Research and practice in thrombosis and haemostasis · 2026
Coagulation activation in anorexia nervosa: increased tissue factor and prothrombin fragment 1+2.
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Egedal Jeanie Meincke, Bladbjerg Else-Marie, Sjögren Jan Magnus, Sprogøe Ulrik, Støving René Klinkby
Аннотация
BACKGROUND: An increased risk of both venous and arterial thromboses in patients with anorexia nervosa (AN) has been established epidemiologically and reported via case reports. However, the coagulation system is incompletely studied in patients with AN.
OBJECTIVES: To investigate the coagulation profile in patients with AN by assessing the tissue factor (TF) and contact activation pathways in plasma and whole blood.
METHODS: In a cross-sectional case-control study, 40 female patients with AN and 40 healthy, age-matched, normal-weight controls were included. Plasma coagulation markers, in vitro thrombin and kallikrein generation, and whole-blood rotational thromboelastometry variables were analyzed and compared between groups.
RESULTS: Patients with AN had significantly higher plasma concentrations of TF, prothrombin fragment 1+2, C1 inhibitor, and high-molecular-weight kininogen and reduced kallikrein generation. No group differences were found in thrombin generation or rotational thromboelastometry variables.
CONCLUSION: In this comparative cross-sectional study, we found that patients with AN exhibit modest coagulation activation, characterized by elevated plasma TF and prothrombin fragment 1+2, alongside increased C1 inhibitor and reduced contact activation potential. This indicates that the balance between coagulation activators and inhibitors is generally maintained, but with an imbalance in the contact activation pathway that does not indicate a procoagulant state. The findings suggest a shift toward in vivo coagulation activation in AN but should be interpreted as hypothesis-generating and warrant confirmation in future studies.
OBJECTIVES: To investigate the coagulation profile in patients with AN by assessing the tissue factor (TF) and contact activation pathways in plasma and whole blood.
METHODS: In a cross-sectional case-control study, 40 female patients with AN and 40 healthy, age-matched, normal-weight controls were included. Plasma coagulation markers, in vitro thrombin and kallikrein generation, and whole-blood rotational thromboelastometry variables were analyzed and compared between groups.
RESULTS: Patients with AN had significantly higher plasma concentrations of TF, prothrombin fragment 1+2, C1 inhibitor, and high-molecular-weight kininogen and reduced kallikrein generation. No group differences were found in thrombin generation or rotational thromboelastometry variables.
CONCLUSION: In this comparative cross-sectional study, we found that patients with AN exhibit modest coagulation activation, characterized by elevated plasma TF and prothrombin fragment 1+2, alongside increased C1 inhibitor and reduced contact activation potential. This indicates that the balance between coagulation activators and inhibitors is generally maintained, but with an imbalance in the contact activation pathway that does not indicate a procoagulant state. The findings suggest a shift toward in vivo coagulation activation in AN but should be interpreted as hypothesis-generating and warrant confirmation in future studies.