Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/16308
Title: Macrophage activation marker soluble CD163 may predict disease progression in hepatocellular carcinoma
Austin Authors: Kazankov, Konstantin;Rode, Anthony;Simonsen, Kira;Villadsen, Gerda Elisabeth;Nicoll, Amanda J;Møller, Holger Jon;Lim, Lucy ;Angus, Peter W ;Kronborg, Ian;Arachchi, Niranjan;Gorelik, Alexandra;Liew, Danny;Vilstrup, Hendrik;Frystyk, Jan;Grønbæk, Henning
Affiliation: Department of Hepatology and Gastroenterology, Aarhus University Hospital, Aarhus, Denmark
Department of Gastroenterology and Hepatology, Royal Melbourne Hospital, Melbourne, Australia
Department of Gastroenterology, Eastern Health, Melbourne, Australia
Department of Clinical Biochemistry, Aarhus University Hospital, Aarhus, Denmark
Gastroenterology and Hepatology
Department of Gastroenterology, Western Hospital, Melbourne, Australia
Epicentre, Royal Melbourne Hospital, Melbourne, Australia
Medical Research Laboratory, Department of Clinical Medicine, Health, Aarhus University, Aarhus, Denmark
Victorian Liver Transplant Unit
Issue Date: 2016
Date: 2015-11-07
Publication information: Scandinavian Journal of Clinical and Laboratory Investigation 2016; 76(1): 64-73
Abstract: BACKGROUND: Tumor associated macrophages are present in hepatocellular carcinoma (HCC) and associated with a poor prognosis. The aim of the present study was to investigate the levels and dynamics of soluble (s)CD163, a specific macrophage activation marker, in patients with HCC. METHODS: In a cohort from Australia, we studied 109 HCC patients, 116 patients with chronic liver disease (CLD), and 52 healthy controls. We examined associations between baseline sCD163 and parameters of HCC severity as well as overall and progression-free survival. In a cohort of 42 Danish HCC patients, we measured sCD163 at baseline and 1, 4 and 12 weeks after ablative treatment. RESULTS: In the Australian cohort, median sCD163 was similarly increased in HCC (5.6[interquartile range 3.5-8.0] mg/L) and CLD (6.1[3.6-9.6] mg/L) patients as compared to controls (2.0[1.5-2.7] mg/L, p < 0.001). sCD163 correlated with Child-Pugh and MELD scores in both HCC and CLD patients. Patients with high sCD163 levels had shorter progression-free survival (p < 0.001), but not overall survival (p = 0.15). In the Danish cohort, patients with HCC progression at 12 weeks had an increase in sCD163. There was no association between sCD163 and HCC size, number, vascular invasion or metastasis in any of the cohorts. CONCLUSIONS: We confirmed increased sCD163 levels in CLD and HCC patients associated with Child-Pugh and MELD scores and portal hypertension, but not with HCC size and number, or metastasis. As a novel finding, baseline sCD163 appeared to predict a rapid HCC progression, as sCD163 increased during follow-up in HCC patients who showed progression.
URI: https://ahro.austin.org.au/austinjspui/handle/1/16308
DOI: 10.3109/00365513.2015.1099722
ORCID: 
Journal: Scandinavian Journal of Clinical and Laboratory Investigation
PubMed URL: https://pubmed.ncbi.nlm.nih.gov/26549495
Type: Journal Article
Subjects: Biomarker
immunity
Inflammation
Liver disease
Prediction
Tumor associated macrophages
Appears in Collections:Journal articles

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