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To pee or not to pee: ammonia hypothesis of hepatic encephalopathy revisited.

机译:撒尿还是不撒尿:重新探讨了氨性肝性脑病的假说。

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Hepatic encephalopathy is a neuropsychiatric syndrome associated with liver failure. Its aetiology has been debated for the past 100 years. Nevertheless, elevated ammonia levels are still believed to play a central role in its pathogenesis. After intestinal production, ammonia is detoxified by the liver. In liver failure, skeletal muscle and brain have been proposed to be alternative, although temporary, ammonia detoxifying organs. However, there is an increasing body of evidence that the kidney, in addition to the gut, is a pivotal organ determining systemic ammonia levels. In the last 20 years, it has been shown that the kidney can switch from an organ of systemic net ammonia production to a net ammonia excretion organ. The kidney plays a central role in the determination of ammonia levels. It is at least as important as the gut and could therefore serve as a target for new treatments for hepatic encephalopathy.
机译:肝性脑病是一种与肝功能衰竭相关的神经精神病综合症。在过去的100年中,其病因一直受到争论。然而,仍然认为氨水平升高在其发病机理中起着核心作用。肠道产生后,氨被肝脏解毒。在肝功能衰竭中,骨骼肌和脑已被提议替代,尽管是暂时的氨解毒器官。然而,越来越多的证据表明,除了肠外,肾脏是决定全身性氨水平的关键器官。在最近的20年中,已经证明肾脏可以从全身性净氨产生器官转换为净氨排泄器官。肾脏在确定氨水平中起着核心作用。它至少与肠一样重要,因此可以作为肝性脑病新疗法的靶标。

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