PO-20 - Crosstalk between the lectin pathway and haemostasis in patients with pulmonary cancer

J B Larsen; T D Christensen; C L Hvas; A M Hvas

doi:10.1016/S0049-3848(16)30153-0

PO-20 - Crosstalk between the lectin pathway and haemostasis in patients with pulmonary cancer

Thromb Res. 2016 Apr:140 Suppl 1:S183. doi: 10.1016/S0049-3848(16)30153-0. Epub 2016 Apr 8.

Authors

J B Larsen¹, T D Christensen², C L Hvas³, A M Hvas¹

Affiliations

¹ Center for Haemophilia and Thrombosis, Department of Clinical Biochemistry, Aarhus University Hospital.
² Department of Thoracic Surgery, Aarhus University Hospital.
³ Department of Anaesthesiology, Aarhus University Hospital; Denmark.

PMID: 27161707
DOI: 10.1016/S0049-3848(16)30153-0

Abstract

Introduction: Recent research has focused on the complement system in cancer, including the lectin pathway of complement activation. Mannose-binding lectin (MBL), a key activator of the lectin pathway, can bind to tumor cell surfaces in vitro, and lectin pathway activation is increased in several types of cancer. The exact role of the complement system in cancer is currently discussed. However, one possible consequence of the increased complement activation could be contribution to the increased thrombosis risk which cancer patients experience. Proteins of the lectin pathway can activate coagulation and impair fibrinolysis in vitro, but the significance of this in a clinical setting is not well understood.

Aim: We aim to investigate associations between lectin pathway and haemostatic activation in patients with lung cancer undergoing thoracoscopic surgery.

Materials and methods: Patients with lung cancer (n=60) eligible for thoracoscopic tumor resection were included as part of a randomized controlled trial, the COPPVATS project (EudraCT no: 2012-002409-23), conducted at the Department of Thoracic Surgery, Aarhus University Hospital. Exclusion criteria were arterial or venous thrombosis within the last three months, other systemic disease than cancer, and anticoagulant treatment prior to inclusion. Blood samples were obtained the day before surgery, perioperatively, and on the 1st and 2nd postoperative days. Laboratory analyses on the complement system include MBL, MBL-associated protease (MASP)-1 and -2, MBL-MASP complex, ficolin-1, -2, and -3 and complement factor C3b. Haemostasis was evaluated with routine coagulation parameters (INR, APTT, fibrinogen, fibrin d-dimer), platelet function, and tissue factor-induced thrombin generation.

Results: Recruitment of the study subjects is concluded, and laboratory work is in progress. The complement analyses and data processing will be performed during early spring 2016, so that results will be ready for presentation on the conference.

Conclusions: The present project will provide new knowledge on lectin pathway activation and the pathogenesis of thrombosis in cancer patients. In the long term, this will help improve the individual risk assessment and lead to new studies on thromboprophylaxis and treatment in conditions with increased complement activation.