The Current Status of Granulocyte-Colony Stimulating Factor to Treat Acute-on-Chronic Liver Failure

被引:19
作者
Engelmann, Cornelius [1 ,2 ,3 ]
Di Martino, Vincent [4 ]
Kerbert, Annarein J. C. [1 ]
Weil-Verhoeven, Delphine [4 ]
Aehling, Niklas Friedemann [2 ]
Herber, Adam [2 ]
Thevenot, Thierry [4 ]
Berg, Thomas [2 ]
机构
[1] UCL, Inst Liver & Digest Hlth, Liver Failure Grp, Royal Free Campus, London, England
[2] Univ Leipzig, Med Ctr, Dept Med 2, Div Hepatol, Liebigstr 21, D-04103 Leipzig, Germany
[3] Charite Univ Med Berlin, Campus Virchow Klinikum, Dept Med, Div Hepatol & Gastroenterol, Berlin, Germany
[4] Hop Jean Minjoz, Serv Hepatol & Soins Intensifs Digestifs, F-25000 Besancon, France
关键词
liver cirrhosis; ACLF; alcoholic hepatitis; growth factors; STEM-CELL MOBILIZATION; G-CSF THERAPY; DECOMPENSATED CIRRHOSIS; IMPROVES SURVIVAL; CD34(+) CELLS; MACROPHAGE POLARIZATION; INFLAMMATORY RESPONSE; ALCOHOLIC HEPATITIS; PARTIAL-HEPATECTOMY; ANIMAL-MODEL;
D O I
10.1055/s-0041-1723034
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Patients with acute-on-chronic liver failure (ACLF) have a devastating prognosis and therapeutic options are limited. Granulocyte-colony stimulating factor (G-CSF) mobilizes immune and stem cells and possess immune-modulatory and proregenerative capacities. In this review, we aim to define the current evidence for the treatment with G-CSF in end-stage liver disease. Several smaller clinical trials in patients with different severity grades of end-stage liver disease have shown that G-CSF improves survival and reduces the rate of complications. Adequately powered multicenter European trials could not confirm these beneficial effects. In mouse models of ACLF, G-CSF increased the toll-like receptor (TLR)-mediated inflammatory response which led to an increase in mortality. Adding a TLR4 signaling inhibitor allowed G-CSF to unfold its proregenerative properties in these ACLF models. These data suggest that G-CSF requires a noninflammatory environment to exert its protective properties.
引用
收藏
页码:298 / 307
页数:10
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