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Abstract Details
The association between soluble CD163, disease severity, and ursodiol treatment in patients with primary biliary cholangitis
Hepatol Commun. 2023 Mar 24;7(4):e0068. doi: 10.1097/HC9.0000000000000068.eCollection 2023 Apr 1.
1Department of Hepatology & Gastroenterology, Aarhus University Hospital, Aarhus, Denmark.
2Institute of Pathology, Aarhus University Hospital, Aarhus, Denmark.
3Department of Clinical Biochemistry, Aarhus University Hospital, Aarhus, Denmark.
4Diagnostic Centre, University Research Clinic for Innovative Patient Pathways, Silkeborg Regional Hospital, Silkeborg, Denmark.
5Department of Internal Medicine, Horsens Regional Hospital, Horsens, Denmark.
6Department of Internal Medicine, Herning Regional Hospital, Herning, Denmark.
7Department of Internal Medicine, Randers Regional Hospital, Randers, Denmark.
8Department of Internal Medicine, Viborg Regional Hospital, Viborg, Denmark.
Abstract
Introduction: The macrophage activation marker soluble (s)CD163 is associated with disease severity and prognosis in patients with primary biliary cholangitis (PBC). Ursodeoxycholic acid (UDCA) treatment attenuates fibrosis progression in PBC patients, but its effect on macrophage activation is unclear. We examined the effect of UDCA on macrophage activation, as determined by sCD163 levels.
Methods: We included 2 cohorts of PBC patients; 1 cohort with prevalent PBC patients, and 1 cohort of incident PBC patients before start of UDCA treatment and with follow-up after 4 weeks and 6 months. We measured sCD163 and liver stiffness in both cohorts. Further, we measured sCD163 and TNF-α shedding in vitro in monocyte-derived macrophages after UDCA and lipopolysaccharide incubation.
Results: We included 100 patients with prevalent PBC [93% women, median age 63 y (interquartile range: 51-70)] and 47 patients with incident PBC [77% women, median age 60 y (49-67)]. Prevalent PBC patients had a lower median sCD163 of 3.54 mg/L (2.77-4.72) than incident PBC patients with a median sCD163 of 4.33 mg/L (2.83-5.99) at inclusion. Patients with an incomplete response to UDCA and patients with cirrhosis had higher sCD163 than responders to UDCA and noncirrhosis patients. After 4 weeks and 6 months of UDCA treatment median sCD163 decreased by 4.6% and 9.0%, respectively. In in vitro experiments, UDCA attenuated shedding of TNF-α, but not sCD163, from monocyte-derived macrophages.
Conclusion: In PBC patients, sCD163 levels correlated with liver disease severity and treatment response to UDCA. Further, after 6 months of UDCA treatment, we observed a decrease in sCD163, which may be related to the treatment.
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