Oral Cerivastatin was prescribed 2 months prior to the onset of retention. With the discontinuation of Cerivastatin, the patient reported modest improvement in symptoms. The findings of this case support the potential risk of permanent bladder selleck compound smooth muscle damage due to statin that may lead to underactive bladder

and urinary retention. “
“It is with great pleasure that the editorial team present to you this compendium of review articles. To provide an update of current knowledge on lower urinary tract symptoms (LUTS) and their underlying pathophysiology, a workshop with experts in the field was arranged in Tokyo on 16–17 July 2011. The presentations and the following discussions were integrated, resulting in the articles presented in this supplement. We hope it will be of interest to both see more clinicians and researchers. Recent studies suggest that some cardiovascular, metabolic and endocrine factors may be associated with the development of LUTS. Yoon describes an association between LUTS and components of metabolic syndrome. This association is clear in men with benign prostatic hyperplasia (BPH), but there is limited data on female LUTS. Tai and Yu indicate that a link between LUTS and metabolic syndrome remains controversial, suggesting that the development of LUTS is a multifactorial process. Aoki and Yokoyama have related nocturia

(one of the most common LUTS) to metabolic syndrome. They show that nocturia can be a marker of metabolic syndrome as well as a precursor of this syndrome. Son et al. overview basic and clinical studies reporting a possible relationship between hypercholesterolemia

Dynein and detrusor overactivity (DO). Using Myocardial Infarction Prone Watanabe Heritable Hyperlipidemia (WHHL-MI) rabbits, Yoshida et al. have evaluated the effects of chronic hyperlipidemia on bladder function. Their results show that young WHHL-MI rabbits have DO, while old WHHL-MI rabbits exhibit both detrusor hyperactivity and impaired detrusor contraction (DHIC). As hyperlipidemia is thought to induce atherosclerosis, arterial occlusive disease, such as atherosclerosis, may cause DO and overactive bladder (OAB) symptoms in men and women through ischemia, hypoxia and oxidative stress in the bladder. Lin and Juan also show that blood flow of the bladder is decreased by bladder outlet obstruction (BOO) and acute overdistention. They suggest that functional impairment of the urinary bladder might partly come from tissue ischemia, ischemia/ reperfusion injury and subsequent oxidative stress. Kuo has comprehensively reviewed recent investigations of the potential biomarkers for OAB, which include urinary and serum biomarkers, and bladder wall thickness, with a particular emphasis on urinary nerve growth factor (NGF) level. Although recent studies have found several potential biomarkers, the author describes that there is no satisfactory one for diagnosis and treatment of OAB.