Xu et al. conclude that changes in gut microbiota in neurocritically ill patients seem to have an impact on their mortality [1]. We would like to add some comments. The authors described an overgrowth of opportunistic pathogens defined as dysbiosis in patients with neurocritical illness. This study had similar results to other studies regarding the appearance of pathogens and disappearance of commensals [2, 3]. Further, the authors said that dysbiosis of the microbiota in neurocritical patients can be reasonably presumed to increase the risk of infection, undernutrition, and unconsciousness [1]. Here we would like to link dysbiosis and unconsciousness, where increased production of ammonia may play an important role. Indeed, bacteria residing in the human gut produce urease which is beneficial in healthy hosts but pathogenic in hosts with liver disease [4]. Urea produced by the liver is both excreted in urine and transported into the colon, where it is hydrolyzed by bacterial urease into carbon dioxide and ammonia [4]. Circulating ammonia is correlated with brain damage in patients with acute or chronic liver disease resulting in hepatic encephalopathy. In Xu’s study, nearly 40% of the patients had liver disease [1]. It is somewhat unfortunate that blood ammonia was not measured. This would have been of great utility to better interpret the results of their study [1, 4]. Xu also suggested that critical illness could lead to microbial translocation, potentially explaining the association between specific pathogens and mortality [1]. Another valid explanation, knowing that there was an overgrowth of enterobacteriaceae in this study [1], could be the translocation of endotoxin [5]. Indeed, translocation of endotoxin can trigger sepsis, septic shock, and secondary peritonitis [5].

中文翻译：

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与昏迷和死亡相关的神经危重症患者的微生物群失调：氨作为潜在的缺失环节

徐等人。得出的结论是，神经危重症患者肠道微生物群的变化似乎对其死亡率有影响 [1]。我们想补充一些意见。作者描述了在神经危重症患者中定义为生态失调的机会性病原体的过度生长。这项研究与其他关于病原体出现和共生体消失的研究结果相似 [2, 3]。此外，作者表示，可以合理推测神经危重症患者的微生物群失调会增加感染、营养不良和昏迷的风险[1]。在这里，我们想将生态失调和无意识联系起来，其中氨的产生增加可能起着重要作用。确实，存在于人体肠道中的细菌会产生脲酶，该酶对健康宿主有益，但对肝病宿主具有致病性 [4]。肝脏产生的尿素会随尿液排出体外并转运到结肠中，在结肠中被细菌脲酶水解成二氧化碳和氨 [4]。循环氨与导致肝性脑病的急性或慢性肝病患者的脑损伤相关。在徐的研究中，近 40% 的患者患有肝脏疾病 [1]。有点遗憾的是没有测量​​血氨。这对于更好地解释他们的研究结果非常有用 [1, 4]。徐还提出，危重疾病可能导致微生物易位，这可能解释了特定病原体与死亡率之间的关联[1]。另一个有效的解释，知道本研究中存在肠杆菌科的过度生长 [1]，可能是内毒素的易位 [5]。事实上，内毒素的易位可引发败血症、感染性休克和继发性腹膜炎 [5]。