CC BY-NC-ND 4.0 · TH Open 2023; 07(02): e155-e167
DOI: 10.1055/a-2087-0314
Original Article

Platelets and the Lectin Pathway of Complement Activation in Patients with Systemic Lupus Erythematosus or Antiphospholipid Syndrome

1   Department of Biomedicine, Aarhus University, Aarhus, Denmark
Anne Troldborg
1   Department of Biomedicine, Aarhus University, Aarhus, Denmark
2   Department of Rheumatology, Aarhus University Hospital, Aarhus, Denmark
Anne-Mette Hvas
3   Faculty of Health, Aarhus University, Aarhus, Denmark
4   Thrombosis and Haemostasis Research Unit, Department of Clinical Biochemistry, Aarhus University Hospital, Aarhus, Denmark
Steffen Thiel
1   Department of Biomedicine, Aarhus University, Aarhus, Denmark
› Author Affiliations
Funding This study was supported by grants from Grosserer LF Foghts, the A.P. Moller Foundation (19-L-0091), and the Danish Rheumatism Association (R184-A6401 and R172-A6101). A.T. was supported by grants from Lundbeck Fonden (R264-2017-3344) and the Danish Rheumatism Association (R172-A6101). Tests for pattern recognition molecules were supported by Danish National Research Foundation through the Center for Cellular Signal Patterns (CellPAT) (DNRF135).


Background Patients with systemic lupus erythematosus (SLE) have an increased risk of thrombosis even when they do not have antiphospholipid syndrome (APS). Interactions between complement activation and activated platelets have been suggested in SLE and APS and could play a role in the increased thrombosis risk.

Objectives To explore factors potentially related to the prothrombotic pathophysiology in patients with SLE, primary APS, and healthy controls, by investigating lectin pathway proteins (LPPs), complement activation, platelet aggregation, and platelet activation.

Methods This cross-sectional cohort study included 20 SLE patients, 17 primary APS, and 39 healthy controls. Flow cytometry and light transmission aggregometry were used to assess platelet activation and aggregation. Using time-resolved immunofluorometric assays, the plasma concentrations of 11 LPPs and C3dg, reflecting complement activation, were measured.

Results H-ficolin plasma concentrations were higher in SLE and APS patients than in controls (p = 0.01 and p = 0.03). M-ficolin was lower in SLE than in APS (p = 0.01) and controls (p = 0.03). MAp19 was higher in APS patients than in SLE patients (p = 0.01) and controls (p < 0.001). In APS patients, MASP-2 and C3dg correlated negatively with platelet activation. Platelet-bound fibrinogen after agonist stimulation and C3dg concentrations correlated negatively with platelet activation.

Conclusion We observed significant differences between SLE and APS patients regarding complement proteins and platelet activation. Particularly the negative correlations between MASP-2 and C3dg with platelet activation only observed in APS patients suggest that interactions between complement activation and platelets differ in SLE and APS.

Supplementary Material

Publication History

Received: 28 October 2022

Accepted: 25 April 2023

Accepted Manuscript online:
05 May 2023

Article published online:
15 June 2023

© 2023. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (

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