can be diagnosed on the basis of characteristic findings at PF ultrasound. In most women, the tape position can be corrected and there is no need for tape removal. [ABSTRACT FROM AUTHOR]

Introduction: Since the soluble receptor activator of the NF-κB ligand (sRANKL) as well as the endogenous anti-resorptive cytokine osteoprotegerin (OPG) are produced by osteoblasts and given that these cells undergo significant changes during antiresorptive treatment, we hypothesized that treatment with bisphosphonates (BP) would be accompanied by changes in serum OPG and sRANKL levels. Methods: In a prospective, randomized controlled trial of previously untreated postmenopausal women with osteoporosis, oral BP therapy (daily doses of either 10 mg alendronate or 5 mg risedronate) in combination with calcium/vitamin D was compared to calcium/ vitamin D treatment alone (control group). Follow-up at 2, 6 and 12 months was completed for 56 patients. Standardized spinal X-rays were performed at baseline, and DEXA measurements at the femoral neck and trochanter were made at baseline and after 1 year. Serum OPG and sRANKL levels were measured with a polyclonal antibody-based ELISA system. Results: After 1 year, there was a nonsignificant loss in neck and trochanteric bone mineral density (BMD) in the CTR group and a mean increase of 3.3% and 4.6% in the combined BP group (both p<0.0001), respectively. Serum levels of C-terminal telopeptides of type I collagen (sCTX) and osteocalcin decreased by 12% and 10% at 12 months in the CTR group and by 43% and 23% in the combined BP group, respectively (all significant). OPG serum levels in the CTR group decreased significantly by 9% at 2 months (p<0.005) and remained below pre-treatment levels at later time points. Both the alendronate- and risedronate-treated patient groups showed unaltered OPG levels after 2 months, but they had significantly increased serum levels at 6 and 12 months. Levels of sRANKL were unchanged throughout the treatment period. Univariate regression analysis demonstrated that changes in serum OPG levels after 12 months of BP treatment were positively and better correlated to BMD changes (trochanter: r =0.59, p<0.0001; neck: r =0.50, p<0.001) than those of sCTX, which showed the expected negative correlation to BMD change (trochanter: r = -0.35, p=0.03; neck: r = -0.23, p=0.16).With multiple regression analyses at 12 months, R² values for 1-year changes in trochanteric BMD of 0.33 (OPG alone) and 0.23 (sCTX alone) were significantly improved to the 0.57 when OPG and sCTX changes were combined (p<0.001). Results for the femoral neck were also statistically significant R²=0.35, p<0.001). BMD and OPG changes in the CTR group were not correlated with each other. Conclusions: We conclude that with BP treatment, changes in serum OPG levels, unlike changes in sCTX levels, are positively correlated to changes in BMD response. The BP-related changes in serum OPG levels during treatment could result from effects on osteoclastogenesis and osteoclast apoptosis as well as from a direct stimulatory effect on osteoblastic OPG production. These changes in OPG levels may be used to predict the individual response of patients to BP treatment. [ABSTRACT FROM AUTHOR]

Copyright of Reproduktionsmedizin is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)