Journal of Intensive Care (Jun 2022)

Soluble mannose receptor CD206 and von Willebrand factor are early biomarkers to identify patients at risk for severe or necrotizing acute pancreatitis

  • Philipp A. Reuken,
  • Jonathan F. Brozat,
  • Stefanie Quickert,
  • Oluwatomi Ibidapo-obe,
  • Johanna Reißing,
  • Anika Franz,
  • Sven Stengel,
  • Ulf K.-M. Teichgräber,
  • Michael Kiehntopf,
  • Christian Trautwein,
  • Andreas Stallmach,
  • Alexander Koch,
  • Tony Bruns

DOI
https://doi.org/10.1186/s40560-022-00619-2
Journal volume & issue
Vol. 10, no. 1
pp. 1 – 12

Abstract

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Abstract Background In acute pancreatitis (AP), microcirculatory dysfunction and leukocyte activation contribute to organ damage, inflammation, and mortality. Given the role of macrophage activation, monocyte recruitment, and microthrombus formation in the early pathogenesis of AP, we examined the macrophage activation marker soluble mannose receptor (sCD206) and the endothelial function marker von Willebrand factor (vWF) in patients admitted for AP. Methods In an exploratory analysis, serum sCD206 and plasma vWF were prospectively analyzed on day 1 and day 3 in 81 patients with AP admitted to the hospital. In addition, blood samples from 59 patients with early AP admitted to the intensive care unit and symptom onset 48 h and/or patients with local complications. Results In the prospective cohort, 17% developed severe/necrotizing pancreatitis compared with 56% in the ICU cohort. Serum concentrations of sCD206 on admission were higher in patients with severe/necrotizing AP than in patients with non-severe edematous AP (prospective: 1.57 vs. 0.66 mg/l, P = 0.005; ICU: 1.76 vs. 1.25 mg/l, P = 0.006), whereas other inflammatory markers (leukocytes, C-reactive protein, procalcitonin) and disease severity (SOFA, SAPS II, APACHE II) did not show significant differences. Patients with severe/necrotizing AP had a greater increase in sCD206 than patients with non-severe edematous AP at day 3 in the prospective cohort. In contrast to routine coagulation parameters, vWF antigen levels were elevated on admission (prospective cohort: 375 vs. 257%, P = 0.02; ICU cohort: 240 vs. 184%, P = 0.03). When used as continuous variables, sCD206 and VWF antigen remained predictors of severe/necrotizing AP after adjustment for etiology and age in both cohorts. Conclusions sCD206 identifies patients at risk of severe AP at earlier timepoints than routine markers of inflammation and coagulation. Prospective studies are needed to investigate whether incorporating early or repeated measurements into the existing scoring system will better identify patients at increased risk for complications of AP.

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