摘要:

The biological activity of blood coagulation factors II, V, VII, VIII, IX, X, XI and XII, fibrinogen and prekallikrein was assessed in 15 healthy subjects and 60 patients with endemic Egyptian hepatosplenomegaly. The degree of liver disease was graded according to the Child-Pugh classification, the intensity of 5. mansoni infection was monitored by determination of circulating schistosome immune complexes (CSIC) level using a monoclonal antibody and hemostasis activation was detected by measurement of hemostatic markers D-dimer and prothrombin fragment 1+2 (F1+2). Functional activity of antithrombin III, α2-antiplasmin and protein C as well as quantitative determination of plasma concentrations of α1-antitrypsin, C1 activator inhibitor and α2-macroglobulin were also carried out. The progressive deterioration of liver function which matched the severity of the disease and the intensity of schistosomal infection led to a reduction in anticoagulant proteins (decreases in antithrombin III and protein C) resulting in hypercoagulability and thrombin generation (increased F1+2) subsequently followed by consumption (prolongation of coagulation screening tests, thrombocytopenia, hypofibrinogenemia and decreased factor VIII resulting in hypocoagulability and secondary fibrinolysis (increased D-dimer and decreased α2-antiplasmin). A significant decline in fibrinogen and factors VII, XII and prekallikrein was detected in bleeders compared with ascitic patients. The decline in factor XII was closely related to CSIC high titers in all disease groups, but was not correlated to D-dimer or F1+2 concentrations. This suggests that circulating schistosome immune complexes may exert an inhibitory effect on contact factor XII which should be taken into account when considering the reasons for schistosomal coagulopathy and bleeding in hepatosplenic schistosomiasis. Blood Coag Fibrinol 9:189–194 × 1998 Lippincott-Raven Publishers.

ISSN:0957-5235    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

The antiphospholipid antibody (APLA) syndrome is defined by the presence of a lupus anticoagulant or markedly elevated plasma levels of anticardiolipin antibodies (ACAs), associated with venous or arterial thromboembolic events, fetal loss or thrombocyto-penia. Familial clustering of raised APLA levels has been described, but the reports are heterogeneous with regard to the characterization of the APLA syndrome, coexisting autoimmune diseases and clinical complications. We describe two siblings with a lupus anticoagulant, elevated ACA-immunoglobulin G levels and systemic lupus erythematosus or related autoimmune disorders. Both patients experienced venous thrombotic complications at an early age. We provide a review of the literature, giving special consideration to the familial occurrence of lupus anticoagulants complicated by venous thrombosis, and emphasize the importance of family screening. Blood Coag Fibrinol 9:195–200 × 1998 Lippincott-Raven Publishers.

ISSN:0957-5235    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

There is little question that the blood clotting process is triggered and causes the vascular occlusion associated with myocardial infarction. Although it is less clear what part blood coagulation events might play in the etiology of coronary artery disease, impaired regulation of anticoagulation or fibrinolysis might be involved. Among anticoagulant and fibrinolytic factors, an elevated plasma plasminogen activator inhibitor-1 (PAI-1) concentration has been identified as a risk factor for the development of myocardial infarction. An association between one polymorphism of the PAI-1 promoter (4G/5G single nucleotide deletion/ insertion at position −675) and plasma PAI-1 levels was described in 1995. However, most recent studies seem to point to the lack of such an association. This is the first report on the frequency of this polymorphism in the Japanese population with respect to the risk of myocardial infarction. Sixty-six patients with myocardial infarction and sixty-two healthy control patients were chosen for the analysis of the PAI-1 promoter 4G/5G genotype with polymerase chain reaction-single strand conformation polymorphism. Five myocardial infarction patients and six in the control group were homozygous for the 4G/4G genotype. Twenty-eight and 27 4G/5G and 33 and 29 5G/5G genotypes were found in myocardial infarction and control groups, respectively. The total frequencies of the 4G and 5G alleles were approximately 30% and 70% in both control and myocardial infarction groups. In conclusion, the PAI-1 promoter genotype is not a risk factor for myocardial infarction in the Japanese population. This is in contrast to the first report in Caucasians, suggesting an interaction with other genetic or environmental factors which influences the risk of myocardial infarction. Blood Coag Fibrinol 9:201–204 × 1998 Lippincott-Raven Publishers.

ISSN:0957-5235    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

The plasma levels of heparin cofactor II were determined in pregnant women who were either normotensive, or had essential hypertension, gestational hypertension or pre-eclampsia during the third trimester and 72 h after delivery. Heparin cofactor II levels in the pre-eclampsia group were depressed. The clinical relevance of this finding is the potential utility of heparin cofactor II plasma levels in the differential diagnostic between non-proteinuric hypertension and pre-eclampsia. Blood Coag Fibrinol 9:205–208 × 1998 Lippincott-Raven Publishers.

ISSN:0957-5235    

出版商:OVID    

年代:1998

数据来源: OVID

ISSN:0957-5235    

出版商:OVID    

年代:1998

数据来源: OVID

ISSN:0957-5235    

出版商:OVID    

年代:1998

数据来源: OVID