title: Prothrombin fragment 1 + 2 measures treatment effect in patients with antiphospholipid syndrome.
abstract: Antiphospholipid syndrome (APS) is characterized by recurrent thrombosis. The anticoagulant management of APS thrombosis remains controversial. Few reports on markers of in vivo activation of coagulation have been reported. To determine whether plasma levels of prothrombin fragment 1 + 2 (F1 +2) correlate with thrombotic risk and treatment effect in patients with APS, plasma F1 + 2 levels were followed in 57 patients with this syndrome for more than 2 years. Clinical findings were also observed in these patients. Plasma levels of F1 + 2 in patients with APS were significantly higher when compared with control subjects (p<.05). These results suggest patients with APS are in a hypercoagulable state. Plasma levels of F1 + 2 significantly decreased following treatment with either aspirin, or aspirin plus warfarin (p<.05 and p<.01, respectively). Recurrent thromboses or spontaneous abortions occurred in all eight patients whose plasma levels of F1 + 2 remained higher than 1 nmol/l after treatment with either aspirin alone or no anticoagulants. These patients were subsequently treated with warfarin as well as aspirin, and plasma levels of F1 + 2 decreased to less than 1 nmol/l, with no additional thrombotic events over the remainder of the 2-year follow-up. No fatal bleeding was observed in treated patients. Our results suggest plasma levels of F1 + 2 are useful indicators of successful treatment. It is also suggested that warfarin plus mini-dose aspirin therapy is effective for patients with APS to protect from recurrent thromboses without harmful side effects. Further, prospective cohort studies are needed to substantiate these associations.
authors.affiliation: Department of Internal Medicine (III), Kanazawa University School of Medicine, Japan. masahide@med.kanazawa-u.ac.jp
authors.forename: M
authors.initials: M
authors.lastname: Yamazaki
authors.forename: H
authors.initials: H
authors.lastname: Asakura
authors.forename: M
authors.initials: M
authors.lastname: Saito
authors.forename: H
authors.initials: H
authors.lastname: Jokaji
authors.forename: C
authors.initials: C
authors.lastname: Uotani
authors.forename: I
authors.initials: I
authors.lastname: Kumabashiri
authors.forename: E
authors.initials: E
authors.lastname: Morishita
authors.forename: K
authors.initials: K
authors.lastname: Aoshima
authors.forename: T
authors.initials: T
authors.lastname: Matsuda
authors.forename: D A
authors.initials: DA
authors.lastname: Triplett
mesh_terms: D016736:Antiphospholipid Syndrome / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D001241:Aspirin / Q000627:therapeutic use; D015415:Biomarkers; D006801:Humans; D010446:Peptide Fragments / Q000032:analysis* / Q000378:metabolism; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D011498:Protein Precursors / Q000032:analysis* / Q000378:metabolism; D011516:Prothrombin / Q000032:analysis* / Q000378:metabolism; D013927:Thrombosis / Q000097:blood* / Q000188:drug therapy / Q000209:etiology; D014859:Warfarin / Q000627:therapeutic use
chemical_list: D015415:Biomarkers; D010446:Peptide Fragments; D010975:Platelet Aggregation Inhibitors; D011498:Protein Precursors; D014859:Warfarin; C029733:prothrombin fragment 1; C044183:prothrombin fragment 2; D011516:Prothrombin; D001241:Aspirin