BLADDER PAIN AND MENOPAUSE

There is no woman who does not find to face, sooner or later, the consequences of small, large hormonal revolutions and in menopause, when estrogen physiologically reduce, are felt not only physical, but also psychological and relational. Estrogens are depute to protect women’s intimate for most of their life and when they fail, the body in general, and the urogenital tract in particular, suffer the wayside. That’s why it is important to act in advance. The estrogen deficiency may induce both anatomical and functional changes of the uro-genital tract resulting in dryness, atrophy and loss of elasticity of the tissues. Changes in functional level of estrogens may be responsible for a disorder characterized by urgency and frequency of urine more or less associated with incontinence. both for the effect on the detrusor musculature and for the batterial flora reduction. And, finally, changes in the urethra, which imply a reduction of urethral tone, are responsible for the classical stress incontinence. In addition the lack of estrogen affects the typical bacterial flora of the uro-genital area, the so called lactobacilli, that have the important function of protecting the environment of the vagina against pathogenic bacteria that, in these conditions, tend to open the door to serious uro-genital infections. The thinning of the urethral and vulvovaginal epithelium is responsible for a exteriorization of bladder and urethral nerve fibers; their easier activation is also triggered by micro-traumas that are generated by the friction of undergarments and sexual intercourses; everything justifies the persistence of symptoms such as bladder pain. Surely the patient is not able to associate the symptom to the estrogenic deficit but usually the woman turns to a gynecologist or urologist.
Any damage or defect of this barrier induced by estrogens deficiency may be responsible for a cascade of inflammatory events that induce bladder pain. Though the real cause of bladder pain syndrome, is not completely known, we are aware that the damage of transitional epithelium due to a persistent bacterial attack, plays a key role in the pathogenesis of this disease. Infact the transitional epithelium, urothelium otherwise said, is covered by a protective layer of glicosoaminoglicani (GAGs) that create a barrier against the urine contents. Thus this protective barrier of glicosoaminoglicani (GAGs) is sensitive to the effect of estrogen and thus seems to be reduced in postmenopausal women favoring urothelial damage. The correct treatment approach involves the use of substances that hit all the potential trigger factors including infections (Candida spp., Escherichia coli, Chlamydia, Ureoplasma, etc.), physical or chemical agents and estrogen deficiency. Obviously, apart from the pain relief it should not be neglected the management of the main precipitating or aggravating factors such as microbial agents and hypoestrogenism. Unfortunately the continuous use of antibiotics is however burdened with the risk of resistance as well as from possible gastrointestinal complications and compromise the quality of life of patients. The recommendations on medical therapy of painful bladder syndrome (BPS / IC) primarily target the symptom relief with analgesics and corticosteroids or substances that circumvent bladder pain.