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  3. 出汗多真的等于排毒好吗?科学揭秘出汗与排毒的真实关系

出汗多真的等于排毒好吗?科学揭秘出汗与排毒的真实关系

深度研究匿名用户发表于 2025年12月25日 17:2428阅读
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1. 出汗的本质:身体的「温控系统」而非「排毒机器」

1.1 出汗是如何发生的?从汗腺到体温调节的全过程

说到出汗,我们可能首先想到的是热得满头大汗,或者运动后的淋漓畅快。但这背后,其实是身体一套精密的“空调系统”在默默工作。这套系统的主角,就是遍布我们全身的汗腺。

咱们身体里主要有两种汗腺:一种叫“小汗腺”,医学上称之为外分泌汗腺(eccrine glands);另一种叫“大汗腺”,学名叫顶泌汗腺(apocrine glands) 1。

“小汗腺”就像是身体里分布最广、数量最多的“微型水泵”,它们几乎覆盖了全身皮肤,尤其在手掌、脚底和额头这些地方特别多。它们的任务很单纯,就是分泌一种清澈的汗液,主要成分是水和少量盐分。当身体内部的温度传感器——特别是大脑深处的下丘脑(hypothalamus)这个“总指挥部” 23——感受到体温升高时,它就会立刻发出指令,通过神经系统通知这些小汗腺开足马力“排水”。这些汗液分泌到皮肤表面,通过蒸发带走身体的热量,就像给身体吹了一阵凉风,从而帮助我们把体温维持在一个舒适的范围 456。这就是我们常说的体温调节功能,也是小汗腺最主要、最重要的作用 17。

而“大汗腺”则相对低调,它们主要集中在腋窝、腹股沟、乳晕等少数区域。相比小汗腺,大汗腺分泌的汗液除了水和盐,还会带有一些蛋白质和脂质 1。这些物质本身没什么味道,但一旦被皮肤表面的细菌分解,就会产生我们熟悉的“体味”。有趣的是,在许多哺乳动物,包括一些非人灵长类动物身上,大汗腺和体毛是协同作用的,它们分泌的物质可能参与了信息交流,比如释放费洛蒙 89。但在人类身上,大汗腺的体温调节作用非常有限,它们更多地与应激反应(比如紧张、恐惧)有关,而不是主要为了降温而工作。所以,从“给身体降温”这个角度来说,小汗腺才是真正的“主力军” 10。

总的来说,我们出汗,尤其是为了降温而出的汗,绝大部分都是由小汗腺分泌的。整个过程就像是身体的“智能温控系统”在自动运行:大脑监测到体温过高,下达指令,汗腺分泌汗液,汗液蒸发带走热量,体温恢复正常。这是一个为了生存而演化出来的精妙机制,确保我们的“核心温度”始终保持稳定。

1.2 传统认知的误区:为何人们会将出汗与排毒联系起来?

既然出汗主要扮演着身体“空调”的角色,那为什么“出汗排毒”的说法会流传得如此广泛,甚至深入人心呢?这其中有历史的渊源,也有我们对“排毒”这个词的模糊理解。

一个重要的起源可能要追溯到中医理论中的“发汗解表”。在中医看来,当身体感受风寒、风热等邪气侵袭时,通过服用辛温或辛凉的药物,促使身体发汗,能将侵入体表的邪气“赶出去”,从而达到治病的效果。例如,麻黄这种中草药,就有很好的发汗作用,常用于治疗感冒、支气管哮喘等疾病 11。而香薷这种植物,则被称为“夏月之麻黄”,能用于夏季感冒,同样具有发汗解表的功效 12。这种“发汗就能把病邪赶走”的观念,在日常生活中被人们简单地理解为“出汗就能排出身体里的坏东西”,也就是“排毒”。这种朴素的思维逻辑,无疑为“出汗排毒论”提供了强大的理论基础。

然而,这里的“排毒”与现代医学所说的“排毒”有着本质的区别。在日常语境中,我们谈论“排毒”时,常常指代的是排出身体内各种“不好的东西”,比如吃了不健康的食物,身体里累积的“垃圾”;或者生活作息不规律,产生的“毒素”;甚至是一些环境污染物,比如重金属。这个概念非常宽泛,几乎包含了所有我们不希望身体里存在的物质。

但在科学上,“毒素”通常指由生物体产生并能对其他生物体造成伤害的物质,或者广义上指任何对身体有害的化学物质。而身体的“排毒”机制,是一个高度复杂且精确的生理过程,主要由特定的器官负责。例如,肝脏是身体主要的解毒器官,通过各种酶系统转化和清除有毒物质;肾脏则是“过滤器”,通过尿液排出代谢废物和多余的水分。

所以,当我们将中医“发汗解表”的经验,套用到现代医学对“毒素”和“排毒”的理解上时,就产生了一种误读。出汗确实能排出一些物质,但这些物质的种类和数量,与肝脏、肾脏等主要排毒器官的工作效率相比,简直是“小巫见大巫”,远远达不到我们想象中“排出身体所有坏东西”的效果。这种概念的模糊性和混淆,是导致“出汗排毒”这个误区广泛传播的重要原因。

2. 人体排毒的核心途径:肾脏、肝脏才是「主力军」

既然出汗并非身体主要的“排毒机器”,那么,我们身体里真正的“排毒主力军”究竟是谁呢?答案就是——肝脏和肾脏。这两个器官就像是身体的“化学工厂”和“精密过滤器”,日夜不停地工作,保障着我们身体的清洁和健康。

2.1 肝脏:代谢解毒的「化学工厂」

想象一下,肝脏就像是一个高度自动化的“中央化学工厂”,专门负责处理各种进入身体的“可疑分子”——无论是我们吃进去的食物残渣、药物,还是环境中接触到的污染物,甚至是我们身体自身代谢产生的一些废物。它的任务就是把这些可能有害的物质“改造”一番,让它们变得无毒或毒性降低,并且更容易被身体排出体外 13。

这个“改造”过程复杂而精妙,主要依靠肝脏细胞内庞大的酶系统来完成。其中最著名的“明星员工”就是细胞色素P450酶(Cytochrome P450 enzymes,简称CYP酶) 14。这些CYP酶就像是工厂里的“初级处理员”,它们能够对许多脂溶性的有害物质进行氧化、还原等“预处理”,比如分解酒精、药物(包括许多化疗药物)和各种环境毒素 14。这个阶段被称为I相反应,通过这一步,很多物质的毒性会被初步降低,或者被转化成更适合下一步处理的形式。

不过,有些物质在I相反应后,可能会变得毒性更强,或者只是“半成品”,还不能直接排出体外。这时候,肝脏里的另一批“高级处理员”——例如谷胱甘肽S-转移酶(Glutathione S-transferases, GSTs)和UDP-葡糖醛酸转移酶(UGTs)就会登场了 1516。它们会把I相反应的产物与身体里的一些小分子(比如谷胱甘肽、葡糖醛酸)结合起来,这个过程叫做II相反应,也叫结合反应。通过结合,这些有害物质的溶解性会大大增加,变得更容易溶于水,这样一来,它们就能随着胆汁进入肠道,或者通过血液循环被肾脏捕捉,最终随尿液排出体外 1315。

举个例子,日常生活中我们接触到的黄曲霉毒素B1 (AFB1) 这种强力致癌物,就是通过肝脏的CYP450酶进行生物转化,然后通过GST酶进行解毒 17。同样,许多药物在体内代谢,也离不开CYP酶的辛勤工作 14。甚至我们身体内产生的胆汁酸,也需要CYP酶和UGT酶的协同作用来调节和解毒,以维持正常生理功能 16。

这个过程就像是一个精密的生产线,各种酶分工协作,确保每一批“原材料”(有害物质)都能被有效处理,最终变成无害的“产品”或易于排出的形式。如果肝脏这个“化学工厂”出了问题,比如发生肝衰竭,这些解毒功能就会严重受损,身体就会积累大量的毒素,危及生命 1819。因此,肝脏在身体的“排毒”工作中,扮演着不可替代的“总工程师”角色。它的效率高低,直接决定了我们身体清除毒素的能力 20。有趣的是,连这些重要的解毒酶本身,也受到身体昼夜节律的精准调控,保证了身体在一天中不同时间段都能高效地进行解毒工作 21。

2.2 肾脏:尿液排泄的「精密过滤器」

如果说肝脏是身体的“化学工厂”,负责把有毒物质“改造”成无害或易于排出的形式,那么肾脏就是身体的“精密过滤器”,专门负责把这些经过改造的废物以及身体自身代谢产生的垃圾,统统从血液中清除出去,最终随尿液排出体外 22。

我们的肾脏,这两个形状像蚕豆、大小和拳头差不多的器官,每天要处理大约200升的血液,将其中的水分、电解质和代谢废物进行精确的过滤和调节 22。它们的工作效率之高、精密度之细,远超任何人工设备。肾脏之所以能做到这一点,全靠里面数百万个微小的“功能单元”,我们称之为肾单位。每个肾单位都包含一个“小球”和一个“小管”,它们是肾脏执行过滤和重吸收任务的关键。

首先,血液带着各种物质(包括营养物质、电解质、水和代谢废物)进入肾单位的第一个关卡——肾小球。肾小球就像一个超精密的“滤网”,它的孔径非常小,只允许小分子物质(如水、电解质、葡萄糖、氨基酸、尿素、肌酐、尿酸等)通过,而体积较大的蛋白质、血细胞等则被“拦截”,留在血液中 22。这个过程叫做肾小球滤过。滤过出来的液体,我们称之为原尿,每天大约会产生180升的原尿!

如果这些原尿全部排出体外,那我们一天得喝多少水才能补充回来?好在,肾脏的聪明之处远不止于此。原尿会接着流经肾单位的第二个部分——肾小管。肾小管就像一条蜿蜒曲折的“回收站”,它会对原尿进行精挑细选的“回收”和“处理”。在这个过程中,大部分水、葡萄糖、氨基酸以及身体需要的电解质(如钠、钾、钙、磷酸盐、镁等)会被重新吸收回血液,防止这些宝贵的物质随尿液流失 232425。这个过程叫做肾小管重吸收。

与此同时,肾小管还会主动地将血液中一些身体不需要的代谢废物和毒素,进一步地分泌到尿液中 2627。比如,肝脏处理过的很多水溶性毒素,以及我们身体自身代谢产生的尿素(蛋白质代谢的终产物)、肌酐(肌肉代谢的产物)、尿酸(嘌呤代谢的产物)等,都会在肾小管这里被“打包”好,等待最终排出 28293031。经过肾小管的“精加工”后,180升的原尿最终只剩下约1.5升的终尿,也就是我们每天排出的尿液。

所以,我们可以看到,肾脏通过肾小球的“粗筛”和肾小管的“精选”,把血液中的代谢废物、多余的电解质和水分,高效且精准地清除出体外。尤其是在清除尿素、肌酐、尿酸等关键代谢废物方面,肾脏是绝对的“主力军”,其排毒功能是维持我们生命活动不可或缺的 31。一旦肾脏功能受损,这些废物就会在体内堆积,引发一系列严重问题,这在医学上被称为氮质血症或尿毒症 32333435。因此,肾脏在人体排毒系统中占据着核心地位,是当之无愧的“精密过滤器”。

2.3 对比:出汗与其他途径的排毒效率差距有多大?

现在我们明白了,肝脏和肾脏才是身体里真正的“排毒高手”。那么,回到最初的问题,出汗在排毒这方面,到底能有多大的贡献呢?答案可能会让你感到有些“失望”:跟肝脏和肾脏相比,汗液排出代谢废物的效率,简直是微乎其微。

我们可以拿最常见的代谢废物之一——尿素来举例。尿素是蛋白质在体内分解后产生的一种废物,主要由肾脏负责过滤并通过尿液排出体外 363738。当我们的肾脏功能正常时,尿液中的尿素浓度是相当高的。但科学研究发现,汗液中尿素的浓度远低于尿液 39。这就像是,身体想清理一屋子的垃圾,肾脏用的是一台大功率吸尘器,而汗腺呢,可能只是一把小小的扫帚,而且还只能扫掉很小一部分。

再从排出的总量来看,我们每天排出的尿液量通常在1.5升左右,而即使大量出汗,比如运动或桑拿,一次出汗量也很难超过几升。把这些数据结合起来看,汗液中排出的尿素总量,相对于肾脏通过尿液排出的总量来说,简直是沧海一粟。

除了尿素,对于其他一些代谢废物和毒素,汗液的排出能力也同样有限。例如,汗液中虽然能检测到极微量的重金属(我们后面会详细讲到),但其排出量与肾脏和肝脏的排出的比例相比,也是不值一提的。

此外,别忘了,我们身体还有另一条重要的排泄途径——粪便。肠道也是身体排除代谢废物、食物残渣以及肝脏通过胆汁排出的某些毒素的重要出口。例如,一些脂溶性的毒素,在肝脏经过处理后,会随着胆汁进入肠道,最终随粪便排出体外。

所以,综合来看,将“排毒”的重任寄希望于出汗,就像是希望一个小小的排气扇能代替整个中央空调系统一样不切实际。出汗的主要功能是调节体温,防止身体过热,这是它无可替代的核心作用。而至于排出体内的代谢废物和毒素,那还是得依靠肝脏和肾脏这两大“主力军”,它们才是真正高效、专业的“排毒专家”。

3. 出汗与排毒的有限关联:仅对特定物质「辅助」

3.1 重金属:出汗能排,但效率远低于尿液

讲了这么多,我们似乎得出结论:出汗对排毒没啥大用。但事情总有例外,对于某些特定的“毒素”——比如重金属,汗液确实能发挥一些辅助作用,但这个作用有多大,还需要我们仔细辨别。

重金属是一类对人体有害的金属元素,比如铅、汞、镉、砷等等。它们没有生理功能,一旦进入人体就很难排出,容易在体内累积,对健康造成危害 40。那么,出汗能排出这些“坏家伙”吗?

一些研究确实发现,在汗液中可以检测到铅(Pb)、镍(Ni)、铜(Cu)、砷(As)和汞(Hg)等重金属 4041。例如,有研究表明,运动出汗可以排出少量的镍和铅 41。甚至有报告提到,在一些重金属暴露较高的个体中,汗液中的某些重金属浓度可能会超过血浆或尿液的浓度,甚至皮肤排出的量可能与尿液的日排泄量相当或更高 40。这意味着,对于某些重金属,汗液确实提供了一条排泄途径。

但是,我们需要清醒地认识到,这种排泄的效率是有限的,并且远远低于主要的排泄途径。举个例子,虽然汗液中可以检测到铅,但身体排出铅的主要途径仍然是粪便和尿液 42。肝脏通过胆汁将一部分铅排入肠道随粪便排出,而肾脏则通过尿液排出。尽管出汗能在一定程度上排出铅,但要显著影响体内铅的累积量,可能需要长期、大量且剧烈的出汗 4043。比如,一项针对运动员和久坐人群的研究发现,运动员的尿液中镉、钨、铍和碲等有毒金属的浓度更高,这暗示了体育活动可能通过增加尿液排泄来帮助清除这些金属,但这项研究主要关注的是尿液排排泄,并未直接比较汗液排泄的效率 43。

此外,一项有趣的实验比较了两种出汗方式对重金属排泄的影响:动态运动出汗和桑拿静坐出汗。结果发现,在动态运动出汗的情况下,汗液中镍、铅、铜和砷的浓度显著高于桑拿静坐出汗的情况 41。这可能表明,剧烈运动时,由于血液循环加速,汗腺分泌更活跃,可能会促使更多的重金属通过汗液排出。但即使是这样,这些研究也只是量化了汗液中重金属的浓度,并没有直接证明出汗是清除体内重金属负荷的有效或主要方法。

总而言之,虽然汗液可以作为重金属的一个次要排泄途径,但指望通过多出汗来“排光”体内的重金属,就像指望用勺子把游泳池里的水舀干一样,效率低下且不切实际。对于健康的普通人来说,身体的肝脏和肾脏才是清除重金属的主力军。只有在极其特殊的情况下,比如重金属中毒,医生才会考虑通过一些特殊的医学干预手段来加速排泄,而不仅仅是依靠出汗。

3.2 出汗方式不同,排毒效果有差异?

刚才我们提到,出汗对排出重金属有些辅助作用。那么,是不是所有的出汗方式,效果都一样呢?这就好比我们要把屋子里的灰尘清理干净,是用扫帚扫,还是用吸尘器吸,效率肯定是不一样的。对于出汗来说,不同的出汗方式,确实可能在“排毒”效果上存在一些差异,这主要体现在运动出汗和桑拿出汗上。

我们日常生活中最常见的两种主动出汗方式,就是运动出汗和桑拿出汗。这两种出汗方式,虽然最终都是身体排出汗液,但它们启动身体机制和生理过程却大不相同。

运动出汗:当我们进行跑步、打球等体育活动时,身体为了给肌肉提供能量,新陈代谢会加快,体温也会随之升高。这时候,大脑的“温控中心”就会命令汗腺分泌汗液来降温。更重要的是,运动时交感神经会变得非常兴奋,这不仅会直接刺激汗腺大量分泌汗液,还会加速全身的血液流动和代谢过程。这种情况下,身体的“代谢工厂”和“过滤器”——肝脏和肾脏——的工作效率也会相应提高。有研究表明,在动态运动出汗时,汗液中像镍、铅、铜、砷等重金属的浓度会显著高于在桑拿房里静坐出汗的情况 41。这意味着,通过运动来出汗,由于身体内部的全面激活,可能会更有效地将一些物质通过汗液排出体外。

桑拿出汗:桑拿或蒸汽浴则是通过外部高温环境,让身体被动地升高体温,从而刺激汗腺分泌汗液。这时候,虽然汗液也会大量排出,但身体内部的生理反应与运动时有所不同。虽然高温也能促进汗液分泌,但由于缺乏运动带来的全身性生理激活,排泄效率可能会受到限制 41。一些研究提示,在桑拿浴中,汗液中的镁和钙含量可能会更高,这可能与汗腺主动调节汗液成分有关 44。还有研究发现,水过滤红外-A(wIRA)桑拿可能会排出比传统运动或湿桑拿更高浓度的无机离子(包括有毒和营养元素) 45。不过,需要注意的是,桑拿过程中身体大量出汗,如果不能及时补充水分,很容易导致脱水,而脱水会进一步影响肾脏的工作效率,反而可能间接限制了身体通过尿液排出废物的能力。

所以,我们可以这样理解:运动出汗就像是给身体做了一次全面的“大扫除”,不仅把“垃圾”扫出去,还把“物流系统”和“处理中心”都调动起来,效率更高。而桑拿出汗则更像是把“垃圾”从表面扫掉一部分,虽然也能出汗,但对身体内部的整体代谢和排泄系统的刺激相对较小。因此,如果单纯从“排毒”的角度考虑,主动运动出汗可能比被动桑拿出汗,对一些物质的排泄效果更明显。但无论是哪种方式,都不能夸大其“排毒”作用,因为和肝脏、肾脏这两个“主力军”比起来,汗液的贡献依然是有限的。

3.3 正常饮食下,汗液排毒的「贡献值」有多小?

我们已经了解,出汗,尤其是在剧烈运动时,确实能排出一些重金属。但这就像往一个大海里滴了几滴水,并不能改变大海的整体水量。对于绝大多数生活在健康环境、饮食正常的普通人来说,汗液在清除体内“毒素”方面的“贡献值”,实际上是微乎其微的,可以说几乎可以忽略不计。

我们每天通过食物、饮水和空气,不可避免地会摄入微量的重金属。例如,我们常吃的鱼类、蔬菜、牛奶中都可能含有微量的铅、镉、镍等重金属 4647484950。这些重金属大部分在进入身体后,会由肝脏和肾脏进行处理和排出,只有一小部分会在体内蓄积。

那么,汗液能排出多少呢?以镉为例,我们日常通过饮食摄入的镉量通常在微克级别。而即便是出汗能排出少量镉,根据研究,汗液中的镉浓度往往比血液中的浓度高,这似乎预示着汗液对镉的排泄有一定作用 40。然而,综合考量每天的汗液总量和其中重金属的浓度,汗液排出的重金属总量,与肝脏和肾脏通过粪便和尿液排出的总量相比,所占比例往往不足1%。也就是说,汗液对重金属的排出量,在健康人群的日常生理排泄中,通常低于总排泄量的1%。

这意味着什么呢?简单来说,如果你是一个健康的普通人,没有职业暴露于重金属的风险,平时饮食均衡,那么你体内的微量重金属绝大部分都由肝脏和肾脏处理掉了。你不需要刻意去“多出汗”来追求额外的“排毒”效果。那种“出汗越多,排毒越好”的说法,在日常生活中是站不住脚的。

所以,与其纠结于汗液排毒的微小贡献,不如把注意力放在更重要的方面:保持健康的生活习惯,比如均衡饮食,避免摄入过多的环境污染物;以及关注肝脏和肾脏的健康,因为它们才是真正为你日夜辛劳的“排毒专家”。

4. 出汗多可能是「健康警报」:警惕病理性多汗

出汗是人体的正常生理现象,是维持体温平衡的关键机制。然而,当我们谈论“出汗多”时,情况就变得复杂起来。并非所有的多汗都代表身体健康,有时,过多的汗水可能是身体发出的“警报”,提示我们警惕某些潜在的健康问题。这种异常的多汗,我们称之为病理性多汗。

4.1 生理性多汗vs病理性多汗:如何区分?

要判断自己的多汗是正常生理反应,还是需要关注的健康信号,关键在于区分生理性多汗和病理性多汗。这两种情况虽然都表现为汗量增多,但它们的发生原因、表现形式和伴随症状却大相径庭。

生理性多汗,顾名思义,是身体在特定刺激下做出的正常反应。它通常具有以下特点:

  • 有明显诱因:比如在高温环境下,身体为了散热而大量出汗,防止中暑。炎炎夏日,户外工作或在没有空调的房间里,出一身汗是很正常的。
  • 运动后:进行剧烈或长时间的体育锻炼后,身体产热增加,汗腺会大量分泌汗液以降低体温,这是运动的正常生理反应。
  • 情绪紧张或焦虑:在面对考试、演讲、面试等压力情境时,或感到紧张、焦虑、恐惧时,交感神经兴奋,也可能导致出汗增多,这是一种应激反应。
  • 食用辛辣食物:吃辣椒、喝热汤等刺激性食物后,身体为了散热也会出汗。
  • 短暂性、可逆性:生理性多汗通常在诱因消失后,汗液分泌会很快恢复正常。

而病理性多汗则不同,它往往提示身体内部存在一些异常情况,需要我们提高警惕。病理性多汗的特征包括:

  • 无明显诱因:最突出的特点是,在没有高温、运动、紧张等诱因的情况下,身体仍然大量出汗。比如在凉爽的环境中,甚至在休息时也汗流浃背 51。
  • 持续性多汗:这种多汗是持续性的,或者反复发作,并且严重到影响日常生活和社交活动 51。
  • 夜间盗汗:如果在睡眠中大量出汗,甚至把衣服和床单都浸湿,且与卧室温度无关,这被称为夜间盗汗,是常见症状之一 52。
  • 局部多汗:虽然生理性多汗也可能局部表现,但病理性多汗有时会呈现出不对称或异常分布的局部多汗。例如,身体一侧出汗多于另一侧,或者只有面部、手掌、脚底等特定区域异常多汗,而身体其他部位正常 5153。这种局限性的多汗可能表明神经通路受损,如中风或交感神经损伤,从而导致出汗异常 54。
  • 伴随其他症状:病理性多汗常常不只是单纯出汗多,还会伴随其他一系列身体不适,这些症状是医生诊断疾病的重要线索 55。
  • 影响生活质量:由于过度出汗,患者可能会感到尴尬、焦虑,甚至影响工作和社交,例如手汗过多导致无法握笔、打字,或腋汗湿透衣服导致社交回避等 51。

简单来说,如果你发现自己出汗增多,且没有明显原因,或者伴随其他不适症状,持续时间较长,甚至影响了正常生活,那么这就很可能是病理性多汗,需要及时就医,找出背后的原因。

4.2 哪些疾病会导致异常多汗?

当出汗不再是为了降温,而是身体内部某些环节出了问题时,它就从一个正常的生理现象变成了疾病的信号。多种疾病都可能以异常多汗为表现,以下是一些常见的例子:

  1. 甲状腺功能亢进(甲亢):甲亢就像是身体的“油门”踩得太猛了。甲状腺分泌过多的甲状腺激素,会加速身体的新陈代谢,导致全身产热增加,体温升高。为了散热,身体就会通过出汗来降低体温,所以甲亢患者常常会感到怕热、多汗,即使在凉爽的环境中也容易出汗 。这通常会伴随着心慌、手抖、食欲旺盛但体重减轻、易怒等其他典型症状 56。

  2. 糖尿病:糖尿病患者由于长期血糖控制不佳,容易引起糖尿病自主神经病变(Diabetic Autonomic Neuropathy, DAN) 5758。自主神经系统负责调节身体的很多无意识功能,包括出汗。当自主神经受损时,汗腺的功能可能出现异常。有些糖尿病患者会出现味觉性出汗(gustatory sweating),即在吃东西时,头部和颈部会大量出汗,尤其是在吃辛辣食物时更为明显 59。另一些患者则可能出现出汗减少甚至无汗症,这会导致皮肤干燥、皲裂,增加感染风险,并且在高温环境中更容易中暑 606162。因此,糖尿病患者出现出汗异常,无论是多汗还是少汗,都可能是神经病变的信号。有趣的是,一项最新的研究也指出,“出汗”是利用机器学习模型预测2型糖尿病患者糖尿病周围神经病变(DPN)风险的五大最显著特征之一 63。

  3. 感染:一些感染性疾病,尤其是慢性感染,常常会引起多汗,特别是夜间盗汗。最典型的就是结核病,尤其是肺结核。结核病患者常表现为长期低热、咳嗽、体重下降,并伴有显著的夜间盗汗,即睡梦中大量出汗,甚至湿透衣物 64656667。其他一些慢性感染,如布鲁氏菌病、艾滋病等,也可能引起多汗。

  4. 更年期综合征:女性在进入更年期(围绝经期、绝经期和绝经后期)时,由于卵巢功能衰退,雌激素水平波动或下降,常常会出现一系列症状,其中最常见的就是潮热(hot flashes)和夜间盗汗(night sweats) 686970。潮热表现为身体突然感到一阵燥热,皮肤发红,并伴随出汗。夜间盗汗则是潮热在夜间的表现形式,严重时可以影响睡眠质量 68。这些症状是体内激素变化导致体温调节功能失衡所致,并非真正的“排毒”反应 70。

  5. 某些肿瘤:虽然相对不常见,但某些恶性肿瘤,特别是淋巴瘤、白血病以及一些实体瘤,也可能导致不明原因的夜间盗汗。这种盗汗通常会伴随着体重减轻、不明原因发热等“B症状” 71。

  6. 精神和神经系统疾病:焦虑症、恐慌症等精神障碍,以及中风、帕金森病、脊髓损伤等神经系统疾病,也可能导致出汗异常,包括全身性多汗或局部性多汗 6071。

  7. 药物副作用:某些药物,如一些抗抑郁药、降糖药、止痛药等,也可能引起多汗作为副作用 72。

当出现无明显诱因的多汗,特别是夜间盗汗、局部异常多汗,或多汗伴随乏力、体重下降、心慌等其他不适症状时,这很可能是身体发出的“健康警报”。这时候,与其盲目追求“排毒”,更重要的是及时就医,让医生帮助查找病因,进行针对性的诊断和治疗。

4.3 特殊人群的出汗异常:尿毒症患者的「反向案例」

要彻底颠覆“出汗多就是排毒好”的观念,没有什么比尿毒症患者的案例更有说服力了。尿毒症,顾名思义,就是身体里尿毒素过高。这通常是由于肾脏功能严重衰竭,无法有效地将代谢废物从血液中清除出去所导致的。在这种情况下,我们可能会直觉地认为,身体为了“排毒”,应该会大量出汗,把多余的毒素排出去。但实际情况却恰恰相反,尿毒症患者的出汗情况,完美地诠释了“出汗多不等于排毒好”的逻辑。

首先,让我们看看尿毒症患者的汗液成分。由于肾脏无法正常工作,血液中的尿素、肌酐等代谢废物浓度会显著升高。研究发现,这些血液中高浓度的废物,也会渗透到汗液中,导致尿毒症患者的汗液中含有更高水平的尿素、肌酐以及钙、镁、磷酸盐等物质 6173747576。有研究显示,尿毒症患者汗液中的尿素氮含量比健康人高出两倍以上 75。甚至有最新的观察性研究发现,血液透析患者在透析过程中,汗液中的尿素和肌酐浓度会随着血液浓度的下降而下降,这表明汗液中的这些物质确实与血液中的水平密切相关 77。这看起来似乎是在“排毒”,对吧?

然而,问题的关键在于,尽管汗液中的毒素浓度提高了,但尿毒症患者的总出汗量却往往是减少的 61。由于肾脏功能受损,他们常常伴有自主神经功能障碍,这种神经病变会影响汗腺的正常功能,导致出汗能力下降,甚至出现无汗症 6178。这就像身体的“排水系统”出了故障,即使水箱里的水再脏,水龙头也拧不动了。部分研究指出,尿毒症患者可能因为出汗减少,更容易出现体温升高、皮肤干燥和感染风险增加等问题 61。

所以,尿毒症患者的案例,是一个非常具有说服力的“反向案例”:

  • 毒素浓度高,但出汗量少:他们的汗液中确实毒素浓度更高,但这并非是身体主动通过出汗来高效“排毒”的表现,而是因为身体内部毒素水平整体升高,汗液作为身体液体的一部分,自然也会含有更高浓度的毒素。
  • 出汗能力受损:更重要的是,由于疾病本身对神经系统的影响,这些患者反而出汗量减少了。这说明,即使身体急需排毒,但当主要排毒器官(肾脏)功能丧失,连带着次要排毒辅助途径(汗腺)的功能也会受到影响。

这有力地证明了,“出汗多不等于排毒好”。相反,当身体的主要排毒器官——肝脏和肾脏——出现问题时,即使汗液中含有较高浓度的毒素,也无法有效清除体内的废物。过度依赖出汗来“排毒”,不仅是缘木求鱼,甚至可能忽视了身体发出的真正健康警报。对于尿毒症患者而言,真正的“排毒”是通过透析等医疗手段来替代肾脏功能,而不是通过出汗。

5. 科学看待出汗:平衡需求,不必追求「排毒」

读到这里,相信你已经明白了,出汗的真正“本职工作”是调节体温,而不是我们常常误以为的“排毒”。肝脏和肾脏才是我们身体里真正的“排毒高手”。那么,我们应该如何科学地看待出汗,而不是盲目地追求所谓的“排毒”效果呢?

5.1 健康出汗的关键:维持体温调节功能

出汗,作为身体的一项基本生理功能,对我们的健康至关重要。它的核心作用在于维持身体内部温度的平衡,这就像给身体安装了一个24小时工作的“智能恒温器”。当外界环境温度升高,或者我们进行体育活动时,身体为了避免过热,就会启动出汗机制。汗液蒸发带走热量,有效地防止了体温过高,从而预防中暑等热相关疾病的发生 79。想象一下,如果没有出汗,我们的身体在炎热的夏天或者剧烈运动后,体温会迅速升高,这会损害细胞和器官的功能,甚至危及生命。儿童由于体表面积与体重之比相对较大,汗腺功能发育不完善,散热效率相对较低,因此比成年人更容易中暑 8081。

除了降温,汗液在皮肤健康方面也扮演着不容忽视的角色。汗液中含有水分,能够帮助维持皮肤表面的湿润。一些研究甚至提出,汗液本身就是一种天然的保湿剂,可以提高皮肤的表面水合作用,有助于维持皮肤屏障功能 8283。健康的皮肤屏障能够抵御外界有害物质的入侵,保护身体免受感染。

所以,我们应该做的,是维护和保持汗腺的正常工作,确保它能够有效地发挥体温调节和皮肤保湿的功能。过度地抑制出汗,比如滥用止汗剂,可能会适得其反。止汗剂通过阻塞汗腺导管来减少出汗,虽然可以在短期内解决腋下潮湿和异味的问题,但如果长期或大面积使用,可能会影响身体正常的散热功能,特别是在高温环境或运动时,增加了中暑的风险。此外,一些止汗剂中含有的铝盐,虽然目前科学界对它与乳腺癌的关联仍在争论中,尚未有定论 848586,但也有一些研究指出,铝可以被皮肤吸收,并有可能在乳腺组织中积累 87。因此,对于止汗剂的使用,应持谨慎态度,避免过度依赖。

总之,健康出汗的关键在于让身体的“温控系统”正常运转。我们应该尊重身体的自然机制,而不是盲目追求“无汗”或“多汗排毒”。当身体需要出汗时,就让它自然地出汗,并及时补充水分和电解质,确保身体能够顺畅地完成体温调节的任务。

5.2 运动出汗的正确打开方式:关注整体健康而非「排毒」

明白了出汗的真正意义后,我们再来看运动出汗。很多人为了“排毒”而特意去剧烈运动,恨不得每次都汗流浃背才作罢。但其实,运动出汗的价值,远不止于那一点点被排出的“毒素”,它的真正魅力在于对整体健康的全面提升。

运动,是身体健康的“万能药”。当我们在运动时,身体会发生一系列积极的变化:

  • 心血管系统更强大:规律的有氧运动,如慢跑、游泳、骑行,能够锻炼我们的心脏和血管,让它们更强壮,泵血效率更高,降低高血压、冠心病等心血管疾病的风险 。研究表明,健康的体育活动有助于改善心血管危险因素,如血脂和血糖水平 。
  • 新陈代谢更高效:运动能加速身体的新陈代谢,帮助身体更好地利用血糖,维持血糖稳定,减少脂肪堆积,从而降低患2型糖尿病和肥胖的风险 88。
  • 骨骼肌肉更坚韧:特别是力量训练,能增强肌肉力量和骨密度,预防骨质疏松和肌肉萎缩,让我们在老年时也能保持良好的活动能力 89。
  • 情绪更愉悦,大脑更清晰:运动是天然的“抗抑郁药”。它能促进大脑分泌内啡肽,带来愉悦感,缓解压力和焦虑。对于患有抑郁症的个体,运动,特别是结合了康复计划的运动,已被证明能有效改善情绪和生活质量 90919293。一项针对中风后抑郁症患者的研究也发现,运动疗法作为非药物治疗的一种,对改善抑郁症状具有积极作用 94。此外,运动还能改善认知功能,减缓老年痴呆的进程。
  • 免疫力更强:适度的运动可以增强身体的免疫功能,让我们更能抵御各种疾病的侵袭。

所以,运动的益处是全方位的,绝不仅仅是为了“出汗排毒”。我们应该关注的是运动带来的这些实实在在的健康回报,而不是盯着汗液中的那点微不足道的“毒素”。

那么,如何才能做到科学运动呢?

  1. 选择适合自己的运动方式:不必追求高强度,适合自己的才是最好的。快走、慢跑、游泳、瑜伽、跳舞、骑行、太极拳,甚至园艺,只要能让你动起来,就是好的运动。对于一些特殊人群,如慢性肾病患者,运动同样能带来显著益处,如改善心肺功能、肌肉力量和整体生活质量 9596979899。
  2. 循序渐进,持之以恒:运动是个长期投资,不能一蹴而就。从少量开始,逐渐增加运动强度和时间。世界卫生组织推荐成年人每周至少进行150分钟的中等强度有氧运动,或75分钟的高强度有氧运动,并结合每周两次的力量训练。
  3. 关注身体感受,而非汗量:运动时感到身体发热、心跳加速、呼吸加快,微微出汗是正常的。但如果出现胸闷、头晕、剧烈疼痛等不适,应立即停止。不必刻意追求“大汗淋漓”才能达到效果。比如,一项对Bikram瑜伽的研究发现,即使是中等强度的瑜伽,也能达到锻炼效果,并非出汗越多效果越好 100。
  4. 运动前热身,运动后拉伸:热身可以帮助身体适应运动强度,减少受伤风险;拉伸则有助于缓解肌肉酸痛,提高身体柔韧性。
  5. 及时补充水分:运动时出汗会丢失大量水分和电解质,一定要及时补充,防止脱水。

总之,运动是健康生活不可或缺的一部分。我们提倡运动,是为了强身健体、愉悦身心,而不是为了所谓的“排毒”。当你通过运动收获了强健的体魄、积极的心态和高质量的生活,那才是运动的真正意义所在。

5.3 异常多汗的应对:及时就医比「排毒」更重要

在前面的章节里,我们已经详细区分了生理性多汗和病理性多汗。现在,是时候再次强调一个非常重要的观念了:如果你发现自己有异常的多汗症状,比起去尝试各种“排毒”偏方,最明智、最负责任的选择是及时就医。

为什么这么说呢?因为异常的多汗,往往不是单纯的“身体排毒”那么简单,它更像是一个“健康警报”,可能预示着身体内部存在着一些需要医生介入的健康问题。试图通过“排毒”来解决病理性多汗,不仅是缘木求鱼,更可能延误疾病的诊断和治疗,带来更严重的后果。

异常多汗可能带来哪些潜在风险?

  1. 延误诊断和治疗:如果把病理性多汗误认为是“身体在排毒”,就会忽视它背后隐藏的疾病信号,比如甲亢、糖尿病、感染(如结核)甚至某些肿瘤。这些疾病如果不能及时发现和治疗,可能会发展到更严重的阶段,增加治疗难度,甚至危及生命。例如,未经治疗的甲亢可能导致心脏病发作或骨质疏松;晚期糖尿病并发症可能导致肾衰竭或截肢;慢性感染可能蔓延全身。
  2. 生活质量严重受损:持续性、无诱因的多汗,尤其是局限性多汗(如手汗症、腋汗症),会给患者带来巨大的困扰。手掌多汗可能影响书写、操作电子设备、甚至握手,导致社交焦虑和职业困境 101102。腋下多汗则可能让衣服总是湿漉漉的,让人感到尴尬和自卑。长期的精神压力和社交障碍,会严重影响患者的心理健康和生活质量 101103。在某些情况下,多汗甚至可能是一种神经系统的过度活跃,如手掌多汗症,通过内窥镜胸交感神经切除术(ETS)治疗后,可以显著降低心血管不良事件的风险,这表明异常多汗可能与某些心血管风险因素存在关联 104。
  3. 盲目“排毒”可能适得其反:市面上流传的很多“排毒”方法,如不当的节食、服用不明成分的保健品、过度蒸桑拿等,不仅没有科学依据,反而可能给身体带来额外的负担甚至伤害。例如,过度的桑拿或高温环境可能导致脱水和电解质紊乱,对于有心血管疾病或肾脏疾病的患者来说,更是非常危险。

什么情况下需要及时就医?

我们前面提到了病理性多汗的几个关键特征,如果出现以下情况,请务必引起重视,及时寻求医生的帮助:

  • 无诱因多汗:在环境凉爽、没有运动或情绪紧张的情况下,仍然大量出汗。
  • 夜间盗汗:在睡眠中大量出汗,甚至湿透衣物和床单,且与卧室温度无关。
  • 伴随其他症状:多汗同时伴有体重减轻、乏力、心慌、手抖、发热、咳嗽、皮肤改变、情绪异常等任何不适症状。
  • 局部异常多汗:身体某个部位(如手、脚、腋下或面部)出汗异常多,并且影响到正常生活。
  • 突发性或持续性加重:以前没有多汗问题,但突然出现,或者多汗症状近期明显加重。

医生会通过详细询问病史、体格检查,并可能安排一些血液检查(如甲状腺功能、血糖、血常规等)、影像学检查(如胸片)或其他专科检查,来寻找导致异常多汗的真正原因。一旦确诊,医生会根据病因进行针对性的治疗,比如调整甲状腺功能、控制血糖、治疗感染、激素替代治疗(对于更年期潮热)105106,甚至对于原发性多汗症,也有多种有效的治疗方案,如止汗剂、离子导入、肉毒素注射,甚至手术治疗 101102103。

记住,身体的任何异常信号都是在向你“说话”。倾听这些信号,并寻求专业的医疗帮助,远比寄希望于模糊的“排毒”概念,更能保障你的健康。

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The general way of looking at short-term temperature regulation has not fundamentaly changed since 1968. Some points nevertheless have been developed and deserve special attention: 1. The influence of water on the skin surface inhibits sweat secretion (55, 106). This fact may be the explanation of sweating fatigue and of discordant conclusions regarding the functioning of the regulator, particularly during exercise in man. 2. Since a large number of studies have shown that appropriate behaviors occur in response to all the stimuli that activate autonomic responses, behavior itself should be considered as an integral part of the thermoregulatory system (1, 2, 16, 18, 19, 21, 23, 25, 31, 32, 34-36, 48, 88, 89, 98, 99, 122, 126, 127, 137). 3. The description of the peripheral input for the control of sweating with regard to mean skin temperature (104) and time dependence (159) has been improved. Among internal temperature sensors those of the spinal cord have been extensively studies (25, 27, 32, 36, 42, 59-63, 71-75, 82, 83, 86, 113-115, 121, 150, 158) and demonstrated to have a sensitivity equal to that of the hypothalamic sensors (73, 75). 4. New hypotheses have been proposed describing the overall mechanism responsible for a constant temperature in the core (58, 96, 97, 135). These stimulating theories have been discussed briefly herein. Mechanisms for the defense against heat and against cold can be dissociated completely from one another. In the same way the control of autonomic responses can be dissociated from the control of behavioral responses. This suggests that temperature regulation is brought about by multiple independent feedback loops. The overall system is well described, in the author's opinion, by the theory of the adjustable set point with proportional control (47).

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Eccrine sweat glands help to maintain homoeostasis, primarily by stabilizing body temperature. Derived from embryonic ectoderm, millions of eccrine glands are distributed across human skin and secrete litres of sweat per day. Their easy accessibility has facilitated the start of analyses of their development and function. Mouse genetic models find sweat gland development regulated sequentially by Wnt, Eda and Shh pathways, although precise subpathways and additional regulators require further elucidation. Mature glands have two secretory cell types, clear and dark cells, whose comparative development and functional interactions remain largely unknown. Clear cells have long been known as the major secretory cells, but recent studies suggest that dark cells are also indispensable for sweat secretion. Dark cell-specific Foxa1 expression was shown to regulate a Ca(2+) -dependent Best2 anion channel that is the candidate driver for the required ion currents. Overall, it was shown that cholinergic impulses trigger sweat secretion in mature glands through second messengers - for example InsP3 and Ca(2+) - and downstream ion channels/transporters in the framework of a Na(+) -K(+) -Cl(-) cotransporter model. Notably, the microenvironment surrounding secretory cells, including acid-base balance, was implicated to be important for proper sweat secretion, which requires further clarification. Furthermore, multiple ion channels have been shown to be expressed in clear and dark cells, but the degree to which various ion channels function redundantly or indispensably also remains to be determined.

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Hyperhidrosis (HH) is a central nervous dysfunction characterized by abnormally increased sweating due to a central dysregulation of sweat secretion. HH significantly affects the quality of life of patients in their private, social and professional environments. Physiologically, sweating is a mechanism that regulates body temperature, but it may also be triggered by emotional or gustatory stimuli. There are two main types of sweat glands: eccrine and apocrine glands. The central nervous system controls sweat secretion through the release of neurotransmitters into the autonomous nervous system (ANS) that activate the sweat glands. The hypothalamus has two separate neuronal pathways, one for thermoregulation and one for emotions. HH may thus be due to either a neuronal dysfunction of ANS regulation leading to a hyperactivity of the sympathetic nervous system, or to abnormal central processing of emotions. Crucially, there is no dysfunction of the sweat glands themselves. Various pathogenic mechanisms have been proposed to be involved in pathological sweat secretion in HH, ranging from structural changes within the ANS to increased expression of aquaporin 5 and upregulation of activin A receptor type 1 in eccrine sweat glands. Although a genetic predisposition has been demonstrated, it remains unclear exactly which genes are involved. To identify new, potential therapeutic targets and to improve treatment options, a good understanding of the signaling pathways involved, the underlying mechanisms, and the genetic components is essential. In this review we discuss the various aspects of sweat physiology and function that are necessary to explain pathological sweating. Our aim is to raise awareness of the complexity of HH to promote a better understanding of the disorder.

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Qingge Zheng, Xiangyu Mu, Shaobin Pan, et al.
J Ethnopharmacol. 2023 May 10;307:116153. doi: 10.1016/j.jep.2023.116153. Epub 2023 Jan 11.
ETHNOPHARMACOLOGICAL RELEVANCE: Ephedrae herba (called Mahuang in China) is the dried herbaceous stem of Ephedra sinica Stapf, Ephedra intermedia Schrenk et C. A. Mey., and Ephedra equisetina Bge. Ephedrae herba has a long history of use as an herb, and it was originally recorded in Sheng Nong's herbal classic. Ephedrae herba has also been widely used as both medicine and food. In the clinic, Ephedrae herba is commonly used for treating colds, bronchial asthma, nasal congestion, and other diseases. AIM OF REVIEW: This review aims to provide a systematic summary on the traditional use, chemical constituents, pharmacological effects, clinical applications, quality control, toxicology, and pharmacokinetics of Ephedrae herba to provide a theoretical basis for further reasonable development of Ephedrae herba in clinical practice and creation of new drugs. MATERIALS AND METHODS: Information on Ephedrae herba was gathered from various sources, including the scientific databases including CNKI, PubMed, SciFinder and ScienceDirect, classical books on traditional Chinese herbal medicine, Ph.D. and M.Sc. dissertations; Baidu Scholar; and from different professional websites. RESULTS: Ephedrae herba is distributed in regions of China and other areas. Ephedra and its compound preparations can be used for colds, bronchial asthma, nasal congestion and other diseases. Approximately 281 chemical constituents have been isolated from Ephedrae herba, including alkaloids, flavonoids, tannins, polysaccharides, volatile oils, organic acids, and other compounds. Among these constituents, alkaloids and volatile oils are the most abundant and represent the major bioactive constituents. Ephedrae herba possesses multiple pharmacological activities, including diuretic effect, anti-allergic effect, blood pressure regulatory, anti-inflammatory effect, anti-oxidation effect and anti-viral effects. Ephedrine hydrochloride and pseudoephedrine hydrochloride are generally selected as indicators for the quantitative determination of Ephedrae herba. The maximum dosage of Ephedrae herba should not exceed 10 g. If overused, adverse reactions such as palpitations, sweating, irritability and insomnia will occur. CONCLUSIONS: Ephedrae herba is an ancient herbal medicine with a broad spectrum of pharmacological activities that has been used for thousands of years in China. It is one of the most commonly used herbal components of the TCM formulas. Hydrochloride and pseudoephedrine are the major bioactive constituents. However, there is a need to further understand the mechanisms of active components of Ephedrae herba. Future studies should perform an in-depth analyses of the pharmacokinetics and mechanisms of toxicity of Ephedrae herba. Quality standards should be developed to correspond to the various application methods to ensure the efficacy of drugs in actual treatment.

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Zhuo-Ying Duan, Yan-Ping Sun, Zhi-Bin Wang, et al.
Molecules. 2024 Apr 10;29(8):1716. doi: 10.3390/molecules29081716.
Moslae Herba (MH) can be used for both medicine and food and has a long history of medicine. MH has the effects of sweating and relieving the exterior, removing dampness and harmonizing, and is mainly used for colds caused by damp heat in summer. It is called "Xiayue Zhi Mahuang" in China. So far, 123 chemical compounds have been isolated and identified from MH, including flavonoids, terpenoids, phenolic acids, phenylpropanoids, and other chemical compounds. Its chemical components have a wide range of pharmacological activities, including antibacterial, antiviral, anti-inflammatory, antioxidant, analgesic sedation, antipyretic, immune regulation, insecticidal, and other effects. In addition, because of its aromatic odor and health care function, MH also has development and utilization value in food, chemical, and other fields. This paper reviewed the research progress of MH in botany, traditional uses, phytochemistry, and pharmacology and provided a possible direction for further research.

13Detoxification pathways in the liver.PubMed

D M Grant
J Inherit Metab Dis. 1991;14(4):421-30. doi: 10.1007/BF01797915.
The liver plays an important rôle in protecting the organism from potentially toxic chemical insults through its capacity to convert lipophiles into more water-soluble metabolites which can be efficiently eliminated from the body via the urine. This protective ability of the liver stems from the expression of a wide variety of xenobiotic biotransforming enzymes whose common underlying feature is their ability to catalyse the oxidation, reduction and hydrolysis (Phase I) and/or conjugation (Phase II) of functional groups on drug and chemical molecules. The broad substrate specificity, isoenzyme multiplicity and inducibility of many of these enzyme systems make them particularly well adapted to handling the vast array of different chemical structures in the environment to which we are exposed daily. However, some chemicals may also be converted to more toxic metabolites by certain of these enzymes, implying that variations in the latter may be important predisposing factors for toxicity. Pharmacogenetic defects of xenobiotic biotransformation enzymes, a subclass of inborn errors of metabolism which are manifested only upon drug challenge, introduce marked variation into human populations for the pharmacokinetics and pharmacodynamics of therapeutic and toxic agents, and thus may have important clinical consequences for drug efficacy and toxicity.

14Cytochrome P450 Structure, Function and Clinical Significance: A Review.PubMed

Palrasu Manikandan, Siddavaram Nagini
Curr Drug Targets. 2018;19(1):38-54. doi: 10.2174/1389450118666170125144557.
BACKGROUND: The cytochrome P450 (CYP) enzymes are membrane-bound hemoproteins that play a pivotal role in the detoxification of xenobiotics, cellular metabolism and homeostasis. Induction or inhibition of CYP enzymes is a major mechanism that underlies drug-drug interactions. CYP enzymes can be transcriptionally activated by various xenobiotics and endogenous substrates through receptor-dependent mechanisms. CYP enzyme inhibition is a principal mechanism for metabolism- based drug-drug interactions. Many chemotherapeutic drugs can cause drug interactions due to their ability to either inhibit or induce the CYP enzyme system. Predictions based on in silico analyses followed by validation have identified several microRNAs that regulate CYPs. Genetic polymorphisms and epigenetic changes in CYP genes may be responsible for inter-individual and interethnic variations in disease susceptibility and the therapeutic efficacy of drugs. OBJECTIVE: The present review is a comprehensive compilation of cytochrome P450 structure, function, pharmacogenetics, pharmacoepigenetics and clinical significance. CONCLUSION: Knowledge about the substrates, inducers, and inhibitors of CYP isoforms, as well as the polymorphisms of CYP enzymes may be used as an aid by clinicians to determine therapeutic strategy, and treatment doses for drugs that are metabolized by CYP gene products.

15Human glutathione S-transferases.PubMed

R Whalen, T D Boyer
Semin Liver Dis. 1998;18(4):345-58. doi: 10.1055/s-2007-1007169.
Human glutathione S-transferases (GSTs) are a functionally diverse family of soluble enzymes of detoxification that use reduced glutathione (GSH) in conjugation and reduction reactions. Toxic electrophiles, including a variety of carcinogens, are substrates for the GSTs and after conjugation or reduction they are more easily excreted into bile or urine. Many of the GSTs have been cloned, and the three-dimensional structures of GSTs from several species, including humans, have been determined. These data have provided significant insight into how the GSTs function as enzymes. Many GST substrates are inducers of GST gene expression; nonsubstrate inducers include H2O2 and other reactive oxygen species. The regulatory elements of several human GST genes have been partially characterized, and the regulation of the GSTs in humans appears to be very different from that in rodents. Several polymorphisms of GST expression occur commonly in humans and have been associated with an increased susceptibility to certain cancers, particularly when combined with other genetic and environmental factors such as smoking. The role of GSTs in protecting cells from injury by toxic electrophiles continues to be developed.

16Novel insights into bile acid detoxification via CYP, UGT and SULT enzymes.PubMed

Vlasia Kastrinou Lampou, Birk Poller, Felix Huth, et al.
Toxicol In Vitro. 2023 Mar;87:105533. doi: 10.1016/j.tiv.2022.105533. Epub 2022 Dec 5.
Bile acid (BA) homeostasis is a complex and precisely regulated process to prevent impaired BA flow and the development of cholestasis. Several reactions, namely hydroxylation, glucuronidation and sulfation are involved in BA detoxification. In the present study, we employed a comprehensive approach to identify the key enzymes involved in BA metabolism using human recombinant enzymes, human liver microsomes (HLM) and human liver cytosol (HLC). We showed that CYP3A4 was a crucial step for the metabolism of several BAs and their taurine and glycine conjugated forms and quantitatively described their metabolites. Glucuronidation and sulfation were also identified as important drivers of the BA detoxification process in humans. Moreover, lithocholic acid (LCA), the most hydrophobic BA with the highest toxicity potential, was a substrate for all investigated processes, demonstrating the importance of hepatic metabolism for its clearance. Collectively, this study identified CYP3A4, UGT1A3, UGT2B7 and SULT2A1 as the major contributing (metabolic) processes in the BA detoxification network. Inhibition of these enzymes by drug candidates is therefore considered as a critical mechanism in the manifestation of drug-induced cholestasis in humans and should be addressed during the pre-clinical development.

17The metabolism and biotransformation of AFB: Key enzymes and pathways.PubMed

Lingling Wang, Qiang Huang, Jun Wu, et al.
Biochem Pharmacol. 2022 May;199:115005. doi: 10.1016/j.bcp.2022.115005. Epub 2022 Mar 19.
Aflatoxins B (AFB) is a hepatoxic compound produced by Aspergillus flavus and Aspergillus parasiticus, seriously threatening food safety and the health of humans and animals. Understanding the metabolism of AFB is important for developing detoxification and intervention strategies. In this review, we summarize the AFB metabolic fates in humans and animals and the key enzymes that metabolize AFB, including cytochrome P450s (CYP450s) for AFB bioactivation, glutathione-S-transferases (GSTs) and aflatoxin-aldehyde reductases (AFARs) in detoxification. Furthermore, AFB metabolism in microbes is also summarized. Microorganisms specifically and efficiently transform AFB into less or non-toxic products in an environmental-friendly approach which could be the most desirable detoxification strategy in the future. This review provides a wholistic insight into the metabolism and biotransformation of AFB in various organisms, which also benefits the development of protective strategies in humans and animals.

18Mechanisms of liver damage.PubMed

M R Losser, D Payen
Semin Liver Dis. 1996 Nov;16(4):357-67. doi: 10.1055/s-2007-1007249.
The liver is implicated in many processes, and its failure induces severe consequences for metabolism, immune response, detoxification and antimicrobial defenses. The mechanisms involved in liver injury are complex and interactive, and can be artificially separated as chemical and immune injuries. The biochemical mechanisms concern various chemicals that are detoxified in the liver via cytochrome P-450 and conjugation. Toxic metabolites may alter plasma membrane, mitochondria, intracellular ion homeostasis, or degratative enzyme activity. Immune mechanisms involve cell cooperation, and are mediated by cytokines, nitric oxide, and complement. Pathologic apoptosis is potentially an important mechanism of acute liver injury. Specific attention is paid here to the more frequent causes of acute liver failure: hypoxia/reoxygenation, liver congestion, acetaminophen poisoning, posttransplant acute liver rejection, severe sepsis, viral hepatitis, and alcoholic liver disease. Knowledge of the intimate mechanisms of liver injury at the cellular level may lead to adaptation of therapeutic strategies that will prevent end-stage liver failure.

19Current concepts in acute liver failure.PubMed

Maximiliano Rovegno, Magdalena Vera, Alex Ruiz, et al.
Ann Hepatol. 2019 Jul-Aug;18(4):543-552. doi: 10.1016/j.aohep.2019.04.008. Epub 2019 May 10.
Acute liver failure (ALF) is a severe condition secondary to a myriad of causes associated with poor outcomes. The prompt diagnosis and identification of the aetiology allow the administration of specific treatments plus supportive strategies and to define the overall prognosis, the probability of developing complications and the need for liver transplantation. Pivotal issues are adequate monitoring and the institution of prophylactic strategies to reduce the risk of complications, such as progressive liver failure, cerebral oedema, renal failure, coagulopathies or infections. In this article, we review the main aspects of ALF, including the definition, diagnosis and complications. Also, we describe the standard-of-care strategies and recent advances in the treatment of ALF. Finally, we include our experience of care patients with ALF.

20The detoxification enzyme systems.PubMed

D J Liska
Altern Med Rev. 1998 Jun;3(3):187-98.
The human body is exposed to a wide array of xenobiotics in one s lifetime, from food components to environmental toxins to pharmaceuticals, and has developed complex enzymatic mechanisms to detoxify these substances. These mechanisms exhibit significant individual variability, and are affected by environment, lifestyle, and genetic influences. The scientific literature suggests an association between impaired detoxification and certain diseases, including cancer, Parkinson's disease, fibromyalgia, and chronic fatigue/immune dysfunction syndrome. Data regarding these hepatic detoxification enzyme systems and the body s mechanisms of regulating them suggests the ability to efficiently detoxify and remove xenobiotics can affect these and other chronic disease processes. This article reviews the myriad detoxification enzyme systems, their regulatory mechanisms, and the dietary, lifestyle, and genetic factors influencing their activities, as well as laboratory tests available to assess their functioning.

21Circadian clock-controlled drug metabolism and transport.PubMed

Mengjing Zhao, Huijie Xing, Min Chen, et al.
Xenobiotica. 2020 May;50(5):495-505. doi: 10.1080/00498254.2019.1672120. Epub 2019 Oct 1.
Metabolism and transport of many drugs oscillate with times of the day (solar time), resulting in circadian time-dependent drug exposure and pharmacokinetics.Time-dependent pharmacokinetics (also known as chronopharmacokinetics) is associated with time-varying drug effects and toxicity.This review summarizes drug-metabolizing enzymes and transporters with rhythmic expressions in the liver, intestine and/or kidney. Correlations of these diurnal proteins with circadian variations in drug exposure and effects/toxicity are covered. We also discuss the molecular mechanisms for circadian control of enzymes and transporters.Mechanism-based chronopharmacokinetics would facilitate a better understanding of chronopharmacology and the design of time-specific drug delivery systems, ultimately leading to improved drug efficacy and minimized toxicity.

22Physiology, RenalPubMed

Ifeanyichukwu Ogobuiro, Faiz Tuma
The renal system consists of the kidney, ureters, and the urethra. The overall function of the system filters approximately 200 liters of fluid a day from renal blood flow which allows for toxins, metabolic waste products, and excess ion to be excreted while keeping essential substances in the blood. The kidney regulates plasma osmolarity by modulating the amount of water, solutes, and electrolytes in the blood. It ensures long term acid-base balance and also produces erythropoietin which stimulates the production of red blood cell. It also produces renin for blood pressure regulation and carries out the conversion of vitamin D to its active form. The renal development, the process of urine production and excretion, and the clinical significance of the renal system will be the focus of this article.

23Renal control of calcium, phosphate, and magnesium homeostasis.PubMed

Judith Blaine, Michel Chonchol, Moshe Levi
Clin J Am Soc Nephrol. 2015 Jul 7;10(7):1257-72. doi: 10.2215/CJN.09750913. Epub 2014 Oct 6.
Calcium, phosphate, and magnesium are multivalent cations that are important for many biologic and cellular functions. The kidneys play a central role in the homeostasis of these ions. Gastrointestinal absorption is balanced by renal excretion. When body stores of these ions decline significantly, gastrointestinal absorption, bone resorption, and renal tubular reabsorption increase to normalize their levels. Renal regulation of these ions occurs through glomerular filtration and tubular reabsorption and/or secretion and is therefore an important determinant of plasma ion concentration. Under physiologic conditions, the whole body balance of calcium, phosphate, and magnesium is maintained by fine adjustments of urinary excretion to equal the net intake. This review discusses how calcium, phosphate, and magnesium are handled by the kidneys.

24Osmotic diuresis.PubMed

F Lang
Ren Physiol. 1987;10(3-4):160-73. doi: 10.1159/000173127.
Osmotic diuresis occurs, if nonreabsorbed solutes such as mannitol impair the reabsorption of water. The reduced reabsorption of volume affects in turn the reabsorption and excretion of solutes. Thus, mannitol leads to modest impairment of proximal tubular reabsorption not only of water, but as well of electrolytes (Na, Cl, K, Pi, Ca, but not Mg), urea, and uric acid. Infusion of hypertonic mannitol increases renal blood flow and the glomerular filtration rate of superficial nephrons. The increased perfusion of medulla leads to wash out of medullary hypertonicity. The decline of medullary osmolarity leads to a marked impairment of water reabsorption in descending limbs and possibly to moderate impairment of NaCl, Ca, and Mg reabsorption in the ascending limbs of Henle's loop. In the collecting duct, inhibition is marked of water and urea reabsorption and modest of NaCl reabsorption. A number of open questions remain, such as the mechanisms underlying decrease of renal vascular resistance, increased proximal tubular reabsorption of magnesium, or impaired NaCl reabsorption in thick ascending limbs.

25Uncertainty in measurement and the renal tubular reabsorption of phosphate.PubMed

Ian Farrance, Robert Frenkel, Kay Weng Choy
Clin Chem Lab Med. 2023 Jul 19;61(12):2178-2185. doi: 10.1515/cclm-2023-0451. Print 2023 Nov 27.
OBJECTIVES: The ratio of tubular maximum reabsorption of phosphate to glomerular filtration rate (TmP/GFR) is used to evaluate renal phosphate transport. TmP/GFR is most probably calculated using the formula described by Kenny and Glen or obtained from the nomogram described by Walton and Bijvoet. Even though the calculation itself is well described, no attention has been given to its measurement uncertainty (MU). The aim of this study is to provide a procedure for evaluating the MU of the Kenny and Glen formula; a procedure which is based on the (GUM). METHODS: TmP/GFR is a quantity value calculated from the input of measured values for serum (plasma) phosphate and creatinine, plus measured values of urine phosphate and creatinine. Given the measurement uncertainty associated with these input quantities, the GUM describes the mathematical procedures required to determine the uncertainty of the calculated TmP/GFR. From a medical laboratory perspective, these input uncertainties are the standard deviations of the respective internal quality control estimates for serum and urine phosphate, plus serum and urine creatinine. RESULTS: Based on representative measurements for the input quantities and their associated standard uncertainties, the expanded relative uncertainty for a calculated TmP/GFR is approximately 3.0-4.5 %. CONCLUSIONS: With the continued relevance of the TmP/GFR procedure and the use of creatinine clearance as an estimate of GFR, the addition of an uncertainty estimate is important as an adjunct to this diagnostic procedure.

26Glutathione-dependent bioactivation.PubMed

Lawrence H Lash
Curr Protoc Toxicol. 2007 Nov;Chapter 6:Unit6.12. doi: 10.1002/0471140856.tx0612s34.
The classical view of the glutathione (GSH) conjugation pathway involves GSH S-transferase (GST)-dependent formation of thioether conjugates between GSH and an electrophilic substrate, processing to yield the corresponding cysteine S-conjugate, which is then converted to an N-acetylcysteine conjugate (or mercapturate). Mercapturates of most GST substrates are rendered more polar and thus readily excreted in urine. In contrast, there is a growing number of GST substrates that, rather than being detoxified, are bioactivated. These substrates include several halogenated solvents, many of which are nephrotoxic because of the tissue distribution of GSH conjugation pathway enzymes and membrane transporters, and prodrugs of certain chemotherapeutic agents. Although the initiating steps are the same regardless of whether the substrate is detoxified or bioactivated, the cysteine conjugate functions as a branch point. Bioactivated cysteine S-conjugates are metabolized in the kidneys by either cysteine conjugate β-lyase or flavin-containing monooxygenase to produce a reactive intermediate.

27Sensing of tubular flow and renal electrolyte transport.PubMed

Eric H J Verschuren, Charlotte Castenmiller, Dorien J M Peters, et al.
Nat Rev Nephrol. 2020 Jun;16(6):337-351. doi: 10.1038/s41581-020-0259-8. Epub 2020 Mar 3.
The kidney is a remarkable organ that accomplishes the challenge of removing waste from the body and simultaneously regulating electrolyte and water balance. Pro-urine flows through the nephron in a highly dynamic manner and adjustment of the reabsorption rates of water and ions to the variable tubular flow is required for electrolyte homeostasis. Renal epithelial cells sense the tubular flow by mechanosensation. Interest in this phenomenon has increased in the past decade since the acknowledgement of primary cilia as antennae that sense renal tubular flow. However, the significance of tubular flow sensing for electrolyte handling is largely unknown. Signal transduction pathways regulating flow-sensitive physiological responses involve calcium, purinergic and nitric oxide signalling, and are considered to have an important role in renal electrolyte handling. Given that mechanosensation of tubular flow is an integral role of the nephron, defective tubular flow sensing is probably involved in renal disease. Studies investigating tubular flow and electrolyte transport differ in their methodology, subsequently hampering translational validity. This Review provides the basis for understanding electrolyte disorders originating from altered tubular flow sensing as a result of pathological conditions.

28Amelioration effects of α-viniferin on hyperuricemia and hyperuricemia-induced kidney injury in mice.PubMed

Xiao-Li Guo, Yan-Yan Gao, Ya-Xin Yang, et al.
Phytomedicine. 2023 Jul 25;116:154868. doi: 10.1016/j.phymed.2023.154868. Epub 2023 May 13.
BACKGROUND: α-Viniferin, the major constituent of the roots of Caragana sinica (Buc'hoz) Rehder with a trimeric resveratrol oligostilbenoid skeleton, was demonstrated to possess a strong inhibitory effect on xanthine oxidase in vitro, suggesting it to be a potential anti-hyperuricemia agent. However, the in vivo anti-hyperuricemia effect and its underlying mechanism were still unknown. PURPOSE: The current study aimed to evaluate the anti-hyperuricemia effect of α-viniferin in a mouse model and to assess its safety profile with emphasis on its protective effect on hyperuricemia-induced renal injury. METHODS: The effects were assessed in a potassium oxonate (PO)- and hypoxanthine (HX)-induced hyperuricemia mice model by analyzing the levels of serum uric acid (SUA), urine uric acid (UUA), serum creatinine (SCRE), serum urea nitrogen (SBUN), and histological changes. Western blotting and transcriptomic analysis were used to identify the genes, proteins, and signaling pathways involved. RESULTS: α-Viniferin treatment significantly reduced SUA levels and markedly mitigated hyperuricemia-induced kidney injury in the hyperuricemia mice. Besides, α-viniferin did not show any obvious toxicity in mice. Research into the mechanism of action of α-viniferin revealed that it not only inhibited uric acid formation by acting as an XOD inhibitor, but also reduced uric acid absorption by acting as a GLUT9 and URAT1 dual inhibitor as well as promoted uric acid excretion by acting as a ABCG2 and OAT1 dual activator. Then, 54 differentially expressed (log FPKM ≥ 1.5, p ≤ 0.01) genes (DEGs) repressed by the treatment of α-viniferin in the hyperuricemia mice were identified in the kidney. Finally, gene annotation results revealed that downregulation of S100A9 in the IL-17 pathway, of CCR5 and PIK3R5 in the chemokine signaling pathway, and of TLR2, ITGA4, and PIK3R5 in the PI3K-AKT signaling pathway were involved in the protective effect of α-viniferin on the hyperuricemia-induced renal injury. CONCLUSIONS: α-Viniferin inhibited the production of uric acid through down-regulation of XOD in hyperuricemia mice. Besides, it also down-regulated the expressions of URAT1 and GLUT9 and up-regulated the expressions of ABCG2 and OAT1 to promote the excretion of uric acid. α-Viniferin could prevent hyperuricemia mice from renal damage by regulating the IL-17, chemokine, and PI3K-AKT signaling pathways. Collectively, α-viniferin was a promising antihyperuricemia agent with desirable safety profile. This is the first report of α-viniferin as an antihyperuricemia agent.

29Xenobiotic-metabolizing enzymes in human lung.PubMed

Ji Y Zhang, Yuefen Wang, Chandra Prakash
Curr Drug Metab. 2006 Dec;7(8):939-48. doi: 10.2174/138920006779010575.
Human lung is a major target organ for all inhaled drugs, environmental toxicants and carcinogens. Recent hypotheses suggesting a role for environmental toxicants in the pathogenesis of lung diseases, such as lung cancer and chronic obstructive pulmonary disease have stimulated interest in research on the xenobiotic metabolizing capability of the lung. Many of the compounds associated with these diseases require enzymatic activation to exert their deleterious effects on pulmonary cells. Interindividual differences in in situ activation and inactivation of xenobiotics may contribute to the risk of developing of lung diseases associated with these compounds. The major xenobiotic metabolizing enzymes, including both phase I and phase II enzymes, have been detected in animal and human lung tissues. Although the lung cytochrome P450 (CYP) and other xenobiotic metabolizing enzymes share many common features with those present in other tissues such as liver, kidney and gut, there are some distinctive differences. It is evident from the studies carried out to date CYP1A1, 1B1, 2A13, 2F1, 2S1 and 4B1 are preferentially expressed in the lung together with CYP2E1 and 3A5. This review provides a detailed picture of major xenobiotic-metabolizing phase I (CYPs, epoxide hydrolases, flavin monooxygenases, etc.) and phase II enzymes (conjugation enzymes, including several transferases) expressed in human lung. The roles of individual metabolizing enzymes and their genetic polymorphisms are also discussed.

30Fuling-Zexie formula attenuates hyperuricemia-induced nephropathy and inhibits JAK2/STAT3 signaling and NLRP3 inflammasome activation in mice.PubMed

Meixi Lu, Jiyuan Yin, Tianshu Xu, et al.
J Ethnopharmacol. 2024 Jan 30;319(Pt 2):117262. doi: 10.1016/j.jep.2023.117262. Epub 2023 Oct 1.
ETHNOPHARMACOLOGICAL RELEVANCE: Fuling-Zexie (FZ) formula, a traditional Chinese herbal prescription composed of Poria cocos (Schwan.) Wolf. (Poria), Pueraria lobate (Willd.) Howe. (Puerariae Lobatae Radix), Alisma orientale (Sam.) Julep. (Alismatis Rhizoma), and Atractylodes lancea (Thunb.) Dc. (Atractylodis Rhizoma), has been clinically used to ameliorate hyperuricemia (HUA) and its associated renal injury. AIM OF STUDY: This study aims to explore the action and mechanism of FZ on renal inflammation and dysfunction caused by HUA. MATERIALS AND METHODS: FZ was orally administered to rapid HUA mouse induced by potassium oxonate (PO) and hypoxanthine (HX) for 7 days. Serum levels of uric acid (UA), creatinine (CRE), blood urea nitrogen (BUN), xanthine oxidase (XOD), adenosine deaminase (ADA), alanine aminotransferase (ALT), aspartate aminotransferase (AST), urine levels of UA, CRE and urinary albumin were determined by biochemical assays. Serum levels of interleukin (IL)-1β and IL-6 were tested by ELISA. Hematoxylin-eosin and Masson staining were used to examine kidney and liver histopathological alterations. The expressions of renal glucose transporter 9 (GLUT9), ATP-binding cassette subfamily G member 2 (ABCG2), organic anion transporter 1 (OAT1), phospho-janus kinase 2 (p-JAK2), p-signal transducer and activator of transcription 3 (p-STAT3), suppression of cytokine signaling 3 (SOCS3), NLR family pyrin domain containing 3 (NLRP3), apoptosis-associated speck-like protein (ASC), and cleaved-cysteinyl aspartate specific proteinase-1 (cleaved-Cas-1) were detected by western blots. The potential protein targets and pathways of FZ intervention on HUA were predicted by network pharmacology. The constituents in FZ aqueous extract were analyzed by UPLC-MS. RESULTS: FZ reduced serum UA, CRE, BUN, and urinary albumin and increased urine UA, CRE levels in HUA mice. In addition, the treatment with FZ to HUA mice inhibited the elevated serum levels of XOD and ADA, and regulated renal urate transports including OAT1, GLUT9 and ABCG2. FZ also attenuated kidney inflammation and fibrosis and downregulated the expressions of IL-1β, p-JAK2, p-STAT3, SOCS3, IL-6, NLRP3, ASC, and cleaved-Cas-1. Thirteen compounds were identified in the FG, including L-phenylalanine, D-tryptophan, 3'-hydroxypuerarin, Puerarin, 3'-Methoxy Puerarin, Daidzin, Pueroside A, formononetin-8-C- [xylosyl (1→6)]-glucoside, Ononin, Alisol I 23-acetate, 16-oxo-alisol A, Alisol C and Alisol A. CONCLUSION: FZ inhibits serum UA generation and promotes urine UA excretion as well as attenuates kidney inflammation and fibrosis in HUA mouse with nephropathy. The underlying mechanism of its action may be associated with suppression of the JAK2/STAT3 signaling pathway and NLRP3 inflammasome activation. This formula may offer a novel source for developing anti-HUA drugs.

31Removal of urea, creatinine, uric acid and inorganic phosphate by a rotating-drum artificial kidney.PubMed

A C KENNEDY, M J GRAY, A DINWOODIE, et al.
Lancet. 1961 Nov 4;2(7210):996-8. doi: 10.1016/s0140-6736(61)90961-8.

32Ambulatory Hemodialysis-Technology Landscape and Potential for Patient-Centered Treatment.PubMed

Nina Hojs, William H Fissell, Shuvo Roy
Clin J Am Soc Nephrol. 2020 Jan 7;15(1):152-159. doi: 10.2215/CJN.01970219. Epub 2019 Nov 14.
CKD is a worldwide health problem and the number of patients requiring kidney replacement therapy is rising. In the United States, most patients with ESKD rely on in-center hemodialysis, which is burdensome and does not provide the same long-term benefits as kidney transplantation. Intensive hemodialysis treatments have demonstrated improved clinical outcomes, but its wider adoption is limited by equipment complexity and patient apprehension. Ambulatory devices for hemodialysis offer the potential for self-care treatment outside the clinical setting as well as frequent and prolonged sessions. This article explains the motivation for ambulatory hemodialysis and provides an overview of the necessary features of key technologies that will be the basis for new wearable and implantable devices. Early work by pioneers of hemodialysis is described followed by recent experience using a wearable unit on patients. Finally, ongoing efforts to develop an implantable device for kidney replacement and its potential for implantable hemodialysis are presented.

33Global epidemiology and outcomes of acute kidney injury.PubMed

Eric A J Hoste, John A Kellum, Nicholas M Selby, et al.
Nat Rev Nephrol. 2018 Oct;14(10):607-625. doi: 10.1038/s41581-018-0052-0.
Acute kidney injury (AKI) is a commonly encountered syndrome associated with various aetiologies and pathophysiological processes leading to decreased kidney function. In addition to retention of waste products, impaired electrolyte homeostasis and altered drug concentrations, AKI induces a generalized inflammatory response that affects distant organs. Full recovery of kidney function is uncommon, which leaves these patients at risk of long-term morbidity and death. Estimates of AKI prevalence range from <1% to 66%. These variations can be explained by not only population differences but also inconsistent use of standardized AKI classification criteria. The aetiology and incidence of AKI also differ between high-income and low-to-middle-income countries. High-income countries show a lower incidence of AKI than do low-to-middle-income countries, where contaminated water and endemic diseases such as malaria contribute to a high burden of AKI. Outcomes of AKI are similar to or more severe than those of patients in high-income countries. In all resource settings, suboptimal early recognition and care of patients with AKI impede their recovery and lead to high mortality, which highlights unmet needs for improved detection and diagnosis of AKI and for efforts to improve care for these patients.

34Acute Kidney Injury: Diagnosis and Management.PubMed

Michael G Mercado, Dustin K Smith, Esther L Guard
Am Fam Physician. 2019 Dec 1;100(11):687-694.
Acute kidney injury is a clinical syndrome characterized by a rapid decline in glomerular filtration rate and resultant accumulation of metabolic waste products. Acute kidney injury is associated with an increased risk of mortality, cardiovascular events, and progression to chronic kidney disease. Severity of acute kidney injury is classified according to urine output and elevations in creatinine level. Etiologies of acute kidney injury are categorized as prerenal, intrinsic renal, and postrenal. Accurate diagnosis of the underlying cause is key to successful management and includes a focused history and physical examination, serum and urine electrolyte measurements, and renal ultrasonography when risk factors for a postrenal cause are present (e.g., older male with prostatic hypertrophy). General management principles for acute kidney injury include determination of volume status, fluid resuscitation with isotonic crystalloid, treatment of volume overload with diuretics, discontinuation of nephrotoxic medications, and adjustment of prescribed drugs according to renal function. Additional supportive care measures may include optimizing nutritional status and glycemic control. Pharmacist-led quality-improvement programs reduce nephrotoxic exposures and rates of acute kidney injury in the hospital setting. Acute kidney injury care bundles are associated with improved in-hospital mortality rates and reduced risk of progression. Nephrology consultation should be considered when there is inadequate response to supportive treatment and for acute kidney injury without a clear cause, stage 3 or higher acute kidney injury, preexisting stage 4 or higher chronic kidney disease, renal replacement therapy, and other situations requiring subspecialist expertise.

35Azotemia(Archived)PubMed

Alka Tyagi, Narothama R. Aeddula
Azotemia is a biochemical abnormality, defined as an elevation or buildup of nitrogenous products (BUN, usually ranging from 7 to 21 mg/dL), creatinine in the blood, and other secondary waste products within the body. Raising the level of nitrogenous waste is attributed to the inability of the renal system to filter waste products adequately, resulting in a decreased glomerular filtration rate (GFR). It is a typical feature of both acute and chronic kidney injury. Azotemia is crucial when discussing the precipitant syndrome of acute kidney injury (AKI), which has 3 subtypes: prerenal, intrinsic, and post-renal azotemia. There are multiple classification systems used to define AKI, including the RIFLE criteria of 2004, the AKIN criteria of 2007, and the KDIGO system of 2012. AKI is generally diagnosed by an increase in creatinine (Cr) of 0.3 mg/dL, a Cr increase greater than 1.5%, or a decrease in creatinine clearance of less than 0.5 mL/kg per hour. This diagnosis is made with urinalysis (UA), urine electrolytes, metabolic panel (CMP/BMP), and a renal ultrasound (US). With these labs, the clinician can discern the classification and etiology of the AKI, which guides clinical management. Azotemia manifests as a constellation of clinical signs and symptoms, accompanied by biochemical abnormalities, and is termed uremia

36Molecular mechanisms of urea transport.PubMed

J M Sands
J Membr Biol. 2003 Feb 1;191(3):149-63. doi: 10.1007/s00232-002-1053-1.
Physiologic data provided evidence for specific urea transporter proteins in red blood cells and kidney inner medulla. During the past decade, molecular approaches resulted in the cloning of several urea transporter cDNA isoforms derived from two gene families: UT-A and UT-B. Polyclonal antibodies were generated to the cloned urea transporter proteins, and their use in integrative animal studies resulted in several novel findings, including: (1) UT-B is the Kidd blood group antigen; (2) UT-B is also expressed in many non-renal tissues and endothelial cells; (3) vasopressin increases UT-A1 phosphorylation in rat inner medullary collecting duct; (4) the surprising finding that UT-A1 protein abundance and urea transport are increased in the inner medulla during conditions in which urine concentrating ability is reduced; and (5) UT-A protein abundance is increased in uremia in both liver and heart. This review will summarize the knowledge gained from studying molecular mechanisms of urea transport and from integrative studies into urea transporter protein regulation.

37[Uremic toxins].PubMed

R Vanholder
Nephrologie. 2003;24(7):373-6.
Uremic toxins are compounds which exert biological action and which are retained in the body of patients with renal failure, whereas they normally should be excreted by the healthy kidneys into the urine. Only few retention solutes conform with the strict definition of uremic toxins. Uremic solutes can be subdivided into small water soluble compounds, small protein bound compounds and middle molecules. Most small water soluble compounds are not very toxic and the toxic ones often show a kinetic behavior that is different from that of urea. The uremic solutes that play a role in inflammation and cardio-vascular complications most often are middle molecules and/or protein bound. Hence, once more, the current marker urea is not representative for their mechanistic behavior.

38Urea and urine concentrating ability: new insights from studies in mice.PubMed

Baoxue Yang, Lise Bankir
Am J Physiol Renal Physiol. 2005 May;288(5):F881-96. doi: 10.1152/ajprenal.00367.2004.
Urea is the most abundant solute in the urine in humans (on a Western-type diet) and laboratory rodents. It is far more concentrated in the urine than in plasma and extracellular fluids. This concentration depends on the accumulation of urea in the renal medulla, permitted by an intrarenal recycling of urea among collecting ducts, vasa recta and thin descending limbs, all equipped with specialized, facilitated urea transporters (UTs) (UT-A1 and 3, UT-B, and UT-A2, respectively). UT-B null mice have been recently generated by targeted gene deletion. This review describes 1) the renal handling of urea by the mammalian kidney; 2) the consequences of UT-B deletion on urinary concentrating ability; and 3) species differences among mice, rats, and humans related to their very different body size and metabolic rate, leading to considerably larger needs to excrete and to concentrate urea in smaller species (urea excretion per unit body weight in mice is 5 times that in rats and 23 times that in humans). UT-B null mice have a normal glomerular filtration rate but moderately reduced urea clearance. They exhibit a 30% reduction in urine concentrating ability with a more severe defect in the capacity to concentrate urea (50%) than other solutes, despite a twofold enhanced expression of UT-A2. The urea content of the medulla is reduced by half, whereas that of chloride is almost normal. When given an acute urea load, UT-B null mice are unable to raise their urinary osmolality, urine urea concentration (Uurea), and the concentration of non-urea solutes, as do wild-type mice. When fed diets with progressively increasing protein content (10, 20, and 40%), they cannot prevent a much larger increase in plasma urea than wild-type mice because they cannot raise Uurea. In both wild-type and UT-B null mice, urea clearance was higher than creatinine clearance, suggesting the possibility that urea could be secreted in the mouse kidney, thus allowing more efficient excretion of the disproportionately high urea load. On the whole, studies in UT-B null mice suggest that recycling of urea by countercurrent exchange in medullary vessels plays a more crucial role in the overall capacity to concentrate urine than its recycling in the loops of Henle.

39Is There a Role for Diaphoresis Therapy for Advanced Chronic Kidney Disease Patients?PubMed

Norio Hanafusa, Bereket Tessema Lodebo, Anuja Shah, et al.
J Ren Nutr. 2017 Sep;27(5):295-302. doi: 10.1053/j.jrn.2017.04.008. Epub 2017 Jun 28.
Diaphoresis therapy to remove water and solutes for the treatment of advanced chronic kidney disease (CKD) and chronic dialysis patients is an inadequately characterized treatment that was first reported over 50 years ago. Intensive diaphoresis, induced by heat treatment with saunas (dry heat) or hot baths (wet heat), can substantially increase cutaneous losses of water, urea, sodium, potassium, chloride, lactate, and possibly other solutes. How effectively diaphoresis therapy might remove many uremic toxins is not known. Diaphoresis therapy is not sufficiently effective to replace dialysis treatments, but theoretically it might be used to delay the start of chronic dialysis, supplement infrequent dialysis therapy, or augment chronic dialysis treatment perhaps especially for dialysis patients with excessive salt and water intake. Diaphoresis might be helpful for managing edema resistant states. Because it is inexpensive, diaphoresis may be particularly valuable in lower income countries where some patients may need to pay for dialysis. Diaphoresis might enhance some aspects of dietary treatment. The short-term and long-term effectiveness, safety, and patient acceptance of diaphoretic therapy need to be more carefully investigated.

40Arsenic, cadmium, lead, and mercury in sweat: a systematic review.PubMed

Margaret E Sears, Kathleen J Kerr, Riina I Bray
J Environ Public Health. 2012;2012:184745. doi: 10.1155/2012/184745. Epub 2012 Feb 22.
Arsenic, cadmium, lead, and mercury exposures are ubiquitous. These toxic elements have no physiological benefits, engendering interest in minimizing body burden. The physiological process of sweating has long been regarded as "cleansing" and of low risk. Reports of toxicant levels in sweat were sought in Medline, Embase, Toxline, Biosis, and AMED as well as reference lists and grey literature, from inception to March 22, 2011. Of 122 records identified, 24 were included in evidence synthesis. Populations, and sweat collection methods and concentrations varied widely. In individuals with higher exposure or body burden, sweat generally exceeded plasma or urine concentrations, and dermal could match or surpass urinary daily excretion. Arsenic dermal excretion was severalfold higher in arsenic-exposed individuals than in unexposed controls. Cadmium was more concentrated in sweat than in blood plasma. Sweat lead was associated with high-molecular-weight molecules, and in an interventional study, levels were higher with endurance compared with intensive exercise. Mercury levels normalized with repeated saunas in a case report. Sweating deserves consideration for toxic element detoxification. Research including appropriately sized trials is needed to establish safe, effective therapeutic protocols.

41Excretion of Ni, Pb, Cu, As, and Hg in Sweat under Two Sweating Conditions.PubMed

Wen-Hui Kuan, Yi-Lang Chen, Chao-Lin Liu
Int J Environ Res Public Health. 2022 Apr 4;19(7):4323. doi: 10.3390/ijerph19074323.
Physiologists have long regarded sweating as an effective and safe means of detoxification, and heavy metals are excreted through sweat to reduce the levels of such metals in the body. However, the body can sweat through many means. To elucidate the difference in the excretion of heavy metals among sweating methods, 12 healthy young university students were recruited as participants (6 men and 6 women). Sweat samples were collected from the participants while they were either running on a treadmill or sitting in a sauna cabinet. After they experienced continuous sweating for 20 min, a minimum of 7 mL of sweat was collected from each participant, and the concentrations of nickel (Ni), lead (Pb), copper (Cu), arsenic (As), and mercury (Hg) were analyzed. The results demonstrated that the sweating method affected the excretion of heavy metals in sweat, with the concentrations of Ni, Pb, Cu, and As being significantly higher during dynamic exercise than during sitting in the sauna (all p < 0.05). However, the concentrations of Hg were unaffected by the sweating method. This study suggests that the removal of heavy metals from the body through dynamic exercise may be more effective than removal through static exposure to a hot environment.

42Nutrition of lead.PubMed

S J DeMichele
Comp Biochem Physiol A Comp Physiol. 1984;78(3):401-8. doi: 10.1016/0300-9629(84)90567-x.
At the levels to which human beings are exposed in the workplace as well as in the general environment, lead has been shown to be a toxic element in most of its chemical forms, whether it is inhaled or ingested in water or food. The four main sources of contamination of food are soil, industrial pollution, agricultural technology and food processing. Reasonable quantities of the metal can be stored by humans in a relatively inert form in bone; lead has an affinity for bone and acts by replacing calcium. Gastrointestinal lead absorption and retention, the major pathway of lead intake, has been shown to vary widely depending on the chemical environment of the gastrointestinal lumen, age and iron stores (nutritional status of the subject). Studies in animals have shown that certain substances bind lead and increase its solubility, thus enhancing its absorption. These dietary components consist of sodium citrate, ascorbate, amino acids, vitamin D, protein and fat, and lactose. Data suggest a three-compartmental pool for lead metabolism: (1) blood; (2) soft tissue (hair, nails, sweat, salivary, gastric, pancreatic and biliary secretions); and (3) skeleton. Lead absorption occurs primarily in the duodenum where lead enters the epithelial mucosal cells. The total bodily amount of lead does not affect lead absorption; lead does not have a feedback mechanism which limits absorption. In the adult rat, lead absorption from the intestinal lumen appears to proceed by both active transport and passive diffusion. Bile is an important route of excretion in the gut.(ABSTRACT TRUNCATED AT 250 WORDS)

43Comparison of urine toxic metals concentrations in athletes and in sedentary subjects living in the same area of Extremadura (Spain).PubMed

F Llerena, M Maynar, G Barrientos, et al.
Eur J Appl Physiol. 2012 Aug;112(8):3027-31. doi: 10.1007/s00421-011-2276-6. Epub 2011 Dec 17.
Cadmium (Cd), tungsten (W), tellurium (Te), beryllium (Be), and lead (Pb), are non-essential metals pervasive in the human environment. Studies on athletes during training periods compared to non-training control subjects, indicate increased loss of minerals through sweat and urine. The aim of this study was to compare the level of these trace elements, determined by inductively coupled plasma mass spectrometry (ICP-MS) in urine samples, between athletes and age-matched sedentary subjects living in the same geographical area, although anthropometric and cardiovascular measurements showed that athletes have significantly (P ≤ 0.001) lower BMI, body fat and heart rate, whereas the muscle and bone percentage was significantly (P ≤ 0.001) higher than in sedentary subjects. The validity of the methodology was checked by the biological certified reference material. Trace element analysis concentrations, expressed in μg/mg creatinine, of five toxic elements in urine from athletes (n = 21) versus sedentary subjects, (n = 26) were as follows: Cd (0.123 ± 0.075 vs. 0.069 ± 0.041, P ≤ 0.05); W (0.082 ± 0.053 vs. < limit of detection); Te (0.244 ± 0.193 vs. 0.066 ± 0.045, P ≤ 0.001), Be (0.536 ± 0.244 vs. 0.066 ± 0.035, P ≤ 0.001); Pb (0.938 ± 0.664 vs. 2.162 ± 1.444 P ≤ 0.001). With the exception of Pb, urine toxic metal concentrations from athletes were higher than from sedentary subjects. This fact suggests that physical activity counteracts, at least in part, the cumulative effect of toxic environment by increasing the urine excretion of toxic metals in trained people.

44Sweat composition in exercise and in heat.PubMed

T Verde, R J Shephard, P Corey, et al.
J Appl Physiol Respir Environ Exerc Physiol. 1982 Dec;53(6):1540-5. doi: 10.1152/jappl.1982.53.6.1540.
Sweat samples were collected from the forearms of eight male volunteers using light gauze pads applied for 20-min periods. Preliminary trials indicated that this technique yielded realistic figures for both sweat volume and sweat composition. Tests were conducted under three conditions: a) outdoor exercise, cool environment; b) indoor exercise, normal room temperatures; and c) sauna exposure. In all environments, proximal forearm samples indicated a larger sweat secretion than distal forearm or hand samples. [Mg2+] decreased as sweat flow increased, but after allowance for interindividual differences of sweat volume, [Na+], [K+], [Ca2+], and [Cl-] were independent of sweat flow rates. The differential effect of sweat flow suggests active regulation rather than contamination. Interindividual differences of sweat composition could not be explained in terms of differences in personal fitness. Sauna bathing yielded sweat with a higher [Mg2+] and [Ca2+] content than did exercise; however, [Na+], [K+], and [Cl-] were similar for the three experimental conditions. Again, the data are best explained in terms of an active regulation of sweat composition. Total ionic losses do not seem sufficient to deplete body mineral reserves unless many days of training are undertaken in a hot climate.

45Effect of water filtration infrared-A (wIRA) sauna on inorganic ions excreted through sweat from the human body.PubMed

Kang-Hee Cho, Sung-Hun Jung, Min-Sun Choi, et al.
Environ Sci Pollut Res Int. 2023 Feb;30(7):18260-18267. doi: 10.1007/s11356-022-23437-3. Epub 2022 Oct 8.
Sweat discharged as a result of exposure to sauna plays an important role in removing inorganic ions accumulated in the body, including heavy metals. In this study, inorganic ions (toxic and nutrient elements) excreted in the form of sweat from the body using a water-filtered infrared-A (wIRA) sauna were determined using inductively coupled plasma sector field mass spectrometry. The analyzed elements included eight toxic elements (Al, As, Be, Cd, Ni, Pb, Ti, and Hg) and 10 nutrient elements (Ca, Co, Cr, Cu, Fe, Mg, Mn, Se, V, and Zn), and their correlations were determined. Analysis of the sweat obtained from 22 people using the wIRA sauna showed a higher inorganic ion concentration than that obtained from conventional activities, such as exercise or the use of wet sauna, and the concentration of toxic elements in sweat was higher in females than in males. Correlation analysis of the ions revealed a correlation between the discharge of toxic elements, such as As, Be, Cd, and Ni, and discharge of Se and V, and Ni was only correlated with Mn. This study provides fundamental information on nutritional element supplementation when using wIRA sauna for detoxification.

46Estimated daily intake and health risk of heavy metals by consumption of milk.PubMed

Amir Ismail, Muhammad Riaz, Saeed Akhtar, et al.
Food Addit Contam Part B Surveill. 2015;8(4):260-5. doi: 10.1080/19393210.2015.1081989. Epub 2015 Sep 22.
Cd, Co, Pb, Cu and Ni were analysed in 480 milk samples by flame atomic absorption spectrophotometry. Mean concentrations were 0.001, 0.061, 0.014, 0.738 and 0.028 mg/kg, respectively. Mean concentration of Cd was very low, whereas Cu exceeded the maximum limits established by the Codex Alimentarius. In some areas, the Pb concentration exceeded the maximum limit as set by the Codex Alimentarius. The highest estimated daily intake (EDI) of Cu calculated for male infants (1-3 year) was 33.534 µg/kg bw/day, while the lowest EDI was recorded for Cd (0.004 µg/kg bw/day) in adult females above 16 years. The results suggested that Cu and Pb from milk in the investigated areas may pose a health risk to the consumers.

47Meta-analysis and health risk assessment of toxic heavy metals in muscles of commercial fishes in Caspian Sea.PubMed

Atefeh Amerizadeh, Mohammad Gholizadeh, Raheleh Karimi
Environ Monit Assess. 2023 Mar 9;195(4):457. doi: 10.1007/s10661-023-11076-1.
Heavy metals from contaminated seafood can have serious consequences for human health. Several studies on the amount of heavy metals in Caspian Sea fish have been conducted to ensure their food safety. This meta-analysis aimed to investigate the levels of five toxic heavy metals; Lead (Pb), Cadmium (Cd), Mercury (Hg), Chromium (Cr), and Arsenic (As) in muscles of commercial fishes of the Caspian Sea with assessing their health risk of developing oral cancer in terms of fish collection place and fish type. A systematic search was performed, and the random effect model was applied for meta-analysis. Finally, 14 studies with 30 different sets of results were included. Our results showed that the pooled estimates for Pb, Cd, Hg, Cr, and As were 0.65 mg/kg (0.52, 0.79), 0.08 mg/kg (0.07, 0.10), 0.11 mg/kg (0.07, 0.15), 1.77 mg/kg (1.26, 2.27), and 0.10 mg/kg (- 0.06, 0.26) respectively. The levels of Pb and Cd were higher than their (FAO/WHO) maximum limits. The Estimated Daily Intake (EDI) of Pb and Cd in Mazandaran, and Hg in Gilan were more than Total Daily Intake (TDI) limits. The consumers' non-carcinogenic risk (THQ) for Hg in Mazandaran and Gilan, and As in Gilan, was unsafe. Carcinogenic risk (CR) for Cr and Cd in all three provinces, and for As in Mazandaran and Gilan, was greater than 1*10 - 4 and was unsafe. The lowest and highest risk levels of oral cancer were for Rutilus kutum and Cyprinus carpio respectively.

48Trace metals in transboundary (India-Myanmar-Bangladesh) anadromous fish Tenualosa ilisha and its consequences on human health.PubMed

Afsana Parvin, Md Kamal Hossain, Afroza Parvin, et al.
Sci Rep. 2023 Nov 15;13(1):19978. doi: 10.1038/s41598-023-47142-4.
Hilsa shad (Tenualosa ilisha, Hamilton, 1822), the highly coveted table fish within the Indian subcontinent, is Bangladesh's most significant single-species fishery. To assess the risk that toxic metals pose to human health, certain health risk indices-estimated daily intake (EDI), target hazard quotient (THQ), total target hazard quotient (TTHQ), and target cancer risk (TR)-were calculated. The hierarchy of toxic metals (µg/g-ww) in Hilsa shad of the bay showed as Zn (13.64 ± 2.18) > Fe (9.25 ± 1.47) > Mn (2.98 ± 0.75) > Cu (0.57 ± 0.18) > Cr (0.23 ± 0.06) > Pb (0.22 ± 0.04) > As (0.08 ± 0.02) > Ni (0.06 ± 0.02) > Co (0.04 ± 0.01) > Cd (0.01 ± 0.003) in the wet season and Zn (11.45 ± 1.97) > Fe (10.51 ± 1.38) > Mn (3.80 ± 0.75) > Cu (0.73 ± 0.17) > Pb (0.30 ± 0.03) > Cr (0.20 ± 0.05) > As (0.09 ± 0.01) > Ni (0.08 ± 0.02) > Co (0.07 ± 0.02) > Cd (0.02 ± 0.004) in the dry season. The EDI of all the examined trace metals indicated no risk to human health from consuming Hilsa fish. The estimation of THQ and TTHQ suggested that the ingestion of both individual and combined trace metals through Hilsa shad consumption was safe from the perspective of human health. Also, there was no evidence of carcinogenic risk for consumers based on the evaluation of the TR value of metals (As, Pb, Cd, and Ni) due to Hilsa shad consumption.

49Evaluation of Potentially Toxic Trace Metals and Associated Health Risk Assessment in Buffalo Milk.PubMed

Aqsa Rafiq, Munir H Shah, Mohamed Mohany, et al.
Int J Environ Res Public Health. 2022 Nov 9;19(22):14678. doi: 10.3390/ijerph192214678.
The contamination of toxic trace metals in the food chain is one of the major threats to human health. Milk is part of a balanced diet, which is essential for proper growth, but the ingestion of contaminated milk may cause chronic health disorders. The present study is focused on the assessment of contamination of toxic trace metals in buffalo milk and the associated health risks to the consumers of Abbottabad, Pakistan. Standard analytical methods were employed to quantify the metal contents in the milk samples collected from various shops and homes in the months from June 2021 to October 2021. Health risk assessment was accomplished by computing estimated daily intake (EDI), health risk index (HRI), target hazard quotient (THQ), hazard index (HI), and target cancer risk (TCR). On a comparative basis, the mean concentration of Cr was found to be highest in both shop and home milk samples (101.3 ± 45.33 and 54.11 ± 24.20 mg/L, respectively), followed by Pb, Zn, Ni, and Cd levels. In buffalo milk collected from homes, the highest concentration of the metals was found in October, followed by July, September, June, and August. In shop milk, the increasing trend of metal contents was July > October > September > June > August. Significantly strong positive relationships were noted between the metal concentrations in the milk samples. Multivariate cluster analysis and principal component analysis exhibited significant anthropogenic contributions of the metals in buffalo milk. Mostly, the EDI and HRI values were exceeding the recommended limits; however, THQ, HI, and TCR showed that the intake of these metals through milk consumption was within the safe limit and thus revealed no significant carcinogenic or non-carcinogenic risks to the consumers. It is high time to ensure the continuous monitoring of organic/inorganic toxins in the milk and concerned authorities should take strict measures to control the contamination of milk and other food products.

50Daily intake of heavy metals and nitrate through greenhouse cucumber and bell pepper consumption and potential health risks for human.PubMed

Amir H Khoshgoftarmanesh, Forough Aghili, Azadeh Sanaeiostovar
Int J Food Sci Nutr. 2009;60 Suppl 1:199-208. doi: 10.1080/09637480902755087. Epub 2009 Mar 27.
Limited information is available on the health quality of greenhouse vegetables. Lead, cadmium, nickel, chromium, and nitrate (NO3-) concentrations in greenhouse cucumber (Cucumis sativa L.) and bell pepper (Capsicum annuum L.) and their dietary intakes were determined. The non-cancer risk for NO3- was determined using the non-cancer hazard quotient. Lead non-cancer risk in children was calculated using the Integrated Exposure-Uptake Biokinetic model. Higher concentrations of cadmium, lead, and chromium were found in bell pepper than cucumber. The mean NO3- concentration in the greenhouse cucumber was about 2.7 times higher than the World Health Organization standard limit. Cadmium, lead, nickel, and chromium daily intake for different populations groups through consumption of the vegetables were < 0.01-0.04, 0.35-1.00, 0.03-0.24, and 0.05-0.27 microg/g, respectively. The dietary intake of NO3- for adult was greater than children. Elevated lead and NO3- concentrations in the greenhouse vegetables are important concerns for consumers. Potential health quality problems in greenhouse products have to be considered.

51The etiology, diagnosis, and management of hyperhidrosis: A comprehensive review: Etiology and clinical work-up.PubMed

Shiri Nawrocki, Jisun Cha
J Am Acad Dermatol. 2019 Sep;81(3):657-666. doi: 10.1016/j.jaad.2018.12.071. Epub 2019 Jan 31.
Hyperhidrosis (HH) is a dermatologic disorder defined by sweat production exceeding thermoregulatory needs. Clinically, HH is diagnosed when excess sweating creates significant emotional, physical, or social discomfort, causing a negative impact on the patient's quality of life. Existing data imply that this condition may affect at least 4.8% of the US population. The etiology of HH may stem from a complex autonomic nervous system dysfunction, resulting in neurogenic overactivity of otherwise normal eccrine sweat glands. Alternatively, HH may be a result of aberrant central control of emotions. This condition is categorized as primary or secondary HH. Approximately 93% of patients with HH have primary HH, of whom >90% have a typical focal and bilateral distribution affecting the axillae, palms, soles, and craniofacial areas. Secondary HH presents in a more generalized and asymmetric distribution and is generated by various underlying diseases or medications. Secondary causes of HH need to be excluded before diagnosing primary HH.

52[Night sweats, a common symptom].PubMed

Yoran van Meeuwen, A S M Dofferhoff, Rebecca J H M Verheggen
Ned Tijdschr Geneeskd. 2024 Oct 16;168:D8039.
Night sweats are a common symptom. There is a lack of a uniform definition and a diagnostic guideline. In this article we propose a structural analysis for all levels of healthcare. First, we need to distinguish night sweats with or without fever. We will then discuss the main differential diagnoses (infection, malignancies, sleeping disorders and medication-related) and emphasize the role of diagnostic clues. A screening for infections, sleeping disorders and a medication review are a must for every patient. Furthermore we will explain the role of PET-CT and bone marrow examination.

53Video-assisted thoracoscopic sympathectomy for Harlequin syndrome.PubMed

Frazer Kirk, Kelsie Crathern, Andrie Stroebel
Eur J Cardiothorac Surg. 2023 Feb 3;63(2). doi: 10.1093/ejcts/ezac577.
Harlequin syndrome is an exceedingly rare condition, characterized by unilateral facial flushing and hyperhidrosis. Postulated to be dysregulated sympathetic nervous system stimulation of the dermal vasculature and blood vessels of the face. There is no clear unifying pathological cause. Due to its heterogeneity and rarity, very little is known about the treatment of it. Hereafter, we describe our experience in successfully curing right-sided Harlequin syndrome through video-assisted thoracoscopic sympathectomy.

54Sweating Disorders.PubMed

Elizabeth A Coon, William P Cheshire
Continuum (Minneap Minn). 2020 Feb;26(1):116-137. doi: 10.1212/CON.0000000000000813.
PURPOSE OF REVIEW: This article reviews disorders of sweating, including hyperhidrosis and anhidrosis due to central or peripheral autonomic nervous system causes. RECENT FINDINGS: Disorders of thermoregulation and sweating may manifest with hyperhidrosis or hypohidrosis/anhidrosis. Primary disorders of hyperhidrosis may significantly impact quality of life yet tend to be benign. Many sweating disorders present with compensatory hyperhidrosis due to areas of anhidrosis. Anhidrosis may occur due to either central or peripheral damage to the autonomic nervous system. The thermoregulatory control of sweating involves central pathways from the hypothalamus to the brainstem and then spinal cord as well as projections to peripheral structures, including the sympathetic chain ganglia, peripheral nerves, and eccrine sweat glands. Disruption at any point of this pathway may lead to impaired sweating. Characterization of sweating dysfunction helps localize different autonomic disorders to guide diagnosis and may allow for evaluation of treatment effect. SUMMARY: Sweating dysfunction manifests in myriad ways, including essential hyperhidrosis, complete anhidrosis with heat intolerance, and compensatory hyperhidrosis due to anhidrosis, and often indicates involvement of underlying central or peripheral autonomic dysfunction.

55Non-menopausal endocrine and non-endocrine causes of flushing and sweating.PubMed

Vikram Lal, Yaasir H Mamoojee, Richard Quinton
Post Reprod Health. 2017 Dec;23(4):177-182. doi: 10.1177/2053369117715371. Epub 2017 Jun 26.
Hot flushes and generalised sweating are relatively common presenting complaints, with hypogonadism an important differential diagnosis in both sexes and menopause being the most typical cause in females of climacteric age. However, a variety of other conditions do need to be carefully considered in respect of eugonadal individuals and also for those hypogonadal ones where properly dosed sex steroid replacement has failed to control flushing and sweating, or where the presentation is atypical. Alternative aetiologies may be immediately obvious from the history and physical examination, but more unusual conditions may require deeper scrutiny. This clinical review elaborates on the non-menopausal endocrine and non-endocrine causes of flushing and sweating, including both common and rarer conditions.

56Reduced serum CLCF1 levels in hyperthyroidism patients and T3-treated mice.PubMed

Xuan Zhou, Yanan Zhang, Youwen Yuan, et al.
J Endocrinol. 2024 Jul 3;262(2). doi: 10.1530/JOE-23-0412. Print 2024 Aug 1.
Characteristic symptoms of hyperthyroidism include weight loss, heart palpitation, and sweating. Thyroid hormones (TH) can stimulate thermogenesis through central and peripheral mechanisms. Previous studies have shown an association between dysfunction of cardiotrophin-like cytokine factor 1 (CLCF1) and cold-induced sweating syndrome, with recent research also indicating a link between CLCF1 and brown adipose tissue thermogenesis. However, it remains unclear whether CLCF1 and TH have synergistic or antagonistic effects on thermogenesis. This study aims to investigate the influence of thyroid hormone on circulating CLCF1 levels in humans and explore the potential possibilities of thyroid hormone in regulating energy metabolism by modulating Clcf1 in mice. By recruiting hyperthyroid patients and healthy subjects, we observed significantly lower serum CLCF1 levels in hyperthyroid patients compared to healthy subjects, with serum CLCF1 levels independently associated with hyperthyroidism after adjusting for potential confounders. Tissue analysis from mice treated with T3 revealed a decrease in CLCF1 expression in BAT and iWAT of C57BL/6 mice. These findings suggest that TH may play a role in regulating CLCF1 expression in adipose tissue.

57Diabetic autonomic neuropathy.PubMed

Aaron I Vinik, Raelene E Maser, Braxton D Mitchell, et al.
Diabetes Care. 2003 May;26(5):1553-79. doi: 10.2337/diacare.26.5.1553.
Diabetic autonomic neuropathy (DAN) is a serious and common complication of diabetes. Despite its relationship to an increased risk of cardiovascular mortality and its association with multiple symptoms and impairments, the significance of DAN has not been fully appreciated. The reported prevalence of DAN varies widely depending on the cohort studied and the methods of assessment. In randomly selected cohorts of asymptomatic individuals with diabetes, approximately 20% had abnormal cardiovascular autonomic function. DAN frequently coexists with other peripheral neuropathies and other diabetic complications, but DAN may be isolated, frequently preceding the detection of other complications. Major clinical manifestations of DAN include resting tachycardia, exercise intolerance, orthostatic hypotension, constipation, gastroparesis, erectile dysfunction, sudomotor dysfunction, impaired neurovascular function, "brittle diabetes," and hypoglycemic autonomic failure. DAN may affect many organ systems throughout the body (e.g., gastrointestinal [GI], genitourinary, and cardiovascular). GI disturbances (e.g., esophageal enteropathy, gastroparesis, constipation, diarrhea, and fecal incontinence) are common, and any section of the GI tract may be affected. Gastroparesis should be suspected in individuals with erratic glucose control. Upper-GI symptoms should lead to consideration of all possible causes, including autonomic dysfunction. Whereas a radiographic gastric emptying study can definitively establish the diagnosis of gastroparesis, a reasonable approach is to exclude autonomic dysfunction and other known causes of these upper-GI symptoms. Constipation is the most common lower-GI symptom but can alternate with episodes of diarrhea. Diagnostic approaches should rule out autonomic dysfunction and the well-known causes such as neoplasia. Occasionally, anorectal manometry and other specialized tests typically performed by the gastroenterologist may be helpful. DAN is also associated with genitourinary tract disturbances including bladder and/or sexual dysfunction. Evaluation of bladder dysfunction should be performed for individuals with diabetes who have recurrent urinary tract infections, pyelonephritis, incontinence, or a palpable bladder. Specialized assessment of bladder dysfunction will typically be performed by a urologist. In men, DAN may cause loss of penile erection and/or retrograde ejaculation. A complete workup for erectile dysfunction in men should include history (medical and sexual); psychological evaluation; hormone levels; measurement of nocturnal penile tumescence; tests to assess penile, pelvic, and spinal nerve function; cardiovascular autonomic function tests; and measurement of penile and brachial blood pressure. Neurovascular dysfunction resulting from DAN contributes to a wide spectrum of clinical disorders including erectile dysfunction, loss of skin integrity, and abnormal vascular reflexes. Disruption of microvascular skin blood flow and sudomotor function may be among the earliest manifestations of DAN and lead to dry skin, loss of sweating, and the development of fissures and cracks that allow microorganisms to enter. These changes ultimately contribute to the development of ulcers, gangrene, and limb loss. Various aspects of neurovascular function can be evaluated with specialized tests, but generally these have not been well standardized and have limited clinical utility. Cardiovascular autonomic neuropathy (CAN) is the most studied and clinically important form of DAN. Meta-analyses of published data demonstrate that reduced cardiovascular autonomic function as measured by heart rate variability (HRV) is strongly (i.e., relative risk is doubled) associated with an increased risk of silent myocardial ischemia and mortality. The determination of the presence of CAN is usually based on a battery of autonomic function tests rather than just on one test. Proceedings from a consensus conference in 1992 recommended that three tests (R-R variation, Valsalva maneuver, and postural blood pressure testing)or longitudinal testing of the cardiovascular autonomic system. Other forms of autonomic neuropathy can be evaluated with specialized tests, but these are less standardized and less available than commonly used tests of cardiovascular autonomic function, which quantify loss of HRV. Interpretability of serial HRV testing requires accurate, precise, and reproducible procedures that use established physiological maneuvers. The battery of three recommended tests for assessing CAN is readily performed in the average clinic, hospital, or diagnostic center with the use of available technology. Measurement of HRV at the time of diagnosis of type 2 diabetes and within 5 years after diagnosis of type 1 diabetes (unless an individual has symptoms suggestive of autonomic dysfunction earlier) serves to establish a baseline, with which 1-year interval tests can be compared. Regular HRV testing provides early detection and thereby promotes timely diagnostic and therapeutic interventions. HRV testing may also facilitate differential diagnosis and the attribution of symptoms (e.g., erectile dysfunction, dyspepsia, and dizziness) to autonomic dysfunction. Finally, knowledge of early autonomic dysfunction can encourage patient and physician to improve metabolic control and to use therapies such as ACE inhibitors and beta-blockers, proven to be effective for patients with CAN.

58Diabetic autonomic neuropathy.PubMed

E Niakan, Y Harati, J P Comstock
Metabolism. 1986 Mar;35(3):224-34. doi: 10.1016/0026-0495(86)90205-2.
The incidence of autonomic dysfunction as a complication of diabetes mellitus is reported to be as high as 20% to 40%. Symptoms of diabetic autonomic neuropathy (DAN) are often vague, and signs difficult to detect on routine physical examination. The early diagnosis of DAN is possible by utilizing several simple noninvasive tests, which may also be helpful in localizing the lesion(s) to specific autonomic pathways. DAN may affect multiple organ systems, to include cardiovascular, gastrointestinal, genitourinary and/or neuroendocrine, and may, in fact, be life-threatening. The same metabolic disturbances of somatic peripheral nerve may also be responsible for DAN. Like somatosensory neuropathy, definitive therapy for DAN is not yet satisfactory, although multiple chemotherapeutic agents have been tried and warrant further investigation.

59Diabetic gustatory sweating.PubMed

Dwight I Blair, Julius Sagel, Ian Taylor
South Med J. 2002 Mar;95(3):360-2.
Gustatory sweating is a potential manifestation of autonomic dysfunction in diabetes. This syndrome is seen in long-standing diabetes and is associated with nephropathy, peripheral neuropathy, and other signs of dysautonomia. Symptoms of profuse head and neck diaphoresis with eating may suggest this clinical diagnosis. We present a patient who had complicated diabetes with symptoms of gustatory sweating and other evidence of dysautonomia. Diagnosis and treatment possibilities are discussed, with a review of the literature and an emphasis on bedside testing.

60Thermoregulation in neuropathies.PubMed

Robert D Fealey
Handb Clin Neurol. 2018;157:777-787. doi: 10.1016/B978-0-444-64074-1.00048-3.
Peripheral neuropathy affecting autonomic and small sensory fibers can cause abnormalities of both autonomic and behavioral thermoregulation. Quantitative autonomic and sensory neurophysiologic tests and quantification of the linear density of intraepidermal nerve fibers potentially can stratify those at risk of impaired thermoregulation during cold and heat challenges. New data relating to thermoregulatory sweating impairment in neuropathy are presented in this chapter. Of 516 neuropathy patients analyzed, 345 were found to have thermoregulatory sweat test (TST) abnormalities with a mean percentage of anterior body surface anhidrosis (TST%) of 12% and a significant reduction in total body sweat rate, although the rate of core temperature rise with heating (slope) was not significantly different from that of patients with a normal TST. However a subset of abnormal TST patients having 25% or greater TST% showed a significantly more rapid rise in core temperature (lower slope) than age- and sex-matched neuropathy patients with a normal TST. Etiologies of neuropathy in this more severe group included diabetes, erythromelalgia, immune-mediated autonomic neuropathy, primary systemic amyloidosis, and neuropathy associated with postganglionic-autonomic degenerative disorders.

61Sweating in Systemic Abnormalities: Uremia and Diabetes Mellitus.PubMed

Hiroyuki Murota
Curr Probl Dermatol. 2016;51:57-61. doi: 10.1159/000446760. Epub 2016 Aug 30.
Sweating disorders are sometimes observed in various systemic diseases that include genetic disorders, organ damage, metabolic impairment, autoimmune diseases, and neuropathic disorders. In these diseases, various symptoms such as autonomic failures, psychopathic disorders, abnormal skin innervation, and sweat gland dysfunction can interact with one another in diverse ways, resulting in impaired sweating. This review focuses on the influence of uremia (with or without hemodialysis) and diabetes mellitus on impaired sweating. Dialysis patients perspire less, but their sweat contains higher levels of uremic toxins than do healthy subjects. Neuropathic disorders in diabetes patients develop in relation to disease severity and can impair sweating. Physicians should consider the development of various problems, such as increased body temperature, dry skin, and increased susceptibility to infection, due to decreased sweating, as they are often found in these systemic abnormalities.

62AnhidrosisPubMed

Chelsea D. Harper, Rene Bermudez
Anhidrosis is the inability to sweat. It is important to recognize anhidrosis as it can be potentially life-threatening due to heat-related illnesses. There are three main causes of anhidrosis, which are peripheral alterations in the eccrine gland itself, idiopathic, and central or neuropathic disease and/or medication that disrupts neural inputs from the anterior hypothalamus to the gland. Causes of central/neuropathic anhidrosis can occur at any level of innervation. The disturbance can occur at the sweating center in the brain, the descending neural tract, or the sweat gland. A disruption will lead to an absence of sweating. Disruption in the neural input can be due to tumors or infarctions of the hypothalamus, pons, or medulla. Spinal cord tumors, injuries, or infarctions can disrupt the neural tract. Other etiologies such as degenerative syndromes (Shy-Drager syndrome), autoimmune autonomic neuropathy, peripheral neuropathy (diabetes, alcohol use disorder, leprosy), and drugs have all been implicated in central/neuropathic anhidrosis. Peripheral alterations that cause anhidrosis can be congenital or acquired. In addition, forms of peripheral alterations can be due to genetic abnormalities such as incontinentia pigmenti, due to local destruction, for example, by a tumor, or obstruction by entities such as psoriasis. As heat intolerance may be due to various underlying disorders, a detailed history is important in establishing the diagnosis. Heat intolerance can cause drowsiness, episodic inability to concentrate while in a hot environment, or fatigue, along with a decrease in the patient's normal sweating, which are clues to the diagnosis of anhidrosis. A detailed history should also include the addition of medications, medical events such as injuries, growths or radiation, alcohol consumption, the presence of autoimmune disease or diabetes mellitus, and family history.

63Diabetic peripheral neuropathy detection of type 2 diabetes using machine learning from TCM features: a cross-sectional study.PubMed

Zhikui Tian, JiZhong Zhang, Yadong Fan, et al.
BMC Med Inform Decis Mak. 2025 Feb 18;25(1):90. doi: 10.1186/s12911-025-02932-w.
AIMS: Diabetic peripheral neuropathy (DPN) is the most common complication of diabetes mellitus. Early identification of individuals at high risk of DPN is essential for successful early intervention. Traditional Chinese medicine (TCM) tongue diagnosis, one of the four diagnostic methods, lacks specific algorithms for TCM symptoms and tongue features. This study aims to develop machine learning (ML) models based on TCM to predict the risk of diabetic peripheral neuropathy (DPN) in patients with type 2 diabetes mellitus (T2DM). METHODS: A total of 4723 patients were included in the analysis (4430 with T2DM and 293 with DPN). TFDA-1 was used to obtain tongue images during a questionnaire survey. LASSO (least absolute shrinkage and selection operator) logistic regression model with fivefold cross-validation was used to select imaging features, which were then screened using best subset selection. The synthetic minority oversampling technique (SMOTE) algorithm was applied to address the class imbalance and eliminate possible bias. The area under the receiver operating characteristic curve (AUC) was used to evaluate the model's performance. Four ML algorithms, namely logistic regression (LR), random forest (RF), support vector classifier (SVC), and light gradient boosting machine (LGBM), were used to build predictive models for DPN. The importance of covariates in DPN was ranked using classifiers with better performance. RESULTS: The RF model performed the best, with an accuracy of 0.767, precision of 0.718, recall of 0.874, F-1 score of 0.789, and AUC of 0.77. With a value of 0.879, the LGBM model appeared to be the best regarding recall Age, sweating, dark red tongue, insomnia, and smoking were the five most significant RF features. Age, yellow coating, loose teeth, smoking, and insomnia were the five most significant features of the LGBM model. CONCLUSIONS: This cross-sectional study demonstrates that the RF and LGBM models can screen for high-risk DPN in T2DM patients using TCM symptoms and tongue features. The identified key TCM-related features, such as age, tongue coating, and other symptoms, may be advantageous in developing preventative measures for T2DM patients.

64Tuberculosis prevention and treatment.PubMed

Anita Toth, Janice Fackelmann, Wendy Pigott, et al.
Can Nurse. 2004 Nov;100(9):27-30.
Tuberculosis (TB) is one of the oldest known diseases and has claimed more lives than any other Today, about one-third of the world's population is infected with TB. In 2003, 1,379 cases of new, active and relapsed TB were reported in Canada. TB is caused by Mycobacterium tuberculosis. Only 10 per cent of infected individuals will develop active TB. Pulmonary TB can be spread by an infectious person through the aerosolization of droplets when coughing, talking, spitting, sneezing or singing. Symptoms of pulmonary TB are a cough with or without sputum production lasting at least three weeks, chest pain, hemoptysis, fever, night sweats, weight loss, lack of appetite, chills and weakness. Extrapulmonary TB is generally not associated with person-to-person spread. Common sites include the throat, lymph nodes, abdomen, intestines, long bones of the legs, spine, kidneys, bladder, skin, eyes and meninges. The risk factors for TB infection and disease include close contact with an active pulmonary TB case, HIV infection or AIDS, inactive disease not adequately treated, low income, underlying medical condition, homelessness, alcoholism, injection drug use, aboriginal background or occupation in health care. Risk settings include travel or residence in an endemic area or work or residence in a correctional facility, shelter, rooming house, residential facility, hospital or long-term care facility. Nurses need to advocate for the prompt diagnosis and isolation of suspected and confirmed TB cases. Knowing when to institute such measures as isolation in a negative pressure room, using respirator masks and limiting interpersonal contacts is vital to the nursing care of TB patients. In addition, the role of the public health department needs to be understood; for example, all jurisdictions have legislated requirements for reporting new positive TB skin tests to public health.

65Predictors and outcomes of disseminated tuberculosis in an intermediate burden setting.PubMed

L Meira, C Chaves, D Araújo, et al.
Pulmonology. 2019 Nov-Dec;25(6):320-327. doi: 10.1016/j.pulmoe.2018.11.001. Epub 2019 Feb 26.
SETTING: University-affiliated hospital located in Porto, North Portugal, an area with a low to intermediate incidence of tuberculosis (TB). OBJECTIVE: To identify predictors and outcomes of disseminated TB (dTB). DESIGN: A cohort of patients diagnosed with TB between 2007 and 2013 was retrospectively analysed. Patients with dTB criteria were characterized and compared to single organ TB cases. Factors independently associated with dTB were determined by multivariate logistic regression analysis. RESULTS: A total of 744 patients were analysed, including 145 with dTB. Independent risk factors for dTB were pharmacological immunosuppression (OR 5.6, 95% CI 2.8-11.3), HIV infection (OR 5.1, 95% CI 3.1-8.3), chronic liver failure or cirrhosis (OR 2.3, 95% CI 1.4-4.1) and duration of symptoms (OR 2.3, 95% CI 1.4-3.8). Compared to single organ TB, the clinical presentation of dTB patients differed by the absence of haemoptysis (OR 3.2, 95% CI 1.3-8.4) and of dyspnoea (OR 1.9, 95% CI 1.2-3.1), presence of weight loss (OR 1.8, 95% CI 1.1-2.9), night sweats (OR 1.7, 95% CI 1.1-2.7) and bilateral lung involvement (OR 4.4, 95% CI 2.8-7.1). Mortality and time until culture conversion were higher for dTB patients, although not reaching statistical significance. CONCLUSION: Immunosuppressive conditions and chronic liver failure or cirrhosis were associated with increased risk of dTB. The haematogenous spread may be dependent on longer symptomatic disease and usually progresses with bilateral lung involvement.

66Does incarceration change the profile of pulmonary tuberculosis in Tunisia?PubMed

Soumaya Ben Saad-Baouab, Islam Mejri, Hedia Bellili, et al.
Tunis Med. 2019 Apr;97(4):541-550.
INTRODUCTION: Tuberculosis of the prisoner remains unknown in Tunisia. The aim of our study was to establish the clinical, radiological, bacteriological and prognostic features of pulmonary tuberculosis in patients with a history of incarceration. METHODS: Case-control study conducted between 2010 and 2016 in two pulmonology departments of Abderrahmane Mami Hospital. The cases were male patients, hospitalized for pulmonary tuberculosis with a history of incarceration. Three controls for one case were randomly selected from the list of male patients hospitalized for pulmonary tuberculosis in the same departments as the cases but with no history of incarceration. RESULTS: The study included 58 cases and 174 controls. The average age of cases was lower than in controls (36,5 years vs 43,4 years; p <0.001). The cases had a significantly worse socioeconomic conditions and educational level with no more frequent social coverage of the disease. Risk factors for TB (smoking, alcoholism, substance abuse, unprotected sex, tuberculosis contagion, viral hepatitis C) were significantly higher among cases. Weight loss and night sweats were significantly more common in both cases, as was undernutrition. Positive bacilloscopies prevailed in the cases (36,5 vs 43,4;p = 0.047). In controls, the institution delay was longer (4.38 days vs 10.24 days; p= 0.004) and the total duration of treatment was lower (7.16 mounths vs 6.55 mounths; p = 0.048). CONCLUSION: Pulmonary TB in prisoner predominates in young people with poor socio-economic status and poor educational attainment. It is associated with several risk factors for TB and malnutrition. Health education in prisons is needed to combat this condition.

67Healthcare seeking patterns for TB symptoms: Findings from the first national TB prevalence survey of South Africa, 2017-2019.PubMed

Sizulu Moyo, Farzana Ismail, Nkateko Mkhondo, et al.
PLoS One. 2023 Mar 15;18(3):e0282125. doi: 10.1371/journal.pone.0282125. eCollection 2023.
BACKGROUND: Although tuberculosis (TB) symptoms have limited sensitivity they remain an important entry point into the TB care cascade. OBJECTIVES: To investigate self-reported healthcare seeking for TB symptoms in participants in a community-based survey. METHODS: We compared reasons for not seeking care in participants reporting ≥1 of four TB screening symptoms (cough, weight loss, night sweats, fever) in the first South African national TB prevalence survey (2017-2019). We used logistic regression analyses to identify sociodemographic and clinical characteristics associated with healthcare seeking. RESULTS: 5,168/35,191 (14.7%) survey participants reported TB symptoms and 3,442/5168 had not sought healthcare. 2,064/3,442(60.0%) participants intended to seek care, 912 (26.5%) regarded symptoms as benign, 399 (11.6%) reported access barriers(distance and cost), 36 (1.0%) took other medications and 20(0.6%) reported health system barriers. Of the 57/98 symptomatic participants diagnosed with bacteriologically confirmed TB who had not sought care: 38(66.7%) intended to do so, 8(14.0%) regarded symptoms as benign, and 6(10.5%) reported access barriers. Among these 98, those with unknown HIV status(OR 0.16 95% CI 0.03-0.82), p = 0.03 and those who smoked tobacco products(OR 0.39, 95% CI 0.17-0.89, p = 0.03) were significantly less likely to seek care. CONCLUSIONS: People with TB symptoms delayed seeking healthcare, many regarded symptoms as benign while others faced access barriers. Those with unknown HIV status were significantly less likely to seek care. Strengthening community-based TB awareness and screening programmes together with self-screening models could increase awareness of the significance of TB symptoms and contribute to improving healthcare seeking and enable many people with TB to enter the TB care cascade.

68Management of Menopausal Symptoms: A Review.PubMed

Carolyn J Crandall, Jaya M Mehta, JoAnn E Manson
JAMA. 2023 Feb 7;329(5):405-420. doi: 10.1001/jama.2022.24140.
IMPORTANCE: Menopause, due to loss of ovarian follicular activity without another pathological or physiological cause, typically occurs between the ages of 45 years and 56 years. During the menopausal transition, approximately 50% to 75% of women have hot flashes, night sweats, or both (vasomotor symptoms) and more than 50% have genitourinary symptoms (genitourinary syndrome of menopause [GSM]). OBSERVATIONS: Vasomotor symptoms typically last more than 7 years and GSM is often chronic. Efficacious treatments for women with bothersome vasomotor symptoms or GSM symptoms include hormonal and nonhormonal options. Systemic estrogen alone or combined with a progestogen reduces the frequency of vasomotor symptoms by approximately 75%. Oral and transdermal estrogen have similar efficacy. Conjugated equine estrogens (CEE) with or without medroxyprogesterone acetate (MPA) were the only hormonal treatments for which clinical trials were designed to examine cardiovascular events, venous thromboembolism, and breast cancer risk. Compared with placebo, the increased risk of stroke and venous thromboembolism associated with CEE (with or without MPA) and breast cancer (with use of CEE plus MPA) is approximately 1 excess event/1000 person-years. Low-dose CEE plus bazedoxifene is not associated with increased risk of breast cancer (0.25%/year vs 0.23%/year with placebo). Bioidentical estrogens approved by the US Food and Drug Administration (with identical chemical structure to naturally produced estrogens, and often administered transdermally) also are available to treat vasomotor symptoms. For women who are not candidates for hormonal treatments, nonhormonal approaches such as citalopram, desvenlafaxine, escitalopram, gabapentin, paroxetine, and venlafaxine are available and are associated with a reduction in frequency of vasomotor symptoms by approximately 40% to 65%. Low-dose vaginal estrogen is associated with subjective improvement in GSM symptom severity by approximately 60% to 80%, with improvement in severity by 40% to 80% for vaginal prasterone, and with improvement in severity by 30% to 50% for oral ospemifene. CONCLUSIONS AND RELEVANCE: During the menopausal transition, approximately 50% to 75% of women have vasomotor symptoms and GSM symptoms. Hormonal therapy with estrogen is the first-line therapy for bothersome vasomotor symptoms and GSM symptoms, but nonhormonal medications (such as paroxetine and venlafaxine) also can be effective. Hormone therapy is not indicated for the prevention of cardiovascular disease.

69Vasomotor symptoms of menopause, autonomic dysfunction, and cardiovascular disease.PubMed

Emma Lee, Miguel Anselmo, Chowdhury Tasnova Tahsin, et al.
Am J Physiol Heart Circ Physiol. 2022 Dec 1;323(6):H1270-H1280. doi: 10.1152/ajpheart.00477.2022. Epub 2022 Nov 11.
Cardiovascular disease (CVD), the leading cause of death among US adults, is more prevalent in menopausal females compared with age-matched males. Vasomotor symptoms of menopause (VMS; hot flashes/flushes and night sweats) are common among females undergoing menopausal transition and have been associated with elevated blood pressure (BP) and increased CVD risk. Autonomic dysregulation of BP has been posited as a contributing factor to the elevated CVD risk in menopausal females with VMS. This review includes ) a brief overview of the relationship between VMS and CVD, ) mechanisms of hot flushes and their potential impact on short- and long-term BP regulation, and ) how the disruption of autonomic function associated with VMS might provide a mechanistic pathway to CVD development. Finally, this review will highlight knowledge gaps and future directions toward better understanding of hot flush physiology and VMS contributions to CVD.

70Understanding the pathophysiology of vasomotor symptoms (hot flushes and night sweats) that occur in perimenopause, menopause, and postmenopause life stages.PubMed

D C Deecher, K Dorries
Arch Womens Ment Health. 2007;10(6):247-57. doi: 10.1007/s00737-007-0209-5. Epub 2007 Dec 12.
Vasomotor symptoms (VMS), commonly called hot flashes or flushes (HFs) and night sweats, are the menopausal symptoms for which women seek treatment during menopause most often. VMS are a form of temperature dysfunction that occurs due to changes in gonadal hormones. Normally, core body temperature (CBT) remains within a specific range, oscillating with daily circadian rhythms. Physiological processes that conserve and dissipate heat are responsible for maintaining CBT, and tight regulation is important for maintenance of optimal internal organ function. Disruption of this tightly controlled temperature circuit results in exaggerated heat-loss responses and presents as VMS. The mechanistic role related to changes in gonadal hormones associated with VMS is not understood. Hormone therapy is the most effective treatment for VMS and other menopausal symptoms. Estrogens are known potent neuromodulators of numerous neuronal circuits throughout the central nervous system. Changing estrogen levels during menopause may impact multiple components involved in maintaining temperature homeostasis. Understanding the pathways and mechanisms involved in temperature regulation, probable causes of thermoregulatory dysfunction, and "brain adaptation" will guide drug discovery efforts. This review considers the processes and pathways involved in normal temperature regulation and the impact of fluctuating and declining hormones that result in VMS during the menopausal transition.

71Persistent Night Sweats: Diagnostic Evaluation.PubMed

Carl Bryce
Am Fam Physician. 2020 Oct 1;102(7):427-433.
Night sweats are a nonspecific symptom that patients commonly experience but rarely discuss with their physicians without prompting. Although many life-threatening causes such as malignancies or infections have been described, most patients who report persistent night sweats in the primary care setting do not have a serious underlying disorder. Conditions commonly associated with night sweats include menopause, mood disorders, gastroesophageal reflux disease, hyperthyroidism, and obesity. If a clinical diagnosis is apparent based on the initial history and physical examination, specific treatment for four to eight weeks may be offered. When the history and physical examination do not reveal a specific cause, physicians should proceed with a systematic and cost-conscious strategy that uses readily available laboratory and imaging studies, such as a complete blood count, tuberculosis testing, thyroid-stimulating hormone levels, HIV testing, C-reactive protein level, and chest radiography. Additional tests that could be considered selectively include computed tomography of the chest and/or abdomen, bone marrow biopsy, polysomnography, and/or additional laboratory studies if indicated. If these results are normal, and no additional disorders are suspected, reassurance and continued monitoring are recommended. The presence of night sweats alone does not indicate an increased risk of death.

72Primary hyperhidrosis: an updated review.PubMed

Mahan Maazi, Alexander Kc Leung, Joseph M Lam
Drugs Context. 2025 Jun 16;14. doi: 10.7573/dic.2025-3-2. eCollection 2025.
BACKGROUND: Hyperhidrosis (HH) is a condition characterized by excessive sweating beyond the physiological needs of thermoregulation. HH can be classified as primary (idiopathic) hyperhidrosis (PHH) or secondary hyperhidrosis (SHH), which is associated with underlying medical conditions, medications or systemic disorders. This narrative review provides an updated overview of PHH, with a focus on epidemiology, aetiopathogenesis, clinical manifestations, diagnostic approaches and current management strategies, particularly highlighting pharmacological and procedural treatment options. METHODS: A literature search was conducted in February 2025 across Ovid Medline, EMBASE and the Cochrane Central Register of Controlled Trials (CENTRAL) using the key term "hyperhidrosis". The review included observational studies, clinical trials, narrative reviews, guidelines and meta-analyses published in the past 10 years. Additional references were identified through manual searches of relevant bibliographies. RESULTS: The global prevalence of PHH is estimated to range between 0.072% and 9%, with PHH accounting for 93% of all HH cases. Whilst the precise pathophysiology remains unclear, PHH is believed to result from sympathetic overactivity, whereas SHH is associated with endocrine, neurological, infectious, malignant and medication-induced causes. PHH is diagnosed clinically and distinguishing between primary and secondary forms is essential. Management options vary based on severity, ranging from topical therapies (antiperspirants, anticholinergics), systemic medications (oral anticholinergics, adrenergic modulators), device-based interventions (iontophoresis, microwave thermolysis), injectable therapies (botulinum toxin) and surgical approaches (sympathectomy, excision, liposuction/curettage). Whilst these interventions can significantly improve symptoms and quality of life, long-term efficacy, recurrence and adverse effects remain concerns. CONCLUSION: PHH significantly impacts the quality life of patients contributing to both physical discomfort and psychosocial distress. An individualized, multi-modal approach is crucial to optimizing management. Further research is warranted to refine existing therapies and evaluate emerging treatment modalities for improved long-term outcomes.

73High concentration of sweat calcium, magnesium and phosphate in chronic renal failure.PubMed

C A Prompt, P M Quinton, C R Kleeman
Nephron. 1978;20(1):4-9. doi: 10.1159/000181189.
Sweat collected from the forearm of chronic renal failure and control patients, after iontophoretic stimulation with pilocarpine, was analyzed for Na, K, Cl, Mg, phosphate and urea. Concentrations of Ca, Mg and phosphate in sweat from chronic renal failure patients were significantly elevated (p less than 0.05) as compared to controls, while the concentrations of Na, K, and Cl were normal. The mean sweat rates and apparent skin conductivities were lower in uremics, but not significantly different from controls (0.05 less than p less than 0.10). Tentatively it is concluded that the increase of Ca, Mg and phosphate in uremic sweat is due to an increase in the secretion of these electrolytes in the secretory portion of the sweat gland, while the reabsorptive duct is normal.

74Uric acid and urea in human sweat.PubMed

Chien-Tsai Huang, Mei-Lien Chen, Li-Ling Huang, et al.
Chin J Physiol. 2002 Sep 30;45(3):109-15.
The present study investigated whether thermal sweating may relieve elevated concentrations of serum uric acid or urea. Concentrations of uric acid and urea were measured in the sweat of sixteen male volunteers, who were treated with external heat after one hour of intense physical exercise. The same analytes were also measured in their urine and serum samples. Furthermore, creatinine and some electrolytes were determined in these specimens. The results show that the concentration of uric acid in the sweat is 24.5 micromol/L, which is only 6.3% of that in serum. The concentration of urea in the sweat is 22.2 mmol/L, which is 3.6 times that in serum. The results indicate that sweat uric acid concentration is quite minimal, and the estimated total uric acid excretion per day in normal physiological range is insignificant. However, the level of sweat urea was found at a much higher concentration than the serum level. No correlation could be established between the level of uric acid in sweat and in serum. There was also no correlation between the level of urea in sweat and that in serum. These results suggest it would not be effective to relieve the elevated serum uric acid concentration by thermal sweating when the renal excretion of uric acid is partly compromised. Nevertheless, the potential of urea excretion via profuse sweating is apparent particularly when the kidneys are damaged or their function is impaired. These findings also suggest that persons who take vigorous exercise or are exposed to hot environments should be well advised to drink adequate fluids since heavy sweating excretes only minimal uric acid, accompanied by significant diminution of urinary output and diminished urinary excretions of uric acid, which may induce elevated levels of serum uric acid.

75Urea transporters and sweat response to uremia.PubMed

Raymond W Keller, James L Bailey, Yanhua Wang, et al.
Physiol Rep. 2016 Jun;4(11). doi: 10.14814/phy2.12825.
In humans, urea is excreted in sweat, largely through the eccrine sweat gland. The urea concentration in human sweat is elevated when compared to blood urea nitrogen. The sweat urea nitrogen (UN) of patients with end-stage kidney disease (ESRD) is increased when compared with healthy humans. The ability to produce sweat is maintained in the overwhelming majority of ESRD patients. A comprehensive literature review found no reports of sweat UN neither in healthy rodents nor in rodent models of chronic kidney disease (CKD). Therefore, this study measured sweat UN concentrations in healthy and uremic rats. Uninephrectomy followed by renal artery ligation was used to remove 5/6 of renal function. Rats were then fed a high-protein diet to induce uremia. Pilocarpine was used to induce sweating. Sweat droplets were collected under oil. Sweat UN was measured with a urease assay. Serum UN was measured using a fluorescent ortho-pthalaldehyde reaction. Immunohistochemistry (IHC) was accomplished with a horseradish peroxidase and diaminobenzidine technique. Sweat UN in uremic rats was elevated greater than two times compared to healthy pair-fed controls (220 ± 17 and 91 ± 15 mmol/L, respectively). Post hoc analysis showed a significant difference between male and female uremic sweat UN (279 ± 38 and 177 ± 11 mmol/L, respectively.) IHC shows, for the first time, the presence of the urea transporters UT-B and UT-A2 in both healthy and uremic rat cutaneous structures. Future studies will use this model to elucidate how rat sweat UN and other solute excretion is altered by commonly prescribed diuretics.

76The Expression of AQP5 and UTs in the Sweat Glands of Uremic Patients.PubMed

Liyi Xie, Li Jin, Jie Feng, et al.
Biomed Res Int. 2017;2017:8629783. doi: 10.1155/2017/8629783. Epub 2017 Nov 27.
PURPOSE: To research the distribution and quantitative changes of UT-A1, UT-B1, and AQP5 in uremic skin tissue. METHODS: 34 cases of uremic patients (UP) and 11 controls were recruited. Immunohistochemistry, immunofluorescence, RT-PCR, and Western Blot were used to identify the proteins in sweat glands. RESULTS: AQP5, UT-A1, and UT-B1 were expressed and localized in human skin basal lines, skin sweat glands, and sweat ducts, both in UP and controls. Compared to controls, AQP5 mRNA abundance was significantly decreased in UP ( < 0.01), and, with the decrease of eGFR, the AQP5 expression was significantly decreased ( < 0.05). By contrast, UT-A1 and UT-B1 mRNA abundance was significantly increased in the skin of UP compared with the control ( < 0.01), and, with the decrease of eGFR, the AQP5 expression was significantly increased ( < 0.05). We found that the gene changes were coincident with the corresponding target proteins. The urea transporter subtypes, UT-A1 and UT-B1, were expressed in the skin basal cell layer and exocrine sweat glands. The abundance of UT-A1 and UT-B1 in uremic sweat glands was significantly increased in UP, while the expression of AQP5 was decreased. CONCLUSION: Elimination of urea through the skin by producing sweat is a potential therapeutic strategy for renal failure patients.

77The correlation of urea and creatinine concentrations in sweat and saliva with plasma during hemodialysis: an observational cohort study.PubMed

Sophie Adelaars, Constantijn J A M Konings, Lieke Cox, et al.
Clin Chem Lab Med. 2024 Jan 23;62(6):1118-1125. doi: 10.1515/cclm-2023-1285. Print 2024 May 27.
OBJECTIVES: Urea and creatinine concentrations in plasma are used to guide hemodialysis (HD) in patients with end-stage renal disease (ESRD). To support individualized HD treatment in a home situation, there is a clinical need for a non-invasive and continuous alternative to plasma for biomarker monitoring during and between cycles of HD. In this observational study, we therefore established the correlation of urea and creatinine concentrations between sweat, saliva and plasma in a cohort of ESRD patients on HD. METHODS: Forty HD patients were recruited at the Dialysis Department of the Catharina Hospital Eindhoven. Sweat and salivary urea and creatinine concentrations were analyzed at the start and at the end of one HD cycle and compared to the corresponding plasma concentrations. RESULTS: A decrease of urea concentrations during HD was observed in sweat, from 27.86 mmol/L to 12.60 mmol/L, and saliva, from 24.70 mmol/L to 5.64 mmol/L. Urea concentrations in sweat and saliva strongly correlated with the concentrations in plasma (ρ 0.92 [p<0.001] and 0.94 [p<0.001], respectively). Creatinine concentrations also decreased in sweat from 43.39 μmol/L to 19.69 μmol/L, and saliva, from 59.00 μmol/L to 13.70 μmol/L. However, for creatinine, correlation coefficients were lower than for urea for both sweat and saliva compared to plasma (ρ: 0.58 [p<0.001] and 0.77 [p<0.001], respectively). CONCLUSIONS: The results illustrate a proof of principle of urea measurements in sweat and saliva to monitor HD adequacy in a non-invasive and continuous manner. Biosensors enabling urea monitoring in sweat or saliva could fill in a clinical need to enable at-home HD for more patients and thereby decrease patient burden.

78Uremic neuropathy: clinical features and new pathophysiological insights.PubMed

Arun V Krishnan, Matthew C Kiernan
Muscle Nerve. 2007 Mar;35(3):273-90. doi: 10.1002/mus.20713.
Neuropathy is a common complication of end-stage kidney disease (ESKD), typically presenting as a distal symmetrical process with greater lower-limb than upper-limb involvement. The condition is of insidious onset, progressing over months. and has been estimated to be present in 60%-100% of patients on dialysis. Neuropathy generally only develops at glomerular filtration rates of less than 12 ml/min. The most frequent clinical features reflect large-fiber involvement, with paresthesias, reduction in deep tendon reflexes, impaired vibration sense, muscle wasting, and weakness. Nerve conduction studies demonstrate findings consistent with a generalized neuropathy of the axonal type. Patients may also develop autonomic features, with postural hypotension, impaired sweating, diarrhea, constipation, or impotence. The development of uremic neuropathy has been related previously to the retention of neurotoxic molecules in the middle molecular range, although this hypothesis lacked formal proof. Studies utilizing novel axonal excitability techniques have recently shed further light on the pathophysiology of this condition. Nerves of uremic patients have been shown to exist in a chronically depolarized state prior to dialysis, with subsequent improvement and normalization of resting membrane potential after dialysis. The degree of depolarization correlates with serum K(+), suggesting that chronic hyperkalemic depolarization plays an important role in the development of nerve dysfunction in ESKD. These recent findings suggest that maintenance of serum K(+) within normal limits between periods of dialysis, rather than simple avoidance of hyperkalemia, is likely to reduce the incidence and severity of uremic neuropathy.

79Heat stress and thermal strain challenges in running.PubMed

Michael F Bergeron
J Orthop Sports Phys Ther. 2014 Oct;44(10):831-8. doi: 10.2519/jospt.2014.5500. Epub 2014 Aug 7.
Running well and safely in the heat is challenging for all runners, from recreational to elite. As environmental heat stress (heat stress modulated or augmented by air temperature, humidity, wind speed, and solar radiation) and the intensity and duration of a training run or race increase, so are metabolic heat production, the parallel need for heat transfer from the body to maintain thermal equilibrium, the consequent increase in blood flow to the skin, and the concomitant sweating response progressively and proportionally amplified. An accumulating total body-water deficit from extensive sweating and escalating level of cardiovascular and thermal strain will, in due course, considerably challenge a runner's physiology, perception of effort, and on-course well-being and performance. However, with the appropriate preparation and modifications to planned running intensity and distance, runners can safely tolerate and effectively train and compete in a wide range of challenging environmental conditions. Clinicians play a key role in this regard as an effective resource for providing the most effective guidelines and making the best overall individual recommendations regarding training and competing in the heat.

80Heat illness in children.PubMed

Jeffrey R Bytomski, Deborah L Squire
Curr Sports Med Rep. 2003 Dec;2(6):320-4. doi: 10.1249/00149619-200312000-00007.
With an increasing number of children and adolescents involved in competitive athletics throughout the calendar year, the sports medicine team must be familiar with preventing and treating heat-related illness. Heat illness is a spectrum of illnesses from heat cramps to heat stroke. Mortality for heat stroke ranges from 17% to 70%, depending on severity and age of the patient. Children are more susceptible to heat illness than adults for many reasons, including a greater surface area to body mass ratio, lower rate of sweating, and slower rate of acclimatization. The prevention of heat illness is based on recognizing and modifying risk factors, which include environmental conditions, clothing, hydration, and acclimatization. Once heat illness is suspected, treatment should begin immediately with rapid cooling procedures started on the field.

81Heat illness. Fluid and electrolyte issues for pediatric and adolescent athletes.PubMed

D L Squire
Pediatr Clin North Am. 1990 Oct;37(5):1085-109. doi: 10.1016/s0031-3955(16)36976-0.
The primary mechanism for maintaining normal body temperature during physical exercise in the heat is the evaporation of sweat. With profuse sweating, water loss far exceeds electrolyte loss. Rigorous exercise in the heat places the athlete at risk for thermoregulatory dysfunction from dehydration. Because children are inherently less efficient thermoregulators than adults, they are at even greater risk for heat illness. The three primary syndromes of heat illness are heat cramps, heat exhaustion, and heat stroke. Treatment of heat illness is based on reduction of body temperature and rehydration. Heat stroke is a true medical emergency with a high mortality rate; immediate reduction of body temperature is critical to the survival of these patients. Prevention of heat illness is based on reducing known risk factors. Physical activity should be modified in the face of high ambient temperature and humidity. The athlete should begin exercise well hydrated; frequent consumption of cold water during exercise decreases likelihood of significant dehydration. After exercise, the athlete should continue drinking to replace fluid losses. Clothing should be lightweight; the more skin exposed, the greater the available evaporative surface. A preseason conditioning program, when combined with an 8- to 14-day period of acclimatization, further reduces the risk of heat injury. Although athletes engaged in endurance sports may benefit from drinking carbohydrate/electrolyte-containing solutions, for the majority of young athletes, cold water remains the preferred choice for fluid replacement during exercise. The relatively greater body surface area of young athletes also places them at risk for hypothermia. Special attention should be given when these athletes are competing under cold environmental conditions.

82Sweat as an Efficient Natural Moisturizer.PubMed

Tetsuo Shiohara, Yohei Sato, Yurie Komatsu, et al.
Curr Probl Dermatol. 2016;51:30-41. doi: 10.1159/000446756. Epub 2016 Aug 30.
Although recent research on the pathogenesis of allergic skin diseases such as atopic dermatitis has focused on defects in skin genes important for maintaining skin barrier function, the fact that excreted sweat has an overwhelmingly great capacity to increase skin surface hydration and contains moisturizing factors has long been ignored: the increase in water loss induced by these gene defects could theoretically be compensated fully by a significant increase in sweating. In this review, the dogma postulating the detrimental role of sweat in these diseases has been challenged on the basis of recent findings on the physiological functions of sweat, newly recognized sweat gland-/duct-related skin diseases, and therapeutic approaches to the management of these diseases. We are now beginning to appreciate that sweat glands/ducts are a sophisticated regulatory system. Furthermore, depending on their anatomical location and the degree of the impairment, this system might have a different function: sweating responses in sweat glands/ducts located at the folds in hairy skin such as on the trunk and extremities could function as natural regulators that maintain skin hydration under quiescent basal conditions, in addition to the better-studied thermoregulatory functions, which can be mainly mediated by those at the ridges. The normal functioning of sweat could be disturbed in various inflammatory skin diseases. Thus, we should recognize sweating disturbance as an etiologic factor in the development of these diseases.

83Sweat is a most efficient natural moisturizer providing protective immunity at points of allergen entry.PubMed

Tetsuo Shiohara, Yoshiko Mizukawa, Yurie Shimoda-Komatsu, et al.
Allergol Int. 2018 Oct;67(4):442-447. doi: 10.1016/j.alit.2018.07.010. Epub 2018 Sep 1.
Although there is a growing acceptance that sweat could play a detrimental role in various allergic skin diseases, the possibility that sweat is also involved in maintenance of skin hydration and skin-specific immune responses has not been acknowledged. We initially describe physiological role of sweat in both maintaining skin hydration and thermoregulation. The purpose of this article is to provide the reader with objective evidence that sweating is intimately linked to vital stratum corneum barrier function and usefulness of application of moisturizers in clinical care of allergic skin diseases. This review also covers how sweating disturbance would leave the skin vulnerable to the development of various allergic skin diseases, such as atopic dermatitis. New therapeutic approaches would specifically target such sweating disturbance in these allergic skin diseases.

84Exploring the Potential Link between Aluminum-Containing Deodorants/Antiperspirants and Breast Cancer: A Comprehensive Review.PubMed

Tony Hangan, Geir Bjorklund, Sergiu Chirila
Curr Med Chem. 2025;32(3):417-433. doi: 10.2174/0109298673269343231025070053.
The potential association between aluminum-containing deodorants/antiperspirants and breast cancer has been investigated and debated. This paper comprehensively analyzes existing literature to examine the evidence and provide insights into this relationship. This comprehensive review discusses aspects related to the absorption and distribution of aluminum compounds, its effects on the induction of oxidative stress, the estrogenic activity of aluminum, and potential disruption of hormonal pathways, and the potential role in breast cancer induction. Currently, available research, consisting of epidemiological studies as well as clinical trials, together with meta-analyses and previously published reviews conducted on identifying the relationship between aluminum-containing deodorants/antiperspirants and the risk of breast cancer were also analyzed and discussed. Societal factors, personal hygiene considerations, and lifestyle changes contribute to the increased usage of antiperspirants, but they do not establish a direct causal connection with breast cancer. Further research employing larger-scale studies and rigorous methodologies must validate the existing findings and explore the underlying mechanisms involved. Continued multidisciplinary research efforts and collaboration between researchers, regulatory bodies, and public health authorities are vital to developing a more definitive understanding of this complex topic.

85Breast Cancer and Deodorants/Antiperspirants: a Systematic Review.PubMed

Mohamed Farouk Allam
Cent Eur J Public Health. 2016 Sep;24(3):245-247. doi: 10.21101/cejph.a4475.
BACKGROUND: Over the last decade, the possible association between underarm deodorants/ antiperspirants use and breast cancer risk has raised important interest in the scientific community. The objective of our systematic review is to estimate the pooled risk of deodorants/antiperspirants use for breast cancer. METHODS: All observational studies that evaluated the association between breast cancer risk and deodorants/antiperspirants use were reviewed. We have only identified two case-control studies, carried out between 2002 and 2006. RESULTS: The first study was conducted in USA and investigated the possible relationship between use of products applied for underarm perspiration and the risk for breast cancer in women aged 20-74 years. This population-based case-control study gathered information by in-person interview. The second study was conducted in Iraq and investigated the possible relationship between use of antiperspirants and the risk for breast cancer in women attending a teaching hospital. This study also gathered information by in-person interview. There was no risk of antiperspirants use in the pooled risk (odds ratio 0.40, 95% confidence interval 0.35-0.46). CONCLUSION: Our comprehensive search has identified an insufficient number of studies to conduct a quantitative review and obtain reliable results. Further prospective studies are strongly needed.

86The Health Effects of Aluminum Exposure.PubMed

Katrin Klotz, Wobbeke Weistenhöfer, Frauke Neff, et al.
Dtsch Arztebl Int. 2017 Sep 29;114(39):653-659. doi: 10.3238/arztebl.2017.0653.
BACKGROUND: Aluminum is regularly taken up with the daily diet. It is also used in antiperspirants, as an adjuvant for vaccination, and in desensitization procedures. In this review, we present the scientifically documented harmful effects of aluminum on health and the threshold values associated with them. METHODS: This review is based on publications retrieved by a selective search of the PubMed and SCOPUS databases on the topic of aluminum in connection with neurotoxicity, Alzheimer's disease, and breast cancer, as well as on the authors' personal experience in occupational and environmental medicine. RESULTS: The reference values for the internal aluminum load (<15 μg/L in urine, <5 μg/L in serum) are especially likely to be exceeded in persons with occupational exposure. The biological tolerance value for occupational exposure is 50 μg of aluminum per gram of creatinine in the urine. For aluminum welders and workers in the aluminum industry, declining performance in neuropsychological tests (attention, learning, memory) has been found only with aluminum concentrations exceeding 100 μg/g creatinine in the urine; manifest encephalopathy with dementia was not found. Elevated aluminum content has been found in the brains of persons with Alzheimer's disease. It remains unclear whether this is a cause or an effect of the disease. There is conflicting evidence on carcinogenicity. The contention that the use of aluminum-containing antiperspirants promotes breast cancer is not supported by consistent scientific data. CONCLUSION: The internal aluminum load is measured in terms of the concentration of aluminum in urine and blood. Keeping these concentrations below the tolerance values prevents the development of manifest and subclinical signs of aluminum toxicity. Large-scale epidemiologic studies of the relationship between aluminum-containing antiperspirants and the risk of breast cancer would be desirable.

87If exposure to aluminium in antiperspirants presents health risks, its content should be reduced.PubMed

Alain Pineau, Bernard Fauconneau, André-Pascal Sappino, et al.
J Trace Elem Med Biol. 2014 Apr;28(2):147-150. doi: 10.1016/j.jtemb.2013.12.002. Epub 2013 Dec 19.
Since aluminium (Al) pervades our environment, the scientific community has for many years raised concerns regarding its safety in humans. Al is present in numerous cosmetics such as antiperspirants, lipsticks and sunscreens. Al chlorohydrate is the active antiperspirant agent in underarm cosmetics and may constitute for Al a key exposure route to the human body and a potential source of damage. An in vitro study has demonstrated that Al from antiperspirant can be absorbed through viable human stripped skin. The potential toxicity of Al has been clearly shown and recent works convincingly argue that Al could be involved in cancerogenic processes. Nowadays, for example, Al is suspected of being involved in breast cancer. Recent work in cells in culture has lent credence to the hypothesis that this metal could accumulate in the mammary gland and selectively interfere with the biological properties of breast epithelial cells, thereby promoting a cascade of alterations reminiscent of the early phases of malignant transformation. In addition, several studies suggest that the presence of Al in human breast could influence metastatic process. As a consequence, given that the toxicity of Al has been widely recognized and that it is not a physiological component in human tissues, reducing the concentration of this metal in antiperspirants is a matter of urgency.

88A 7-Month Multidisciplinary Healthy Lifestyle Intervention Effectively Improved Cardiometabolic Risk Profile of Firefighters.PubMed

Daniel Rodrigues Ferreira Saint-Martin, Kevin Alves Barreto, Edgard M K Von Koenig Soares, et al.
J Occup Environ Med. 2024 Aug 1;66(8):605-614. doi: 10.1097/JOM.0000000000003116. Epub 2024 Apr 12.
OBJECTIVE: We investigated the effect of a 7-month healthy lifestyle intervention on cardiometabolic risk factors (CMRF) among male career military firefighters (FFs). METHODS: Forty-nine FFs participated in a 7-month workplace multiddisciplinary healthy lifestyle intervention designed to reduce CMRF through exercise, diet, and improved sleep. Medical assessments, accelerometry, and surveys at the beginning and end determined program effectiveness. RESULTS: At the end of the intervention period, there was a significant improvement in measures of body composition and blood glucose. The prevalence of hypertension also decreased significantly ( P < 0.01). The 57% of participants who fully adhered to the program had significantly greater improvements across multiple CMRF. Participants increased their physical activity and improved their diet following the intervention. CONCLUSIONS: This healthy lifestyle intervention was effective in changing behavior and lowering cardiometabolic risk among FFs.

89Resistance training and Down Syndrome: A narrative review on considerations for exercise prescription and safety.PubMed

Geiziane Leite Rodrigues Melo, Ivo Vieira de Sousa Neto, Eduardo Fernandes da Fonseca, et al.
Front Physiol. 2022 Sep 27;13:948439. doi: 10.3389/fphys.2022.948439. eCollection 2022.
The current manuscript reviews the literature on the health effects of resistance training (RT) for individuals with Down syndrome (DS), focusing on this training modality's methodology, application, and safety. The literature has mentioned that early aging in this population is associated with loss of muscle strength, lower lean and bone mass, and increased obesity. It is necessary to propose non-pharmacological measures for prevention and health promotion. Thus, this review suggests a current research-based RT guide for individuals with DS. This review is divided into three sections: Section 2 briefly reviews DS and the effects on structural and functional decline and how exercise and physical activity can influence health aspects in this population; Section 3 summarizes the evidence for RT prescription; Section 4 briefly reviews the health and potential benefits of RT in individuals with DS. The findings from this review suggest that most individuals with DS should engage in moderate-intensity RT at least 2 days a week and perform RT on the major muscle groups and include balance training. The RT program should be modified and adapted according to individuals' characteristics and limitations. RT promotes positive, health-related benefits such as increasing strength, improving body composition, improving functional capacity and balance, reducing inflammatory status and oxidative stress, and improving the immune system. The RT protocols summarized in this current review provide guidance, critical conclusions, and novel research settings, which could be useful to coaches, clinicians, and researchers to effectively design RT program for individuals with DS.

90Depression and cardiovascular disease: a clinical review.PubMed

David L Hare, Samia R Toukhsati, Peter Johansson, et al.
Eur Heart J. 2014 Jun 1;35(21):1365-72. doi: 10.1093/eurheartj/eht462. Epub 2013 Nov 25.
Cardiovascular disease (CVD) and depression are common. Patients with CVD have more depression than the general population. Persons with depression are more likely to eventually develop CVD and also have a higher mortality rate than the general population. Patients with CVD, who are also depressed, have a worse outcome than those patients who are not depressed. There is a graded relationship: the more severe the depression, the higher the subsequent risk of mortality and other cardiovascular events. It is possible that depression is only a marker for more severe CVD which so far cannot be detected using our currently available investigations. However, given the increased prevalence of depression in patients with CVD, a causal relationship with either CVD causing more depression or depression causing more CVD and a worse prognosis for CVD is probable. There are many possible pathogenetic mechanisms that have been described, which are plausible and that might well be important. However, whether or not there is a causal relationship, depression is the main driver of quality of life and requires prevention, detection, and management in its own right. Depression after an acute cardiac event is commonly an adjustment disorder than can improve spontaneously with comprehensive cardiac management. Additional management strategies for depressed cardiac patients include cardiac rehabilitation and exercise programmes, general support, cognitive behavioural therapy, antidepressant medication, combined approaches, and probably disease management programmes.

91Exercise training for adults undergoing maintenance dialysis.PubMed

Amelie Bernier-Jean, Nadim A Beruni, Nicola P Bondonno, et al.
Cochrane Database Syst Rev. 2022 Jan 12;1(1):CD014653. doi: 10.1002/14651858.CD014653.
BACKGROUND: Dialysis treatments weigh heavily on patients' physical and psychosocial health. Multiple studies have assessed the potential for exercise training to improve outcomes in adults undergoing dialysis. However, uncertainties exist in its relevance and sustainable benefits for patient-important outcomes. This is an update of a review first published in 2011. OBJECTIVES: To assess the benefits and safety of regular structured exercise training in adults undergoing dialysis on patient-important outcomes including death, cardiovascular events, fatigue, functional capacity, pain, and depression. We also aimed to define the optimal prescription of exercise in adults undergoing dialysis. SEARCH METHODS: In this update, we conducted a systematic search of the Cochrane Kidney and Transplant Register of Studies up to 23 December 2020. The Register includes studies identified from CENTRAL, MEDLINE, EMBASE, the International Clinical Trials Register (ICTRP) Search Portal and ClinicalTrials.gov as well as kidney-related journals and the proceedings of major kidney conferences. SELECTION CRITERIA: Randomised controlled trials (RCTs) and quasi-RCTs of any structured exercise programs of eight weeks or more in adults undergoing maintenance dialysis compared to no exercise or sham exercise. DATA COLLECTION AND ANALYSIS: Two authors independently assessed the search results for eligibility, extracted the data and assessed the risk of bias using the Cochrane risk of bias tool. Whenever appropriate, we performed random-effects meta-analyses of the mean difference in outcomes. The primary outcomes were death (any cause), cardiovascular events and fatigue. Secondary outcomes were health-related quality of life (HRQoL), depression, pain, functional capacity, blood pressure, adherence to the exercise program, and intervention-related adverse events. MAIN RESULTS: We identified 89 studies involving 4291 randomised participants, of which 77 studies (3846 participants) contributed to the meta-analyses. Seven studies included adults undergoing peritoneal dialysis. Fifty-six studies reported aerobic exercise interventions, 21 resistance exercise interventions and 19 combined aerobic and resistance training within the same study arm. The interventions lasted from eight weeks to two years and most often took place thrice weekly during dialysis treatments. A single study reported death and no study reported long-term cardiovascular events. Five studies directly assessed fatigue, 46 reported HRQoL and 16 reported fatigue or pain through their assessment of HRQoL. Thirty-five studies assessed functional capacity, and 21 reported resting peripheral blood pressure. Twelve studies reported adherence to exercise sessions, and nine reported exercise-related adverse events. Overall, the quality of the included studies was low and blinding of the participants was generally not feasible due to the nature of the intervention. Exercise had uncertain effects on death, cardiovascular events, and the mental component of HRQoL due to the very low certainty of evidence. Compared with sham or no exercise, exercise training for two to 12 months may improve fatigue in adults undergoing dialysis, however, a meta-analysis could not be conducted. Any exercise training for two to 12 months may improve the physical component of HRQoL (17 studies, 656 participants: MD 4.12, 95% CI 1.88 to 6.37 points on 100 points-scale; I² = 49%; low certainty evidence). Any exercise training for two to 12 months probably improves depressive symptoms (10 studies, 441 participants: SMD -0.65, 95% CI -1.07 to -0.22; I² = 77%; moderate certainty evidence) and the magnitude of the effect may be greater when maintaining the exercise beyond four months (6 studies, 311 participants: SMD -0.30, 95% CI 0.14 to -0.74; I² = 71%). Any exercise training for three to 12 months may improve pain (15 studies, 872 participants: MD 5.28 95% CI -0.12 to 10.69 points on 100 points-scale; I² = 63%: low certainty evidence) however, the 95% CI indicates that exercise training may make little or no difference in the level of pain. Any exercise training for two to six months probably improves functional capacity as it increased the distance reached during six minutes of walking (19 studies, 827 participants: MD 49.91 metres, 95% CI 37.22 to 62.59; I² = 34%; moderate certainty evidence) and the number of sit-to-stand cycles performed in 30 seconds (MD 2.33 cycles, 95% CI 1.71 to 2.96; moderate certainty evidence). There was insufficient evidence to assess the safety of exercise training for adults undergoing maintenance dialysis. The results were similar for aerobic exercise, resistance exercise, and a combination of both aerobic and resistance exercise. AUTHORS' CONCLUSIONS: It is uncertain whether exercise training improves death, cardiovascular events, or the mental component of HRQoL in adults undergoing maintenance dialysis. Exercise training probably improves depressive symptoms, particularly when the intervention is maintained beyond four months. Exercise training is also likely to improve functional capacity. Low certainty evidence suggested that exercise training may improve fatigue, the physical component of quality of life, and pain. The safety of exercise training for adults undergoing dialysis remains uncertain.

92Evidence-based labor management: postpartum care after vaginal delivery (part 6).PubMed

Fabrizio Zullo, Daniele Di Mascio, Vincenzo Berghella
Am J Obstet Gynecol MFM. 2023 Jul;5(7):100977. doi: 10.1016/j.ajogmf.2023.100977. Epub 2023 Apr 22.
In the setting of postpartum care after vaginal delivery, rooming-in is associated with a higher rate of exclusive breastfeeding rate at hospital discharge, but there is insufficient evidence to support or refute rooming-in to increase breastfeeding at 6 months. Education and support for breastfeeding are valuable interventions to promote initiation of breastfeeding whether it is offered by a healthcare professional, nonhealthcare professional, or peer. A combined intervention, a professional provider-led intervention, having a protocol available for the provider training program, and implementation during both the prenatal and postnatal periods increased the rate of exclusive breastfeeding for 6 months. There is no single effective treatment for breast engorgement. Breast massage, continuing breastfeeding, and pain relief are recommended by national guidelines. Nonsteroidal anti-inflammatory drugs and acetaminophen are better than placebo for relief of pain caused by uterine cramping and perineal trauma; acetaminophen is effective in breastfeeding individuals who underwent episiotomy; and local cooling pain relievers have been shown to reduce perineal pain for 24 to 72 hours, compared with no treatment. There is insufficient evidence to assess the safety and efficacy of postpartum routine universal thromboprophylaxis after vaginal delivery. Anti-D immune globulin administration is recommended in Rhesus-negative individuals who have given birth to a Rhesus-positive infant. There is very low-quality evidence that a universal complete blood count is useful in reducing the risk of receiving blood products. In the absence of any postpartum complication, there is insufficient evidence to recommend a routine postpartum ultrasound. Measles, mumps, and rubella combination; varicella; human papillomavirus; and tetanus, diphtheria, and pertussis vaccines should be administered in nonimmune individuals in the postpartum period. Smallpox and yellow fever vaccines should be avoided. Individuals undergoing postplacental placement are more likely to use an intrauterine device at 6 months than those advised to follow-up for placement during outpatient postpartum care. An implant is safe and effective for immediate postpartum contraception. There is insufficient evidence to support or refute the routine administration of micronutrient supplements in breastfeeding women. Placentophagia does not provide any benefits and exposes mothers and offspring to infectious risks. Therefore, it should be discouraged. Because of the low level of evidence, there is insufficient data to assess the efficacy of home visits in the postpartum period. There is insufficient evidence to recommend when to resume daily activities, and individuals should be counseled to return to prepregnancy level of activity or exercise when comfortable. Sexual activity, housework exercise, driving, climbing stairs, and lifting weights should be resumed as soon as postpartum individuals want. A behavioral educational intervention reduces depression symptoms and increases breastfeeding duration. Physical activity after delivery is protective against postpartum mood disorders. There is no strong evidence that supports early discharge after vaginal delivery compared with standard discharge (ie, ≥48 hours).

93Psychocardiology in the elderly.PubMed

Brigita Novak Sarotar, Mitja Lainscak
Wien Klin Wochenschr. 2016 Dec;128(Suppl 7):474-479. doi: 10.1007/s00508-016-1139-x. Epub 2016 Nov 28.
The population is rapidly aging worldwide and the burden of chronic disease follows along. Frequently, diseases go hand in hand and cardiovascular disease and mental health problems are no exception. Symptoms of depression in the elderly are often overlooked and untreated because they coincide with other problems encountered by the elderly. Older adults with depressive symptoms have poorer functioning compared to those with chronic medical conditions. The burden of cardiovascular disease also remains a leading cause of morbidity and mortality. Bidirectional associations between depression and cardiovascular diseases are described with a focus on psychosocial factors affecting cardiac functioning and disease outcome.

94Effectiveness of non-pharmacological therapies for treating post-stroke depression: A systematic review and network meta-analysis.PubMed

Yunhao Yi, Weijie Zhao, Shimeng Lv, et al.
Gen Hosp Psychiatry. 2024 Sep-Oct;90:99-107. doi: 10.1016/j.genhosppsych.2024.07.011. Epub 2024 Jul 22.
OBJECTIVE: Post-stroke depression (PSD) is a common neurological and psychiatric sequelae following a stroke, often surpassing the primary effects of the stroke due to its strong correlation with high mortality rates. In recent years, non-pharmacological therapy has garnered significant attention as a supplementary treatment for PSD, becoming widely adopted in clinical practice. However, the efficacy of specific intervention strategies remains unclear. This study aimed to conduct a network meta-analysis (NMA) of published studies to compare the efficacy of different non-pharmacological therapies for treating PSD. METHOD: We systematically searched five databases from inception through March 2024 to identify randomized controlled trials (RCTs) evaluating non-pharmacological therapies for the treatment of PSD. We considered individual intervention and intervention class. Intervention classes included traditional Chinese medicine (TCM), non-invasive electrotherapy stimulation (NIES), psychotherapy (PT), exercise therapy, hyperbaric oxygen, and combined interventions. The NMA was conducted using R and Stata software, following a frequency-based methodology. Assessment of methodological quality and risk of bias was conducted using the Risk of Bias assessment tool 2.0. Therapies were ranked using the P-score, and box-plots visualization, meta-regression, and sensitivity analysis, were performed to assess transitivity, heterogeneity, and consistency, respectively. RESULTS: The NMA included 43 studies with a total of 3138 participants. Random-effects models revealed significant efficacy for acupuncture (ACUP) (P-score = 0.92; pooled standardized mean difference (95% CI): -3.12 (-4.63 to -1.60)) and transcranial direct current stimulation (P-score = 0.85; -2.78 (-5.06 to -0.49)) compared to the treatment as usual (TAU) group. In categorical comparisons, TCM_PT (P-score = 0.82; -1.91 (-3.54 to -0.28)), TCM (P-score = 0.79; -1.65 (-2.33 to -0.97)), and NIES (P-score = 0.74; -1.54 (-2.62 to -0.46)) showed significant differences compared to TAU group. Furthermore, our results indicated no significant difference between PT and the control groups. However, Confidence in Network Meta-Analysis results indicated very low overall evidence grade. CONCLUSION: Limited evidence suggests that ACUP may be the most effective non-pharmacological therapy for improving PSD, and TCM_PT is the best intervention class. However, the evidence quality is very low, underscoring the need for additional high-quality RCTs to validate these findings, particularly given the limited number of RCTs available for each therapy.

95Advances in exercise therapy in predialysis chronic kidney disease, hemodialysis, peritoneal dialysis, and kidney transplantation.PubMed

Thomas J Wilkinson, Mara McAdams-DeMarco, Paul N Bennett, et al.
Curr Opin Nephrol Hypertens. 2020 Sep;29(5):471-479. doi: 10.1097/MNH.0000000000000627.
PURPOSE OF REVIEW: Chronic kidney disease (CKD) is characterized by poor levels of physical activity which contribute to increased morbidity across the disease trajectory. The short nature, small samples, and poor methodology across most studies have failed to translate the role of exercise in CKD into its adoption as a frontline adjunct therapeutic option. This review focuses on recent advances surrounding the benefits of exercise interventions across the CKD spectrum. RECENT FINDINGS: Key recent advances in exercise studies have focused on the efficacy of novel intervention strategies across the CKD spectrum. These include high-intensity interval training, virtual reality gaming, intradialytic yoga, electrical stimulation of muscles, blood flow restriction training, and protocols combining exercise with nutritional supplementation. Research is also beginning to explore the role of prehabilitation for patients prior to dialysis and kidney transplantation. SUMMARY: Studies continue to demonstrate wide-ranging benefits of exercise across CKD; however, implementation of exercise remains scarce. Future research needs include evaluating the efficacy of larger and/or more comprehensive interventions on clinically important outcomes. It is hoped with increasing global evidence, high-quality clinical studies, and sustained clinician and patient engagement, exercise programs will become better prioritized in the nephrology field.

96Exercise and chronic kidney disease: potential mechanisms underlying the physiological benefits.PubMed

Nicolette C Bishop, James O Burton, Matthew P M Graham-Brown, et al.
Nat Rev Nephrol. 2023 Apr;19(4):244-256. doi: 10.1038/s41581-022-00675-9. Epub 2023 Jan 17.
Increasing evidence indicates that exercise has beneficial effects on chronic inflammation, cardiorespiratory function, muscle and bone strength and metabolic markers in adults with chronic kidney disease (CKD), kidney failure or kidney transplants. However, the mechanisms that underlie these benefits have received little attention, and the available clinical evidence is mainly from small, short-duration (<12 weeks) exercise intervention studies. The available data, mainly from patients with CKD or on dialysis, suggest that exercise-mediated shifts towards a less inflammatory immune cell profile, enhanced activity of the NRF2 pathway and reduced monocyte infiltration into adipose tissue may underlie improvements in inflammatory biomarkers. Exercise-mediated increases in nitric oxide release and bioavailability, reduced angiotensin II accumulation in the heart, left ventricular remodelling and reductions in myocardial fibrosis may contribute to improvements in left ventricular hypertrophy. Exercise stimulates an anabolic response in skeletal muscle in CKD, but increases in mitochondrial mass and satellite cell activation seem to be impaired in this population. Exercise-mediated activation of the canonical wnt pathway may lead to bone formation and improvements in the levels of the bone-derived hormones klotho and fibroblast growth factor 23 (FGF23). Longer duration studies with larger sample sizes are needed to confirm these mechanisms in CKD, kidney failure and kidney transplant populations and provide evidence for targeted exercise interventions.

97Effects of exercise programs on physical function and activity levels in patients undergoing hemodialysis: a randomized controlled trial.PubMed

Borja Perez-Dominguez, Jose Casaña-Granell, Rafael Garcia-Maset, et al.
Eur J Phys Rehabil Med. 2021 Dec;57(6):994-1001. doi: 10.23736/S1973-9087.21.06694-6. Epub 2021 Apr 7.
BACKGROUND: There are still many barriers when implementing exercise routines within daily dialysis care, even though benefits are well-known. Developing cost-effective strategies is necessary to overcome these barriers and include exercise as a complementary therapy in dialysis. AIM: To compare several exercise programs on hemodialysis patient's functional capacity and health-related quality of life. DESIGN: This study was a 16-week follow-up, two-parallel group trial with balanced randomization. SETTING: Participants in this study belonged to a private hospitalized care center. POPULATION: Referred sample of 71 patients that suffered end-stage chronic kidney disease who underwent hemodialysis for at least 3 months and had a medical stable condition. METHODS: Thirty-six participants performed for 16 weeks an intradialytic exercise program lead by the nursing staff of the hemodialysis unit and 35 a home-based program supervised by physical therapists of the hospital. RESULTS: The main researcher and the data analyst were both blinded to participant allocation. There was a significant effect in time for both groups. Participants improved significantly in the Short Performance Physical Battery (SPPB), One-Leg Heel-Rise (OLHR) and 6 Minute-Walk Test (6MWT), and in the Physical Activity Scale for the Elderly (PASE) and Short Survey Form 36 (SF-36) questionnaires. CONCLUSIONS: Nurse-led and home-based exercise interventions produce beneficial effects involving physical function, activity levels and health-related quality of life in patients undergoing hemodialysis. CLINICAL REHABILITATION IMPACT: The study emphasizes the importance of exercise rehabilitation routines in fragile populations such as dialysis patients, and the potential to overcome barriers for its daily implementation.

98Exercise in Patients on Dialysis: A Multicenter, Randomized Clinical Trial.PubMed

Fabio Manfredini, Francesca Mallamaci, Graziella D'Arrigo, et al.
J Am Soc Nephrol. 2017 Apr;28(4):1259-1268. doi: 10.1681/ASN.2016030378. Epub 2016 Dec 1.
Previous studies have suggested the benefits of physical exercise for patients on dialysis. We conducted the Exercise Introduction to Enhance Performance in Dialysis trial, a 6-month randomized, multicenter trial to test whether a simple, personalized walking exercise program at home, managed by dialysis staff, improves functional status in adult patients on dialysis. The main study outcomes included change in physical performance at 6 months, assessed by the 6-minute walking test and the five times sit-to-stand test, and in quality of life, assessed by the Kidney Disease Quality of Life Short Form (KDQOL-SF) questionnaire. We randomized 296 patients to normal physical activity (control; =145) or walking exercise (=151); 227 patients (exercise =104; control =123) repeated the 6-month evaluations. The distance covered during the 6-minute walking test improved in the exercise group (mean distance±SD: baseline, 328±96 m; 6 months, 367±113 m) but not in the control group (baseline, 321±107 m; 6 months, 324±116 m; <0.001 between groups). Similarly, the five times sit-to-stand test time improved in the exercise group (mean time±SD: baseline, 20.5±6.0 seconds; 6 months, 18.2±5.7 seconds) but not in the control group (baseline, 20.9±5.8 seconds; 6 months, 20.2±6.4 seconds; =0.001 between groups). The cognitive function score (=0.04) and quality of social interaction score (=0.01) in the kidney disease component of the KDQOL-SF improved significantly in the exercise arm compared with the control arm. Hence, a simple, personalized, home-based, low-intensity exercise program managed by dialysis staff may improve physical performance and quality of life in patients on dialysis.

99Effects of intradialytic exercise for advanced-age patients undergoing hemodialysis: A randomized controlled trial.PubMed

Hiroki Yabe, Kenichi Kono, Tomoya Yamaguchi, et al.
PLoS One. 2021 Oct 22;16(10):e0257918. doi: 10.1371/journal.pone.0257918. eCollection 2021.
Previous reports have shown the benefits of intradialytic exercise to patients undergoing hemodialysis. However, most of those studies assessed the effects of exercise in middle-aged patients and little is known about advanced-age patients undergoing hemodialysis. Therefore, the present randomized controlled trial was performed to determine the effectiveness of exercise therapy in advanced-age patients undergoing hemodialysis. This non-blinded, randomized controlled parallel trial enrolled a total of 101 patients who were randomly assigned to intradialytic exercise (n = 51) or usual care (n = 50) groups. The training program included both resistance and aerobic exercises and was performed three times per week for 6 months. The aerobic exercise intensity was adjusted to a target Borg score of 13 for 20 minutes. Four types of resistance exercises were performed using elastic tubing, with three sets of 10 exercises performed at moderate intensity (13/20 on the Borg scale). The usual care group received standard care. Lower extremity muscle strength, Short Physical Performance Battery score, and 10-m walking speed were the outcomes and were evaluated before the hemodialysis session and after 6 months of training. There were statistically significant improvements in Short Physical Performance Battery score (effect size, 0.57; 95% confidence interval, 0.15‒1.95) in the exercise group relative to the control group. There were no statistically significant differences in lower extremity muscle strength or in the 10-m walking speed between the two groups. These findings suggest that 6 months of intradialytic training could improve physical function in older patients undergoing hemodialysis.

100The physiological responses to Bikram yoga in novice and experienced practitioners.PubMed

Jessica L Pate, Michael J Buono
Altern Ther Health Med. 2014 Jul-Aug;20(4):12-8.
CONTEXT: Bikram yoga has gained a large following, possibly because of widespread claims boasting energy expenditure of up to 1000 calories per session. However, these claims are unfounded because no scientific study has investigated the metabolic response to a complete, standardized Bikram yoga class. OBJECTIVES: This study intends to determine energy expenditure, heart rate, and sweat rate in novice and experienced practitioners from a standardized Bikram yoga class. SETTING: Data were collected in the environmental chamber of the Exercise Physiology Laboratory at San Diego State University in California, USA. PARTICIPANTS: Male (n = 5) and female (n = 19) participants between the ages of 18 and 57 y were recruited through flyers in yoga studios throughout San Diego. Participants were classified as experienced or novice practitioners, having completed ≥20 or <20 sessions, respectively. INTERVENTIONS: Participants were guided through a standardized 90-min yoga class performed in a hot environment using Bikram's Standard Beginning Dialogue, while expired gas was collected and heart rate was recorded. OUTCOME MEASURES: Energy expenditure, calculated via oxygen uptake, and heart rate were determined for each posture and transition period. In addition, sweat rate and core temperature were recorded for each participant. RESULTS: Mean (±SD) relative VO2 for the entire 90-min session was 9.5 ± 1.9 mL × kg-1 × min-1, ranging from 6.0 to 12.9 mL × kg-1 × min-1. Mean absolute energy expenditure was 286 ± 72 kcals, ranging from 179 to 478 kcals. Independent sample t tests revealed significant differences (P < .05) in relative energy expenditure, heart rate, ending core temperature, and sweat rate between experience levels. Mean relative energy expenditure was 3.7 ± 0.5 kcal/kg in novice practitioners and 4.7 ± 0.8 kcal/kg in experienced practitioners. Percentage of predicted maximum heart rate and sweat rate were 72.3% ± 10.6% and 0.6 ± 0.2 kg/h in novice practitioners and 86.4% ± 5.2% and 1.1 ± 0.5 kg/h in experienced participants. All postures were classified as light-to-moderate intensity according to the American College of Sports Medicine (ACSM) standards. CONCLUSIONS: Bikram yoga meets requirements for exercise of light-to-moderate intensity and, theoretically, could be used for weight maintenance or weight loss if practiced several times per week.

101Primary Hyperhidrosis in Children: Current Perspectives and Therapeutic Options.PubMed

Keri A Wallace
Pediatr Ann. 2025 Jun;54(6):e196-e202. doi: 10.3928/19382359-20250321-03. Epub 2025 Jun 1.
Primary hyperhidrosis is a common condition that often begins before age 18 years and frequently presents to the pediatric primary care provider. It can have significant negative impacts on a child's quality of life (QOL) and emotional well-being. There are a variety of treatment options available that have been shown to decrease symptoms, as well as improve QOL. These treatments include over-the-counter antiperspirants, prescription antiperspirants, topical anticholinergics, iontophoresis, systemic anticholinergics, injectable botulinum toxin, and surgical sympathectomy. Treatment of this condition is lifelong and often nuanced. It is imperative for the pediatric practitioner to be well versed in the risks and benefits, as well as proper usage, of these various therapeutic modalities. With this knowledge, effective treatment plans can be crafted to improve both the physical and mental health of affected children. .

102Hyperhidrosis and botulinum toxin A: patient selection and techniques.PubMed

Richard G Glogau
Clin Dermatol. 2004 Jan-Feb;22(1):45-52. doi: 10.1016/j.clindermatol.2003.11.007.
Focal idiopathic excessive eccrine sweating presents most commonly as an affliction of three anatomically distinct area: the axillae, the palms and soles, and the upper face. The true incidence is not known, but about half of the patients referred to us with this condition have at least one first-degree relative similarly affected. Only a fraction of patients afflicted are thought to seek medical care because of the social stigma, lack of understanding on the part of medical providers as to the cause and nature of the problem, and, until now, lack of effective nonsurgical therapy. A large social sample is required to accurately measure both the incidence and the exact nature of the genetic influence.

103Examining hyperhidrosis: an update on new treatments.PubMed

Carolyn I Jacob
Am J Manag Care. 2018 Dec;24(23 Suppl):S496-S501.
Primary hyperhidrosis is a debilitating condition that causes significant distress and financial burden for affected patients, triggering them to seek medical care for their excessive sweating. Once a diagnosis of primary hyperhidrosis has been established, treatment is initiated to help control sweat production and increase quality of life. While there are no current guidelines in the United States for the treatment of primary hyperhidrosis, there are International Hyperhidrosis Society guidelines that clinicians can use. Currently, a step-therapy approach with the least invasive treatments prioritized first is recommended; the patient's reported disability should also be taken into consideration when selecting a first-line treatment. This update will discuss new treatment modalities, surgical procedures, associated comorbidities, and the impact on managed care of hyperhidrosis, so clinicians can tailor therapy, improve outcomes, and increase patient satisfaction.

104Risk reduction of long-term major adverse cardiovascular events after endoscopic thoracic sympathectomy in palmar hyperhidrosis.PubMed

Chun-An Cheng, Chun-Gu Cheng, Hsin Chu, et al.
Clin Auton Res. 2017 Dec;27(6):393-400. doi: 10.1007/s10286-017-0464-0. Epub 2017 Sep 19.
PURPOSE: Palmar hyperhidrosis (PH) is excessive sweating of the palms resulting from sympathetic overactivity, and patients who undergo endoscopic thoracic sympathectomy (ETS) show reduced cardiac demand after 1 year and improved cerebral perfusion within 2-4 weeks. However, the long-term risks of major adverse cardiovascular events (MACE) following ETS remain unclear. METHODS: We searched the Longitudinal National Health Insurance Database in Taiwan and identified PH patients (International Classification of Disease, Ninth Revision, Clinical Modification diagnostic code 708.8) from the outpatient database and patients who underwent ETS (procedure code 05.29) from the inpatient database between 2000 and 2010; furthermore, we excluded patients younger than 18 years of age or older than 65 years of age. We defined MACE as stroke (diagnostic codes 430-437), myocardial infarction (diagnostic code 410), or death. Patients followed until the first cardiac event or December 31, 2010. Risk factors were identified using a multivariable Cox proportional hazards regression. RESULTS: The incidence of MACE was significantly lower in patients with ETS (0.76%) than without (1.67%). In PH patients, ETS significantly reduced the risk of MACE (adjusted hazard ratio 0.473; 95% confidence interval 0.277-0.808). CONCLUSION: PH patients who underwent ETS showed a reduced risk of MACE over a long-term follow-up period. This result could provide support for patients with PH who are considering undergoing ETS because of its additional cardiovascular benefits.

105[Advances and risks in estrogen therapy in the perimenopause].PubMed

C Lauritzen
Wien Klin Wochenschr. 1983 Oct 28;95(20):748-51.
Treatment with oestrogens in the perimenopause can regulate dysfunctional uterine bleeding and positively influence unpleasant subjective feelings such as sweating, dizziness, nervousness and lack or incapability of concentration. Oestrogens are especially successful in reactive depression and in the therapy of insomnia. Their positive effect on atrophic changes of the genitalia and in combating urge incontinence is also of therapeutic importance. Of particular socio-medical importance is their beneficial effect on postmenopausal osteoporosis. Side effects like weight gain, increase in blood pressure or changes in coagulation parameters are not observed during therapy with natural oestrogens in the usual doses. The incidence of thrombosis, embolism and myocardial infarction is not increased when oestrogens are given in the perimenopause. The controversy with respect to an increased incidence of endometrial carcinoma after long-term therapy with oestrogens may be based on an incorrect mode of administration as used on the Anglo-American scene. Excess dosage, continuous instead of intermittent therapy, lack of addition of progestational agents and a neglect of contraindications and risk factors may have led to the 3- to 8-fold increased incidence of endometrial carcinoma after oestrogen therapy in the studies from these areas.

106Hot FlashesPubMed

Tania Lugo, Maggie Tetrokalashvili
Hot flashes are sudden-onset, spontaneous, and episodic sensations of warmth usually felt on the chest, neck, and face immediately followed by sweating. They are the most common reason women seek medical care during the perimenopausal period, especially if the symptoms impair quality of life. The onset of hot flashes can be associated with perspiration, heart palpitations, headache, weakness, fatigue, faintness, and anxiety, and warm environments, hot drinks, or emotional stress can trigger them. Hot flashes are variable in terms of duration, severity, and frequency. Frequency and severity can increase during the transition to menopause and peak approximately 1 year after the final menstrual period. They can persist for 6 months to several years, usually decreasing in frequency and intensity over time after the final menstrual period. On average, they last less than 5 minutes. The average frequency varies from 10 times daily to several times weekly. The mean duration is 1.2 years.