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関連論文:
img  1:  Etiology and outcome of acute liver failure: retrospective analysis of 50 patients treated at a single center.
 
著者: Akira Hiramatsu, Shoichi Takahashi, Hiroshi Aikata, Takahiro Azakami, Yoshio Katamura, Tomokazu Kawaoka, Kiminori Uka, Keitaro Yamashina, Shintaro Takaki, Hideaki Kodama, Soo Cheol Jeong, Michio Imamura, Yoshiiku Kawakami, Kazuaki Chayama
雑誌名: J Gastroenterol Hepatol. 2008 Aug;23(8 Pt 1):1216-22. doi: 10.1111/j.1440-1746.2008.05402.x. Epub 2008 Jul 10.
Abstract/Text BACKGROUND AND AIM: Acute liver failure (ALF) remains a devastating disease carrying considerable mortality. Since deceased donor liver transplantation is rarely performed in Japan, the artificial liver support system (ALS) and living donor liver transplantation (LDLT) are the main modalities used for treatment of ALF. The aim of this study was to analyze the outcome of ALF patients and to evaluate therapies for ALF according to etiology.
METHODS: Fifty consecutive patients with ALF were treated between January 1990 and December 2006. Prior to 1997, patients received ALS only. After 1997, ALS and/or LDLT were applied. LDLT was performed in 10 patients.
RESULTS: Four of 15 (27%) pre-1997 ALF patients survived, and 16 of 35 (46%) post-1997 ALF patients survived, including eight who underwent LDLT. The causes of ALF were acute hepatitis B virus (HBV) infection in 18%, severe acute exacerbation (SAE) of chronic HBV infection in 18%, autoimmune hepatitis (AIH) in 8%, and cryptogenic hepatitis in 44%. In total, 67% of the patients with ALF caused by acute HBV infection and AIH were cured without LDLT; only 11% of patients with ALF caused by SAE of HBV and 24% of cryptogenic hepatitis were successfully treated without LDLT. Notably, 80% of patients with cryptogenic hepatitis who underwent LDLT survived.
CONCLUSION: Since 1997, the survival rate of ALF patients has increased, mainly due to the introduction of LDLT. Liver transplantation should be performed especially in patients with ALF caused by SAE of HBV and cryptogenic hepatitis.

PMID 18637059  J Gastroenterol Hepatol. 2008 Aug;23(8 Pt 1):1216-22. doi: 10.1111/j.1440-1746.2008.05402.x. Epub 2008 Jul 10.
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