【Lucus Su】評論

氨（NH3）於肝臟經由 urea cycle 轉變為毒性較低之urea。肝臟因為肝細胞衰竭或血液分流而無法清除毒性物質，血液中氨及其他毒性物質濃度就會增加，氨（NH3）及其他中小分子毒性物質可以通過 blood-brain barrier，於急性肝衰竭氨（NH3）可直接作用於大腦皮質、腦幹及脊髓產生胞突結合後抑制（post-synaptic inhibition）。1. Yang SS, Wu CH, Chiang TR, et al. Somatosensory evoked potentials in subclinical porto-systemic encephalopathy: a comparison with psychometric tests. Hepatology 1998;27: 357-61. 2. Chu NS, Yang SS, Liaw YF. Evoked potentials in liver disease. J Gastroenterol Hepatol 1997;12:s288-93. 3. Butterworth RF. The neurobiology of hepatic encephalopathy. Semi Liv Dis 1996;235-44. 4. Blei AT, Larsen FS. Pathophysiology of cerebral edema in fulminant hepatic failure. J Hepatology 1999;31:771-6. 5. Gane EJ, Portmann BC, Naoumov NV, et al. Long-term outcome of hepatitis C infection after liver transplantation. N Engl J Med 1996;334:815-20. 6. Markowitz JS, Martin P, Conrad AJ, et al. Prophylaxis against hepatitis B recurrence following liver transplantation using combination Lamivudine and hepatitis B immune globulin. Hepatology 1998;28:585-9.