Association of lower urinary tract syndrome with peripheral arterial occlusive disease

Lin, Weihong; Andersson, Karl Erik; Lin, Cheng Li; Kao, Chia Hung; Wu, Hsi Chin

doi:10.1371/journal.pone.0170288

Cited by 18 publications

(18 citation statements)

References 37 publications

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“…In support, Uzun et al also founds a positive correlation between patients with metabolic syndrome (ie, central obesity, hypertension, dyslipidemia, and hyperglycemia) and symptoms of OAB, suggesting that metabolic syndrome could be an etiologic pathway for the onset of OAB. Similarly, Lin et al found an increased likelihood of a broad spectrum of LUTS amongst adults with peripheral arterial occlusive disease from a cohort study of 72 084 adults.…”

Section: Discussionmentioning

confidence: 91%

Vascular measures of atherosclerosis in detrusor overactivity and controls

Ladanchuk

Kwak

Bates

et al. 2018

Neurourology and Urodynamics

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Section: Discussionmentioning

confidence: 91%

Vascular measures of atherosclerosis in detrusor overactivity and controls

Ladanchuk

Kwak

Bates

et al. 2018

Neurourology and Urodynamics

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“…18 Patients were not required to have a diagnosis of OAB (International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) diagnosis codes 596.51; 596.59; 788.1x; 788.3x), as lower urinary tract symptoms are likely under-coded. 24 …”

Section: Methodsmentioning

confidence: 99%

“…Discontinuation of antimuscarinics may also have been confounded by comorbid conditions and medications; therefore, several comorbidities were examined using the Elixhauser Comorbidity algorithm, 24 modified to include medications used to treat hypertension, diabetes, and hypothyroidism. Other comorbid conditions diagnosed in older adults and comorbid conditions that may be associated with discontinuation of antimuscarinics, along with medications used to treat these conditions, including osteoporosis, Parkinson’s disease, glaucoma, high cholesterol, constipation, weakness, and falls were also assessed.…”

Section: Methodsmentioning

confidence: 99%

Antimuscarinic use and discontinuation in an older adult population

Vouri

Schootman

Strope³

et al. 2019

Archives of Gerontology and Geriatrics

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Introduction: Although antimuscarinics are typically the first-line pharmacological treatment option for overactive bladder, patients often discontinue therapy. The aim of this research project is to identify the rate of antimuscarinic discontinuation, switching, and continuation and differences in discontinuation among different antimuscarinics. Methods: Using the 5% random sample of Medicare Claims Data, we identified a cohort of patients aged ≥ 66 years old who newly initiated antimuscarinics between January 1, 2007 and December 31, 2012. Treatment discontinuation was defined as no subsequent fills of the initial antimuscarinic in the days’ supply plus a 30 day grace period. We ascertained percentages of patients who discontinued antimuscarinics, switched antimuscarinics, or died within 12 months of antimuscarinic initiation. Cox proportional hazards models were used to determine time to discontinuation of individual antimuscarinics relative to oxybutynin immediate-release (IR). Results: Among the 42,886 new-users of antimuscarinics, 71.8% discontinued, 10.8% switched, and 3.2% died prior to antimuscarinic discontinuation or switching while only 14.2% continually filled an antimuscarinic for one year. In the multivariable analysis, patients who were initiated on oxybutynin extended-released (ER), tolterodine, trospium, darifenacin, solifenacin, and fesoterodine were significantly less likely to be discontinued therapy compared to oxybutynin IR (p<0.001). Conclusion: After one year of antimuscarinic initiation, only 14% of older adult patients continuously utilized their initial antimuscarinic therapy suggesting a need for clinical interventions to improve continual use of antimuscarinics.

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“…In clinical studies, Lin et al studied 36,042 patients and reported a significant correlation between LUTS and the prevalence of atherosclerotic arterial occlusive disease. 1 Gibbons et al reported that American Urological Association Symptom Score (AUA-SS) is significantly higher in patients with vascular disease risk factors in comparison with patients without vascular risk factors. 2 Other studies revealed low bladder blood flow in the elderly population and found a close correlation between decreased bladder perfusion and LUTS in both men and women.…”

Section: Introductionmentioning

confidence: 99%

<p>Regulation of Cellular Stress Signaling in Bladder Ischemia</p>

Yang¹,

Li²,

Azad³

et al. 2020

RRU

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Introduction The etiology of lower urinary tract symptoms in patients with non-obstructed non-neurogenic bladder remains largely unknown. Clinical studies divulged a significant correlation between reduced bladder blood flow and low bladder compliance. Animal models of bladder ischemia displayed structural modifications, characterized by loss of smooth muscle cells and accumulation of connective tissue in the bladder wall. The underlying mechanisms contributing to structural damage in bladder ischemia remain largely elusive. We previously reported that structural modifications in bladder ischemia correlate with upregulated stress proteins and cell survival signaling, suggesting the potential role of cellular stress in ischemic damage. However, stress response molecules and downstream pathways eliciting bladder damage in ischemia remain largely undetermined. Methods Using a rat model of bladder ischemia along with a cell culture hypoxia model, we investigated stress signaling molecules in the ischemic bladder tissues and hypoxic bladder smooth muscle cells. Results Our data suggest simultaneous upregulation of two major cellular stress-sensing molecules, namely apoptosis signal-regulating kinase 1 (ASK1) and caspase-3, implying degenerative insult via stress signaling pathway in bladder ischemia. Consistent with bladder ischemia, incubation of cultured human bladder smooth muscle cells at low oxygen tension increased both ASK1 and caspase-3 expression, insinuating hypoxia as an essential factor in ASK1 and caspase-3 upregulation. Gene deletion of ASK1 by ASK1 siRNA in cultured smooth muscle cells prevented caspase-3 upregulation by hypoxia, suggesting caspase-3 regulation by ASK1 under the ischemic/hypoxic conditions. Upregulation of ASK1 and caspase-3 in rat bladder ischemia and human bladder smooth muscle cell hypoxia was associated with subcellular structural modifications consistent with the initial stages of apoptotic insult. Conclusion Our data suggest that stress sensing by ASK1 and caspase-3 may contribute to subcellular structural damage and low bladder compliance. The ASK1/caspase-3 pathway may provide therapeutic targets against cellular stress and degenerative responses in bladder ischemia.

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Association of lower urinary tract syndrome with peripheral arterial occlusive disease

Cited by 18 publications

References 37 publications

Vascular measures of atherosclerosis in detrusor overactivity and controls

Vascular measures of atherosclerosis in detrusor overactivity and controls

Antimuscarinic use and discontinuation in an older adult population

<p>Regulation of Cellular Stress Signaling in Bladder Ischemia</p>

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