Metabolic syndrome and lower urinary tract symptoms secondary to benign prostatic hyperplasia.
Metabolic syndrome and lower urinary tract symptoms secondary to benign prostatic hyperplasia.
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DOI：
10.1007/s11934-996-0008-y
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发表时间：
2006-07-01
影响因子：
2.6
通讯作者：
McVary, Kevin T
中科院分区：
文献类型：
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作者：
Kasturi, Sanjay;Russell, Shane;McVary, Kevin T
最近越来越多的证据指向下尿路症状（LUTS）与代谢综合征的存在之间的关系。最近的流行病学发现支持了这种关系。可能的病理生理联系也被提出来解释这两种综合征之间的关系。在美国，肥胖症的日益流行使这成为一个日益相关的问题。动物研究支持自主神经系统（ANS）过度活动与泌尿系统症状的发展、膀胱依从性低下、代偿性前列腺增生以及使用α -阻滞剂对其进行阻塞之间的联系。作为代谢综合征一部分的ANS过度活动与良性前列腺增生（BPH）继发的LUTS之间似乎存在显著联系。然而，ANS的过度活动不太可能导致LUTS的发展。相反，ANS的过度活动在LUTS的严重程度高于固有基础强度方面起着关键作用，这是由每个BPH患者的泌尿生殖系统解剖/病理生理特征决定的。本文将代谢综合征定义为超重（内脏腹部脂肪分布）、血脂异常、高血压、葡萄糖代谢受损、c反应蛋白升高（慢性炎症）、自主交感神经过度活跃等异常的集合，假设胰岛素抵抗是潜在的致病机制。
Increasing evidence recently has pointed toward a relationship between lower urinary tract symptoms (LUTS) and the presence of metabolic syndrome. This relationship has been supported by recent epidemiologic findings. Possible pathophysiologic links also have been proposed to explain the relationship between these two syndromes. The increasing prevalence of obesity in the United States makes this an increasingly relevant problem. Animal studies support a link between autonomic nervous system (ANS) overactivity and the development of urinary symptoms, low bladder compliance, compensatory prostatic hyperplasia, and blockage of the same using alpha-blockade. There appears to be a significant link between ANS overactivity as part of the metabolic syndrome and LUTS secondary to benign prostatic hyperplasia (BPH). However, it is unlikely that ANS overactivity could be responsible for the development of LUTS. Rather, ANS overactivity plays a key role in increasing the severity of LUTS above an intrinsic basal intensity that is determined by the genitourinary anatomic/pathophysiologic characteristics of each BPH patient. This paper defines metabolic syndrome as a collection of abnormalities, including being overweight (visceral abdominal fat distribution), dyslipidemia, hypertension, impaired glucose metabolism, elevated C-reactive protein (chronic inflammation), and autonomic-sympathetic overactivity, with insulin resistance as the hypothesized underlying pathogenic mechanisms.