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Hepatic macrophage activation predicts clinical decompensation in chronic liver disease
  1. Anthony Rode1,
  2. Amanda Nicoll1,
  3. Holger Jon Møller2,
  4. Lucy Lim3,
  5. Peter W Angus3,
  6. Ian Kronborg4,
  7. Niranjan Arachchi4,
  8. Alexandra Gorelik5,
  9. Danny Liew5,
  10. Konstantin Kazankov6,
  11. Hendrik Vilstrup6,
  12. Henning Grønbæk6
  1. 1 Department of Gastroenterology & Hepatology, Royal Melbourne Hospital, Melbourne, Australia
  2. 2 Department of Clinical Biochemistry, Aarhus University Hospital, Aarhus, Denmark
  3. 3 Victorian Liver Transplant Unit & Department of Gastroenterology, Austin Hospital, Melbourne, Australia
  4. 4 Department of Gastroenterology, Western Hospital, Melbourne, Australia.
  5. 5 Melbourne EpiCentre, University of Melbourne and Melbourne Health, Australia
  6. 6 Department of Hepatology & Gastroenterology, Aarhus University Hospital, Aarhus, Denmark
  1. Correspondence to Dr Anthony Rode, Department of Gastroenterology & Hepatology, Royal Melbourne Hospital, Grattan St, Parkville, Melbourne 3150, Australia; arode{at}iinet.net.au

https://doi.org/10.1136/gutjnl-2012-304135

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    Hepatic macrophages (Kupffer cells) play important roles in inflammation and portal hypertension in patients with chronic liver disease (CLD).1 We recently showed that plasma soluble CD163 (sCD163), a specific marker for macrophage activation, is produced within and released from the liver with a direct relationship to the portal venous pressure gradient.2 ,3 We hypothesised that: (1) sCD163 is elevated in patients with CLD with previous clinical decompensation; and (2) sCD163 is a marker for CLD progression and clinical deterioration.

    We measured sCD163 in 52 controls and 116 consecutive patients with CLD (89% cirrhosis) caused by chronic hepatitis C (36%), alcohol (30%), non-alcoholic fatty liver disease (11%), chronic hepatitis B (10%); other liver diseases (12%) accounted for the remainder of the cases. Cirrhosis was diagnosed by consistent examination and radiological findings, or by liver biopsy. All controls had no history or clinical examination signs of CLD, and normal liver function tests. They were followed for a median of …

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    Footnotes

    • Contributors AR: study conception and design, acquisition of data, analysis and interpretation of data; drafting the article and revision; final approval; AN, HJM, PWA, IK, NA, AG, DL, KK, HV and HG: study conception and design, analysis and interpretation of data; drafting the article and revision; final approval; LL: study conception and design, data collection, analysis and interpretation of data; drafting the article and revision; final approval.

    • Funding The Novo Nordisk Foundation supported HG with a clinical research grant. The study was supported by The Danish Council for Strategic Research (TRAIN 10-092797).

    • Competing interests None.

    • Patient consent Obtained.

    • Ethics approval Melbourne Health HREC.

    • Provenance and peer review Not commissioned; externally peer reviewed.