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

Autor: Engelmann C; Liver Failure Group, Institute for Liver and Digestive Health, University College London, Royal Free Campus, London, United Kingdom.; Division of Hepatology, Department of Medicine II, Leipzig University Medical Center, Leipzig, Germany.; Division of Hepatology and Gastroenterology, Department of Medical, Campus Virchow-Klinikum, Charité - Universitätsmedizin Berlin, Berlin, Germany., Martino VD; Service d'Hépatologie et de Soins Intensifs Digestifs, Hôpital Jean Minjoz, 25000 Besançon, France., Kerbert AJC; Liver Failure Group, Institute for Liver and Digestive Health, University College London, Royal Free Campus, London, United Kingdom., Weil-Verhoeven D; Service d'Hépatologie et de Soins Intensifs Digestifs, Hôpital Jean Minjoz, 25000 Besançon, France., Aehling NF; Division of Hepatology, Department of Medicine II, Leipzig University Medical Center, Leipzig, Germany., Herber A; Division of Hepatology, Department of Medicine II, Leipzig University Medical Center, Leipzig, Germany., Thévenot T; Service d'Hépatologie et de Soins Intensifs Digestifs, Hôpital Jean Minjoz, 25000 Besançon, France., Berg T; Division of Hepatology, Department of Medicine II, Leipzig University Medical Center, Leipzig, Germany.
Jazyk: angličtina
Zdroj: Seminars in liver disease [Semin Liver Dis] 2021 Aug; Vol. 41 (3), pp. 298-307. Date of Electronic Publication: 2021 May 15.
DOI: 10.1055/s-0041-1723034
Abstrakt: 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.
Competing Interests: None.
(Thieme. All rights reserved.)
Databáze: MEDLINE