leptin and Urinary-Bladder--Overactive

We examined 11 women aged 19-26 years (mean age 22.5±3.5 years) with secondary amenorrhea complaining frequent urination over 1.5 years and repeatedly, but unsuccessful treated for overactive bladder and chronic cystitis. The rare cause of sustained urination disorders in young female patients of reproductive age was established: development of secondary amenorrhea caused by weight loss ("cosmetic" amenorrhea) with subsequent estrogene deficit and urogenital atrophy. Morphological examination of the bladder mucosa, an important clue to the diagnosis, helps to identify the true cause of dysuria, urogenital atrophy of the bladder mucosa, in secondary ("cosmetic") amenorrhea, and determine future course of etiopathogenic treatment of sustained dysuria in young women. The treatment is often effective in case of proper and timely diagnosis and the absence of irreversible changes.

Topics: Adult; Amenorrhea; Case-Control Studies; Cystitis; Dysuria; Estradiol; Estrogens; Female; Follicle Stimulating Hormone; Humans; Leptin; Luteinizing Hormone; Mucous Membrane; Urinary Bladder; Urinary Bladder, Overactive; Weight Loss

Overactive bladder is a common condition and is significantly known to affect quality of life in both men and women. It is usually associated with urinary urgency, frequency, nocturia with or without urinary incontinence. The exact aetiology of overactive bladder is unknown. The two main theories put forward include (a) disruption of central control of the bladder by excessive suprapontine excitation or reduced suprapontine inhibition (b) Peripheral abnormality due to excessive cholinergic excitation (increases release of acetylcholine which is calcium dependent) or reduced neuropeptidergic inhibition. The other factors which contribute to its cause include increase in caffeine intake and behavioural problems. Therefore the initial treatments are based on excluding pathology and implementing behavioural changes, bladder training and caffeine reduction. Anticholinergic drugs are the main pharmacological agents used in the treatment of overactive bladder and they are usually used in conjunction with the above treatment methods. Recently, an increase in serum leptin levels has been associated with overactive bladder symptoms. This possibly is not true because leptin actually reduces Ca2+ influx in the smooth muscle. The addition of increasing doses of leptin on uterine smooth muscle (in vitro) has shown to inhibit spontaneous as well as induced uterine contractions (myometrial biopsies taken from obese women) by reducing Ca2+ influx in obese women compared to normal weight women. We believe it may have similar action on the bladder and therefore expect inhibition of the bladder detrusor smooth muscle contraction rather than stimulation which may lead to overactive bladder symptoms. This action can be considered anticholinergic rather than cholinergic and therefore should improve overactive bladder symptoms. So could this hormone (leptin) be used as a new novel agent for treating women suffering with overactive bladder symptoms?

Topics: Female; Humans; Leptin; Urinary Bladder, Overactive