Testosterone – not just a replacement therapy
Testosterone – not just a replacement therapy
复制标题
睾酮——不仅仅是替代疗法
DOI：
10.1111/j.1742-1241.2006.01112.x
复制
发表时间：
2006
影响因子：
2.6
通讯作者：
G. Jackson
中科院分区：
文献类型：
--
作者：
G. Jackson
我们大多数人将睾丸激素与正常的男性发育联系在一起-声音变深，能量水平持续，肌肉质量和力量增加，性欲保持。此外，睾丸激素会导致阴毛和体毛的生长（尽管它也会导致秃顶），有益于骨骼强度，但也可以降低高密度脂蛋白（HDL）胆固醇。然而，HDL胆固醇降低的影响似乎仅影响HDL 3c，这是抗动脉粥样硬化作用最小的亚组分，总体上没有记录到致动脉粥样硬化或抗动脉粥样硬化作用（1）。然而，有几份报告指出，低睾酮水平与冠状动脉疾病以及性欲降低、疲劳增加、肌肉无力、骨质疏松症、抑郁症、注意力不集中和勃起功能障碍（艾德）之间存在联系（2，3）。在这个问题上，Shabsigh等。提供了一个全面的审查睾酮在治疗艾德的作用（4）。除了采取彻底的历史澄清问题是否是性欲（性欲），艾德或两者兼而有之（重要的是，因为男性可能等同于艾德与性欲在他们的脑海中时，他们的驱动器是正常的），有一个建议，筛选所有男性与艾德从50岁的性腺功能减退症。上午气温最高，应在上午10点前采集样本。Shabsigh et al.（4）强调睾酮替代疗法在治疗艾德方面的重要性，通常与5型磷酸二酯酶抑制剂（西地那非、他达拉非、伐地那非）联合使用，尤其是在性腺功能减退和艾德风险患者中，如2型糖尿病患者，以及具有多种血管疾病风险因素的患者，这些血管疾病可能被归类为代谢综合征（1，4）。睾酮水平的问题之一是实验室之间在正常范围的定义上的差异。然而，如果我们接受8-12至35-45 nmol/L的范围，由于范围的宽度，这仍然存在问题。对于大多数男性来说，12 nmol/L的水平可能是完全正常的，但对某些人来说还不够，因此需要有临床和生化相关性。如果患有艾德和正常睾酮水平低的男性对磷酸二酯酶5型抑制剂没有完全反应，他可能以与Shabsigh等人类似的方式受益于睾酮替代疗法。的论文（4）。50岁以上的男性性腺功能减退通常被称为“男性更年期”，尽管技术上该术语是晚发性性腺功能减退（洛）或老年男性雄激素下降（ADAM）。治疗可改善身心健康、生活质量（包括性生活）、骨密度增加，并可能对整体血管有益。负面影响包括加重现有的前列腺癌，但不会导致前列腺癌，减少精子数量，因此需要检查家庭对孩子的意图，以及增加红细胞压积（红细胞增多症男性需要仔细监测）。在睾酮治疗性腺功能减退症和代谢综合征的综述中，有人认为不仅用睾酮治疗性腺功能减退症，而且这样做可以减缓或阻止代谢综合征向明显的糖尿病或心血管疾病的进展（1）。低睾酮与男性主动脉粥样硬化之间的联系被发现与其他风险因素无关，但在女性中并非如此，作者提出了使用睾酮来防止男性动脉粥样硬化的诱人问题（1）。当English等人质疑生理上高水平的雄激素导致男性冠心病相对风险增加的概念时，报告了与冠状动脉正常的男性相比雄激素水平较低，他们指出替代治疗对生活质量的潜在益处，没有增加心血管风险和潜在益处（3）。最近，睾酮给药已被证明对心绞痛和洛缺失的男性具有抗缺血潜力，睾酮替代可逆转心血管风险（5-7）。在患有冠心病的男性中，测量睾酮应该是评估的一部分，特别是如果艾德和/或糖尿病共存。只有在出现包括艾德在内的雄激素缺乏的明显体征或症状时，才提倡替代治疗，但长期心血管风险降低和症状管理潜力值得进一步研究。替代睾酮可以导致终身受益的生活质量，但低睾酮的检测也应该触发其他血管危险因素的搜索，而治疗进展。
Most of us associate testosterone with normal male development – the voice deepens, the energy levels are sustained, muscle mass and strength is increased and sex drive is maintained. In addition, testosterone causes the growth of pubic and body hair (though it can also lead to baldness) and benefits bone strength, but can also decrease high-density lipoprotein (HDL) cholesterol. However, the impact of a reduction in HDL cholesterol only appears to affect HDL3c, which is the least antiatherogenic subfraction, and overall no atherogenic or antiatherogenic effects have been recorded (1). There are, however, several reports of a link between low testosterone levels and coronary artery disease as well as the more predictable reduction in libido, increased fatigue, muscle weakness, osteoporosis, depression, poor concentration and erectile dysfunction (ED) (2,3). In this issue, Shabsigh et al. provide an overall review of the role of testosterone in the treatment of ED (4). In addition to taking a thorough history clarifying whether the problem is sex drive (libido), ED or both (important because men may equate ED with sex drive in their minds when their drive is normal), there is a recommendation to screen all men with ED from 50 years of age for hypogonadism. Testosterone is at its highest in the morning and samples should be obtained before 10 AM. Shabsigh et al. (4) emphasise the importance of testosterone replacement therapy with regard to treating ED usually in combination with a phosphodiesterase type 5 inhibitor (sildenafil, tadalafil, vardenafil), especially in those at risk for hypogonadism and ED, such as type 2 diabetics, and those with multiple risk factors for vascular disease which may be clustered as the metabolic syndrome (1,4). One of the problems with testosterone levels is the variability between laboratories in the definition of the normal range. However, if we accept a range from 8–12 to 35–45 nmol/L this still presents a problem because of the width of the range. A level of 12 nmol/L may be perfectly normal for most men but not adequate for some, so there needs to be a clinical and biochemical correlation. If a man with ED and low normal testosterone is not responding fully to a phosphodiesterase type 5 inhibitor, he may benefit from testosterone replacement therapy in a similar manner to those in Shabsigh et al.’s paper (4). Hypogonadism in men over 50 years is often known as the ‘andropause’ though technically the terms are late onset hypogonadism (LOH) or androgen decline in the ageing male (ADAM). Treatment improves physical and mental well-being, quality of life (including sex life), bone density increases and there may be an overall vascular benefit. Negatives include aggravating existing prostate cancer but not causing prostate cancer, reducing sperm count so a check needs to be made on family intentions regarding children, and increasing haematocrit (polycythaemic men need careful monitoring). In the review of testosterone therapy in hypogonadism and the metabolic syndrome, an argument was made to not only treat the hypogonadism with testosterone, but also in doing so, the metabolic syndrome’s progression to overt diabetes or cardiovascular disease could be slowed or stopped (1). The link between a low testosterone and aortic atherosclerosis in men was found to be independent of other risk factors but not in women, and the authors raised the tantalising question of using testosterone to protect against atherogenesis in men (1). When English et al. challenged the concept that physiologically high levels of androgens accounted for men’s increased relative risk for coronary disease, reporting lower levels of androgens when compared to men with normal coronary arteries, they pointed out the potential benefit of replacement therapy on quality of life with no increased cardiovascular risk and a potential benefit (3). More recently testosterone administration has been shown to have anti-ischaemic potential in men with angina and the LOH with cardiovascular risks reversed by testosterone replacement (5–7). In men presenting with coronary disease, measuring testosterone should be part of the assessment, especially if ED and/or diabetes coexist. Replacement can only be advocated if there are clear signs or symptoms of androgen deficiency including ED, but the long-term cardiovascular risk reduction and symptom management potential merits further study. Replacing testosterone can lead to a lifelong benefit on quality of life but the detection of a low testosterone should also trigger a search for other vascular risk factors whilst treatment progresses.