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Plasminogen Activity (plasminogen + activity)
Selected AbstractsLigneous inflammation involving the female genital tractJOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH (ELECTRONIC), Issue 4 2007Abdullah Karaer Abstract Ligneous inflammation is a rare disease characterized by progressive growth of ligneous plaques on mucosal surfaces. Involvement of the female genital tract is an unusual condition. We present a patient with multifocal ligneous inflammation involving her genital tract, oral mucosa and conjunctiva. Plasminogen functional activity was 18% of normal (reference: 55,145%). Molecular analysis exhibited that her genetic status is homozygous for a combination of three polymorphisms. But no true mutation could be found in all 19 exons of the plasminogen gene. We did not observe any clinical changes, although plasminogen activity has improved in the course of 5 months of oral contraceptive therapy Most gynecologists are unfamiliar with this diagnosis and pathologists with wide experience in gynecology are unaware of this disease. However, the histology of lesions is characteristic and a diagnosis can be made quite easily once it has been considered. [source] A study on associations between antiprothrombin antibodies, antiplasminogen antibodies and thrombosisJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 4 2003M. J. A. Simmelink Summary., Anti-prothrombin antibodies are a frequent cause of lupus anticoagulant (LAC), a thrombotic risk factor. Prothrombin shares structural homology with plasminogen, a kringle protein with an important role in fibrinolysis. Cross-reactivity between antiprothrombin antibodies and plasminogen has been described. To study associations between LAC, IgG and IgM class antiprothrombin and antiplasminogen antibodies, plasminogen activity levels and thrombosis in selected patients with systemic autoimmune diseases. Patients included forty-six consecutive LAC-positive patients (29 with systemic lupus erythematosus (SLE); 33 with a thrombotic history), 38 patients without LAC (36 with SLE; seven with a history of thrombosis) and 40 healthy controls. In the total group of 84 patient samples, the prevalence of antiprothrombin and antiplasminogen antibodies was 30 and 38%, respectively. There was no significant relationship between the presence of these antibodies. In contrast to presence of antiplasminogen antibodies, presence of antiprothrombin antibodies was statistically significant related to thrombosis. Thirteen samples had antiprothrombin and antiplasminogen antibodies of similar isotype (IgG, n= 4; IgM, n= 9). Of these, all but one had LAC and 11/13 came from patients with a history of thrombosis. Simultaneous presence of IgM-class antiprothrombin and antiplasminogen antibodies had a significant association with thrombosis. Levels of plasminogen activity were similar in samples from healthy controls and patients (with or without antiplasminogen antibodies or thrombosis). Anti-prothrombin antibodies and antiplasminogen antibodies occur frequently in patients with systemic autoimmune disease. Anti-prothrombin antibodies, but not antiplasminogen antibodies are a risk factor for thrombosis. Anti-plasminogen are in most cases unrelated to antiprothrombin antibodies. [source] The first two Japanese cases of severe type I congenital plasminogen deficiency with ligneous conjunctivitis: Successful treatment with direct thrombin inhibitor and fresh plasma,,AMERICAN JOURNAL OF HEMATOLOGY, Issue 6 2009Takashi Suzuki A 71-year-old woman and her elder sister developed ligneous conjunctivitis after ocular surgery. Laboratory tests demonstrated that the proband and her sister had 6.6% and 8.1% of plasminogen activity, and 1.2 and 1.4 mg/dl of antigen, respectively. Thus, they were diagnosed as having severe type I plasminogen deficiency, for the first time, in Japan. DNA sequencing and PCR-RFLP analyses revealed that these two cases are homozygotes of a novel A-to-G mutation at the obligatory splicing acceptor site in intron-C. Both cases were satisfactorily treated with a direct thrombin inhibitor, topical Argatroban, and topical plasma obtained from their healthy family members. Am. J. Hematol. 2009. © 2009 Wiley-Liss, Inc. [source] ,2 -glycoprotein i is a cofactor for tissue plasminogen activator,mediated plasminogen activationARTHRITIS & RHEUMATISM, Issue 2 2009Chunya Bu Objective Regulation of the conversion of plasminogen to plasmin by tissue plasminogen activator (tPA) is critical in the control of fibrin deposition. While several plasminogen activators have been described, soluble plasma cofactors that stimulate fibrinolysis have not been characterized. The purpose of this study was to investigate the effects of ,2 -glycoprotein I (,2GPI), an abundant plasma glycoprotein, on tPA-mediated plasminogen activation. Methods The effect of ,2GPI on tPA-mediated activation of plasminogen was assessed using amidolytic assays, a fibrin gel, and plasma clots. Binding of ,2GPI to tPA and plasminogen was determined in parallel. The effects of IgG fractions and anti-,2GPI antibodies from patients with antiphospholipid syndrome (APS) on tPA-mediated plasminogen activation were also measured. Results Beta2 -glycoprotein I stimulated tPA-dependent plasminogen activation in the fluid phase and within a fibrin gel. The ,2GPI region responsible for stimulating tPA activity was shown to be at least partly contained within ,2GPI domain V. In addition, ,2GPI bound tPA with high affinity (Kd ,20 nM), stimulated tPA amidolytic activity, and caused an overall 20-fold increase in the catalytic efficiency (Kcat/Km) of tPA-mediated conversion of Glu-plasminogen to plasmin. Moreover, depletion of ,2GPI from plasma led to diminished rates of clot lysis, with restoration of normal lysis rates following ,2GPI repletion. Stimulation of tPA-mediated plasminogen activity by ,2GPI was inhibited by monoclonal anti-,2GPI antibodies as well as by anti-,2GPI antibodies from patients with APS. Conclusion These findings suggest that ,2GPI may be an endogenous regulator of fibrinolysis. Impairment of ,2GPI-stimulated fibrinolysis by anti-,2GPI antibodies may contribute to the development of thrombosis in patients with APS. [source] | ||||||||||