Department of Gastroenterology, Kagoshima City Hospital, 37-1 Uearatacho, Kagoshima, Kagoshima, Japan.
Department of Human and Environmental Sciences, Graduate School of Medical and Dental Sciences, Kagoshima University, Sakuragaoka, Kagoshima, Japan.
Clin J Gastroenterol. 2021 Apr;14(2):650-655. doi: 10.1007/s12328-020-01313-2. Epub 2021 Jan 5.
Hyperammonemia is often experienced as a complication of liver cirrhosis, but it is not well known that hyperammonemic encephalopathy is induced by urease-splitting bacteria in the urinary tract. We report two cases of hyperammonemia in two women in their 80s with liver cirrhosis. Both cases were treated as hepatic encephalopathy with usual treatment, but there was no improvement. Urinalysis showed marked alkalinuria and urine culture showed urease-splitting bacteria, which were thought to be related to the pathology. After drainage of urine and administration of antimicrobials, the blood ammonia level decreased and the urine pH level normalized. The mechanism of this is that ammonia is produced by the degradation of urinary urea by urease-producing bacteria in the bladder, and in the presence of dysuria, it is absorbed into the blood circulation from the bladder venous plexus, leading to hyperammonemia.Urine findings should be confirmed when a patient with liver disease develops hyperammonemia or is unresponsive to conventional hepatic encephalopathy treatment.
高氨血症常作为肝硬化的并发症出现，但人们并不清楚，血氨性脑病是由泌尿道中的脲酶分解细菌引起的。我们报告了两名 80 多岁患有肝硬化的老年女性的高氨血症病例。这两种情况均按肝性脑病进行常规治疗，但没有改善。尿分析显示明显的碱尿，尿液培养显示有脲酶分解细菌，这被认为与该病理有关。在进行尿液引流和使用抗生素治疗后，血氨水平降低，尿液 pH 值恢复正常。其机制是，氨由膀胱中的产脲酶细菌分解尿尿素产生，在排尿不畅的情况下，它从膀胱静脉丛吸收到血液中，导致高氨血症。当患有肝病的患者出现高氨血症或对常规肝性脑病治疗无反应时，应确认尿液结果。
