title: Clinical significance of the venous occlusion test on systemic lupus erythematosus patients with a focus on changes in blood levels of tissue plasminogen activator, von Willebrand factor antigen, and thrombomodulin.
abstract: We investigated the clinical significance of the venous occlusion (VO) test on patients with systemic lupus erythematosus (SLE) with or without circulating lupus anticoagulant (LA) concerning whether changes in the blood coagulation and fibrinolysis system in vivo subsequent to VO reflect mechanical stimulation of the endothelium or presence/development of endothelial damage. The tissue plasminogen activator antigen (tPA:Ag) before VO was much lower in the LA-positive patients than in the LA-negative ones (p < 0.01) and the von Willebrand factor antigen (VWF:Ag) pre-VO was significantly higher in the patient group, regardless of LA status, than in the control group (p < 0.01). But the mean increment in tPA:Ag and VWF:Ag post-VO, when expressed as the percentage of the baseline level, showed no appreciable difference between LA-positive and -negative groups. Thrombomodulin (TM) basically, on the other hand, was higher in the patients of either LA status than in the controls (p < 0.01) with a significant post-VO increase in the SLE group, which was more marked in the LA-positive patients, against no substantial change in the controls (p < 0.01). It is known that tPA and VWF:Ag are released simply as a result of endothelial stimulation and that the release of TM is preceded by endothelial damage. Based on the present results, we may well conclude that (1) the endothelium is functionally intact in SLE patients, (2) an injury of the endothelium, possibly as a consequence of vasculitis, preexists in LA-positive patients, and thus to measure the TM response to VO would offer a helpful tool in diagnosing the preexisting endothelial damage in these clinical settings.
authors.affiliation: Department of Medicine, Teikyo University School of Medicine, Tokyo, Japan.
authors.forename: J
authors.initials: J
authors.lastname: Matsuda
authors.forename: K
authors.initials: K
authors.lastname: Kawasugi
authors.forename: K
authors.initials: K
authors.lastname: Gohchi
authors.forename: N
authors.initials: N
authors.lastname: Saitoh
authors.forename: M
authors.initials: M
authors.lastname: Tsukamoto
authors.forename: M
authors.initials: M
authors.lastname: Kazama
authors.forename: T
authors.initials: T
authors.lastname: Kinoshita
mesh_terms: D000328:Adult; D001132:Arm / Q000098:blood supply*; D005260:Female; D006801:Humans; D016682:Lupus Coagulation Inhibitor / Q000097:blood; D008180:Lupus Erythematosus, Systemic / Q000097:blood*; D010980:Platelet Membrane Glycoproteins / Q000032:analysis; D011956:Receptors, Cell Surface / Q000032:analysis*; D018179:Receptors, Thrombin; D013917:Thrombin / Q000032:analysis; D010959:Tissue Plasminogen Activator / Q000097:blood*; D014111:Tourniquets; D014680:Veins; D014841:von Willebrand Factor / Q000032:analysis*
chemical_list: D016682:Lupus Coagulation Inhibitor; D010980:Platelet Membrane Glycoproteins; D011956:Receptors, Cell Surface; D018179:Receptors, Thrombin; D014841:von Willebrand Factor; D013917:Thrombin; D010959:Tissue Plasminogen Activator