Clinical and Experimental Rheumatology 2013; 31: 000-000. Degradation of neutrophil extracellular traps is decreased in patients with antiphospholipid syndrome J. Lefler 1 , L. Stojanovich 2 , Y. Shoenfeld 3 , G. Bogdanovic 2 , R. Hesselstrand 4 , A.M. Blom 1 1 Dept. of Laboratory Medicine, Section of Medical Protein Chemistry, Lund University, Malmö, Sweden; 2 Dept. of Internal Medicine, “Bezhanijska Kosa” University Medical Center, Belgrade, Serbia; 3 Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel Aviv, Israel; 4 Dept. of Clinical Sciences, Section of Rheumatology, Lund University, Lund, Sweden. Abstract Objective A decreased ability to degrade neutrophil extracellular traps (NETs) is seen in a subgroup of patients with systemic lupus erythematosus (SLE) and correlates with the presence of autoantibodies. Antiphospholipid syndrome (APS) can develop secondary to SLE or as a primary disease. In the current study we investigated the ability of sera from patients with APS to degrade NETs. The presence of antibodies against NETs and neutrophil remnants were also determined in the same patients. Methods In the study, 106 patients with APS (73 primary and 33 secondary), 76 patients with systemic sclerosis (SSc) and 77 healthy donors as control samples were included. NETs generated from neutrophils isolated from healthy volunteers were incubated with patient sera, followed by measurement of degraded NETs or deposited IgG. Results Sera of APS patients had a decreased ability to degrade NETs compared to healthy controls, with no difference between primary and secondary APS. Sera from SSc patients did not differ signiicantly from healthy controls in the ability to degrade NETs. A decreased degradation of NETs correlated weakly to increased levels of antibodies against NETs/ neutrophil remnants in patients with primary APS, but stronger in patients with secondary APS. Conclusion The ability to degrade NETs is decreased in a subgroup of patients with APS and is associated with antibodies against NETs and speciic clinical manifestations in those patients. Key words neutrophils, extracellular space, antiphospholipid syndrome, autoantibodies, systemic sclerosis