Potential Biomarkers in the Study of Overactive Bladder in Women

Pelvic organ prolapse Pelvic organ prolapse (POP) is a clinical condition that, although it is not life-threatening, significantly affects patients' quality of life. POP affects more than 30% of females in the general population. Among those, the majority is free of symptoms and do not need any medical assistance. However, according to US statistics, almost 20% of women will be candidates for some type of surgery to restore POP during their lifetime.

Urinary incontinence Urinary incontinence (UI) is used to describe any loss of urine through the urethra. It is a common patient complaint but not a specific disease. UI significantly affects patients' quality of life. UI is classified in 3 subtypes: stress UI (SUI) (loss of urine on effort, coughing etc.), urgency UI (UUI) (loss of urine involuntary and combined by urgency) and mixed UI (MUI) (combination of the two). UUI is the second most common type of UI in women, and it is estimated that 20-40% of women who visit outpatient clinic healthcare services have UUI. Regarding women with SUI, the surgical intervention by using a tension free vaginal tape is a successful method. Considering females with UUI, the pharmacological treatment is a long-lasting and effective alternative.

Pathophysiology of overactive bladder in women with POP Few evidence exist regarding the etiology of OAB in women with POP. POP itself is considered an important mechanism for the development of OAB. Several studies have suggested that patients with POP have a lower peak of maximum flow rate (Q max) during urination compared to patients without concomitant prolapse. In addition, the average flow rate (Q ave) in women with detrusor overactivity appears to be lower as well. It is possible that obstructive urination is involved in the creation of the detrusor overactivity in patients with POP . In studies with patients who underwent POP surgery, had improvement of OAB symptoms, and the urinary flow rates were mainly improved postoperatively.

The first theory that attempts to explain how prolapse induces the OAB symptoms is the possible damage of bladder nerve pathways that happens in women with obstructive voiding. In these patients, hypersensitivity and decreased secretion of acetylcholine (Ach), which is the major neurotransmitter of the urinary bladder, was found in comparison to asymptomatic patients. Ischemia and bladder wall hypoxia caused by bladder dilatation and contractions may play an important role in this damaged neural pathway in cases of prolapse and obstructive urination.

The second theory focuses on the bladder detrusor muscle. The urinary bladder is a hollow sac-like cavity connected with the ureters, where the urine is collected, and a funnel extension, the bladder neck connected to the urethra. The urinary bladder is lined with transitional epithelial tissue that is able to stretch significantly to accommodate large volumes of urine. The main part of the wall is formed by smooth muscle layers provide the urinary bladder with its ability to expand and contract. It is commonly referred to as the detrusor muscle. In cases where there is a reduction in the cell-site electrical activity propagation or in the cell membrane instability, the transmission of the cell-to-cell electrical activity signal is activated. As a result, the detrusor muscle becomes hypersensitive and the patient develops OAB symptoms.