Statins not only have a
lipid-lowering effect but also reduce
inflammation and have an antithrombotic effect. Since
hypercoagulability assessed by
thrombin generation assay (TGA) and increased formation of neutrophil extracellular traps (NET) were demonstrated in diabetes, we investigated whether
statin therapy in diabetes modifies coagulation status and NET formation. Twenty-five consecutive patients with diabetes were recruited. Global coagulation assays (prothrombin time [PT], activated partial thromboplastin time [aPTT], and TGA) and NET
markers (DNA-
histone complex,
cell-free DNA, and
neutrophil elastase) were measured before and after 3-month moderate-intensity
statin therapy. In addition, all
coagulation factors and 3 anticoagulation factors were measured.
Statin therapy significantly reduced endogenous
thrombin potential (ETP) value and blood
lipids but did not change the PT and aPTT values or NET formation markers.
Statin significantly decreased not only
coagulation factors (II, V, VIII, IX, and X) but also the anticoagulation factor
antithrombin.
Statin-induced reduction of
factor V and X significantly contributed to the reduction of ETP value. The extent of reduction in
coagulation factors correlated with that of anticoagulation factors, but not that of
cholesterol. It is possible to use TGA as a global coagulation assay that can detect coagulation status modified by
statin therapy. Additional studies are needed to evaluate the clinical implications of
statin-induced simultaneous reduction of coagulation and anticoagulation factors.