对门体脑病(PSE)的常规疗法是通过结肠变化降低血氨,即减少结肠脲分解菌(新霉素)或降低结肠的pH(乳果糖)这样把氨转变成铵并集聚在结肠内。这两种药物疗法产生诸如氮血症,吸收障碍(新霉素)和腹泻(乳果糖)等讨厌的付作用。而且对昏迷或不配合的病人两者均不能胃肠道外给药。支链氨基酸溶液可在更严重的病例中经胃肠道外使用。然而,这种药物昂贵并在长期使用时需有一条中心静脉道路,增加了感染的危险。另外,这些药物中的任何一种也不是对所有病人均有治疗效果。在过去的研究中,发现小儿患先天性尿素合成障碍时血清氨水平升高而用苯甲酸钠和苯乙酸钠治疗已取得效益。这些替代途径占剩余 Conventional therapy for portal encephalopathy (PSE) is to convert ammonia to ammonium and accumulate in the colon by reducing blood ammonia through colon changes, ie reducing colon ureaplasma (neomycin) or lowering the pH of the colon (lactulose). Both drug therapies produce nasty side effects such as azotemia, malabsorption (neomycin) and diarrhea (lactulose). And for comatose or uncooperative patients both can not be administered parenterally. Branched-chain amino acid solutions can be used parenterally in more serious cases. However, this drug is expensive and requires a central venous access for long-term use, increasing the risk of infection. In addition, none of these drugs have a therapeutic effect on all patients. In the past study, found that children suffering from congenital urethral synthesis of serum ammonia levels increased with sodium benzoate and sodium phenylacetate treatment has been effective. These alternatives account for the rest