Karen L Thomsen1,2, Francis P Robertson3, Peter Holland-Fischer2, Brian R Davidson3, Rajeshwar P Mookerjee2, Holger J Møller4, Rajiv Jalan2, Henning Grønbæk1. 1. Department of Hepatology & Gastroenterology, Aarhus University Hospital, Aarhus, Denmark. 2. Liver Failure Group, UCL Institute for Liver and Digestive Health, University College London, United Kingdom. 3. Division of Surgery and Interventional Science, Royal Free Campus, University College London, United Kingdom. 4. Department of Clinical Biochemistry, Aarhus University Hospital, Aarhus, Denmark.
Abstract
BACKGROUND/ OBJECTIVES: Soluble CD163 (sCD163), a macrophage activation marker, is upregulated in conditions of macrophage proliferation and activation. Elevated sCD163 levels have been associated with liver disease severity and progression. During liver transplantation, the implanted liver is exposed to ischaemia and reperfusion injury, resulting in an acute inflammatory response and macrophage activation. The relationship between sCD163 levels during liver transplantation and the development of early allograft dysfunction (EAD) has not been investigated. METHODS: We included 27 cirrhosis patients (age 55 [range 32-72] years, 23 men) on the waiting list for liver transplantation. Alcohol consumption and viral hepatitis were the most frequent causes for cirrhosis. Patients were characterised by standard biochemical analysis and based on clinical disease severity scores. Information about donor, graft and course of the liver transplantation was recorded. sCD163 levels were measured at the time of liver transplantation before surgery, 2 h after reperfusion, and then at 24 h after transplantation. RESULTS: We observed above-normal sCD163 levels at baseline (5.9 mg/L [4.7-8.8]). Two hours after reperfusion, sCD163 levels increased significantly from baseline (8.4 mg/L [7.4-10.9]; P < 0.01). Twenty-four hours after transplantation, sCD163 levels were significantly reduced compared with baseline (3.7 mg/L [2.9-5.5]; P < 0.01). However, in patients with EAD (n = 16), sCD163 levels were increased compared with patients without EAD (4.1 [3.2-7.4] vs. 3.1 [2.8-3.8] mg/L; P = 0.03). CONCLUSIONS: We observed elevated sCD163 levels in patients with EAD after liver transplantation, confirming macrophage activation to play a role in EAD. Thus, sCD163 may be used as an early marker for EAD after liver transplantation, but larger studies are warranted to validate these findings.
BACKGROUND/ OBJECTIVES: Soluble CD163 (sCD163), a macrophage activation marker, is upregulated in conditions of macrophage proliferation and activation. Elevated sCD163 levels have been associated with liver disease severity and progression. During liver transplantation, the implanted liver is exposed to ischaemia and reperfusion injury, resulting in an acute inflammatory response and macrophage activation. The relationship between sCD163 levels during liver transplantation and the development of early allograft dysfunction (EAD) has not been investigated. METHODS: We included 27 cirrhosis patients (age 55 [range 32-72] years, 23 men) on the waiting list for liver transplantation. Alcohol consumption and viral hepatitis were the most frequent causes for cirrhosis. Patients were characterised by standard biochemical analysis and based on clinical disease severity scores. Information about donor, graft and course of the liver transplantation was recorded. sCD163 levels were measured at the time of liver transplantation before surgery, 2 h after reperfusion, and then at 24 h after transplantation. RESULTS: We observed above-normal sCD163 levels at baseline (5.9 mg/L [4.7-8.8]). Two hours after reperfusion, sCD163 levels increased significantly from baseline (8.4 mg/L [7.4-10.9]; P < 0.01). Twenty-four hours after transplantation, sCD163 levels were significantly reduced compared with baseline (3.7 mg/L [2.9-5.5]; P < 0.01). However, in patients with EAD (n = 16), sCD163 levels were increased compared with patients without EAD (4.1 [3.2-7.4] vs. 3.1 [2.8-3.8] mg/L; P = 0.03). CONCLUSIONS: We observed elevated sCD163 levels in patients with EAD after liver transplantation, confirming macrophage activation to play a role in EAD. Thus, sCD163 may be used as an early marker for EAD after liver transplantation, but larger studies are warranted to validate these findings.
Authors: Katharine A Hintz; Athos J Rassias; Kathleen Wardwell; Marcia L Moss; Peter M Morganelli; Patricia A Pioli; Alice L Givan; Paul K Wallace; Mark P Yeager; Paul M Guyre Journal: J Leukoc Biol Date: 2002-10 Impact factor: 4.962
Authors: Jonathan I Goldstein; Katharine A Goldstein; Kathleen Wardwell; Scott L Fahrner; Katie E Goonan; Matthew D Cheney; Mark P Yeager; Paul M Guyre Journal: Atherosclerosis Date: 2003-10 Impact factor: 5.162
Authors: P S Kamath; R H Wiesner; M Malinchoc; W Kremers; T M Therneau; C L Kosberg; G D'Amico; E R Dickson; W R Kim Journal: Hepatology Date: 2001-02 Impact factor: 17.425
Authors: Moritz von Frankenberg; Markus Golling; Arianeb Mehrabi; Hagen Nentwich; Ernst Klar; Thomas W Kraus Journal: Transpl Int Date: 2003-07-15 Impact factor: 3.782
Authors: Shaojun Shi; Eliano Bonaccorsi-Riani; Ivo Schurink; Thierry van den Bosch; Michael Doukas; Karishma A Lila; Henk P Roest; Daela Xhema; Pierre Gianello; Jeroen de Jonge; Monique M A Verstegen; Luc J W van der Laan Journal: Front Immunol Date: 2022-05-17 Impact factor: 8.786