Author:
Kondo Takayuki,Fujimoto Kentaro,Fujiwara Kisako,Yumita Sae,Ishino Takamasa,Ogawa Keita,Nakagawa Miyuki,Iwanaga Terunao,Koroki Keisuke,Kanzaki Hiroaki,Inoue Masanori,Kobayashi Kazufumi,Kiyono Soichiro,Nakamura Masato,Kanogawa Naoya,Ogasawara Sadahisa,Nakamoto Shingo,Chiba Tetsuhiro,Kato Jun,Fujiwara Keiichi,Kato Naoya
Abstract
AbstractThe pathogenesis of acute liver failure (ALF) involves cell death. Necroptosis is a newly suggested programmed cell death, and receptor-interacting protein kinase 3 (RIPK3) has been reported as a marker for necroptosis. However, there are few reports on necroptosis in ALF. Therefore, we evaluated the role of cell death markers such as cytokeratin (CK) 18, cleaved CK (cCK) 18, and RIPK3 in ALF, as well as cytokines and hepatocyte growth factor (HGF). Seventy-one hospitalized patients with acute liver injury (38 nonsevere hepatitis [non-SH]/22 severe hepatitis [SH]/11 ALF) were studied. No significant difference was found for cytokines, but a substantial increase in HGF levels was found following the severity of hepatitis. The non-SH group had lower levels of CK18 and cCK18 than the SH/ALF group. RIPK3 was significantly lower in the non-SH/SH group than in the ALF group. HGF, RIPK3, and albumin levels were found to be important predictive variables. The present study suggests that cCK18, CK18, and RIPK3 are associated with the severity of hepatitis. RIPK3 and other markers related cell death may be useful for understanding the pathogenesis of ALF and as a prognostic marker of acute liver injury.
Publisher
Springer Science and Business Media LLC
Cited by
2 articles.
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