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Biomedical subjects

J F Schved

Publications and source records attributed to J F Schved.

At least 19 recordsLinked to original sources
PubMed1992

Procoagulant activity of endotoxin or tumor necrosis factor activated monocytes is enhanced by IgG from patients with lupus anticoagulant.

The effect of lupus anticoagulant (LA) positive plasma on the expression of human monocyte procoagulant activity (PCA) was studied. LA positive plasma were able to enhance the endotoxin or TNF alpha induced monocyte associated PCA. The monocyte PCA had the characteristic of tissue factor activity (factor VII, factor X dependence). The enhancement of monocyte PCA could be confirmed using purified LA positive IgG. The stimulating effect was supported by the F(ab')2 fragments.

Adult↗
PubMed1992

Study of the protein S system in HIV-infected patients: acquired protein S deficiency or unsuitable assays?

The plasma protein S (PS) system was studied in 120 HIV seropositive patients (CDC classification: group II: n = 35; group III: n = 6; groups IVA, IVC2 or IVE, n = 38; groups IVB, IVC1 or IVD, n = 41). Total PS antigen and C4b-binding protein (C4b-BP) values were not significantly different from control values. Free protein S levels assessed by an immunological method in the supernatant of PEG-precipitated plasma samples (PEG-fPS) were below the normal limit in 85 patients, lower values being found in patients with advanced HIV disease. No correlation was found between PEG-fPS levels and C4b-BP or total PS levels. At least 25 patients had a low functional PS value. Low functional levels of PS were found in each clinical group although there was no difference in the distribution of functional PS values among groups. Crossed immuno-electrophoresis showed an abnormal distribution of PS in some patients, but failed to confirm the marked decrease of free PS in patients with very low PEG-fPS. An impairment of the protein S system is observed in HIV-infected patients. However, the discrepancies found in some patients among the results of the various PS-related assays should lead to a cautious interpretation concerning the incidence of PS deficiency in HIV-infected patients.

Adult↗
PubMed1992

Autoantibody to plasma fibrinopeptide A in a patient with a severe acquired haemorrhagic syndrome.

We describe a 50-year-old man with a severe acquired haemorrhagic syndrome. He had slightly prolonged clotting times using bovine thrombin, human thrombin and reptilase. His plasma contained a polyclonal IgG which interfered with the generation of fibrin monomers without inhibiting the aggregation of preformed monomers. The inhibitor delayed thrombin-induced fibrinopeptide A release. The IgG bound to insolubilized synthetic fibrinopeptide A (one binding site per molecule) and, with higher affinity, to fibrinogen (two binding sites per molecule). It did not bind to insolubilized fibrin monomers. The IgG did not impair the catalytic activity of thrombin toward a small synthetic substrate but inhibited the binding of thrombin to fibrinogen without binding to thrombin. The binding of the anti-fibrinopeptide A autoantibody to fibrinogen might have impaired thrombin-induced fibrinogen to fibrin conversion in vivo. This may have favoured the reported haemorrhagic syndrome which was associated with severe chronic renal insufficiency.

Autoantibodies↗
PubMed1992

Meningococcaemia in an adult with hereditary C4b-binding protein deficiency: study of the variations of the protein S system.

Serial studies of the plasma protein C-protein S system were performed during the clinical course of a pregnant woman with meningococcaemia who recovered under therapy. The patient had limited purpura fulminans skin lesions and hereditary C4b-binding protein deficiency was suspected. This diagnosis was confirmed in the patient 1 year after delivery and also by family studies. During the meningococcaemia, an initial mild and transient acquired protein C deficiency was seen but no protein S deficiency was observed despite consumption of the latter protein. As C4b-binding protein partial deficiency is associated with high free protein S and protein S activity, this may have protected against acquired protein S deficiency during meningococcaemia.

Adult↗
PubMed1992

von Willebrand factor antigen, tissue-type plasminogen activator antigen, and risk of death in human immunodeficiency virus 1-related clinical disease: independent prognostic relevance of tissue-type plasminogen activator.

Tissue-type plasminogen activator, von Willebrand factor, and plasminogen-activator inhibitor type 1 plasma levels were measured at first consultation in 85 consecutive patients infected with human immunodeficiency virus. Patients were assigned to three groups according to clinical status: mild disease group, intermediate group, and acquired immunodeficiency syndrome group. Significant differences were found in von Willebrand factor, tissue-type plasminogen activator, and plasminogen-activator inhibitor type 1 plasma levels among the three groups: severe clinical status was associated with higher von Willebrand factor, tissue-type plasminogen activator, and plasminogen-activator inhibitor type 1 plasma levels. Significant correlations were found among these three parameters, such known biologic prognostic indicators of human immunodeficiency virus infection as IgA, anti-p24 antibodies, p24 antigenemia, CD4+ lymphocytes, beta 2-microglobulin, and the clinical status. The prognostic relevance of plasma von Willebrand factor and tissue-type plasminogen activator levels at the time of entry into the study was then investigated in a cohort of 65 of the 85 patients who had follow-up during a median period of 22 months. The median survival time for all patients was 39 months after the first consultation. A plasma von Willebrand factor level greater than 200% of the control value had a positive predictive value of 86% for determining nonsurvivors; the median survival time for such patients was 9 months after the first consultation. A positive predictive value of 100% in recognizing nonsurvivors was found for tissue-type plasminogen factor plasma levels greater than 20 ng/ml; the median survival time for these patients was 2 months after the first consultation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

[Endothelial mediators regulating vascular tonus].

Vascular endothelium is the unavoidable interface between blood and tissues. Its role as regulator of vascular tone is discussed here. The endothelium possesses different receptors for vasoactive mediators. These receptors activate the endothelial cells which in turn may produce secondary mediators acting on smooth muscle cells by activating or inhibiting their contraction. Such mediators are the endothelins which have a vasoconstrictor effect, and prostacyclin or endothelium-derived relaxation factors (EDRF) which have a vasodilator effect. Thus, the vascular endothelium and the mediators it secretes play a crucial role in vascular tone physiology.

Endothelins↗
PubMed1991

Venous occlusion and chronic cigarette smoking: dose-dependent decrease in the measurable release of tissue-type plasminogen activator and von Willebrand factor.

This study was aimed at examining the effect of chronic cigarette smoking on a venous occlusion test. Two groups of young healthy men, a control group of 20 non-smoking subjects and a group of 21 smoking subjects having an average consumption of 17.6 packages.day-1.years (SD 8.6) were studied. Venous occlusion performed in smokers did not induce a significant measurable release of von Willebrand factor (vWF). The release of tissue-type plasminogen activator (t-PA) was significantly weaker for the smokers than for the control group (P less than 0.02). An inverse correlation was found between the cumulative parameter of tobacco consumption and the measurable amount of t-PA Ag or vWF Ag released during venous occlusion (r' = -0.994 and r' = -0.889). Cigarette smoking is thus associated with disturbances of the biological response to this venous occlusion test.

Adult↗
PubMed1991

[Fibrinolytic activity in traumatic hemothorax fluids].

Twenty-nine patients, 15 to 85-year-old (mean: 50 years) who presented with a pleural effusion after trauma were studied. The blood content of pleural fluid was confirmed by thoracocentesis. None of the patients had been taking anticoagulant drugs during the fortnight preceding the trauma. Thoracocentesis was always carried out less than 90 min after the trauma. The following parameters were measured in the haemothorax liquid samples: clotting fibrinogen fraction (Fg C), fibrin degradation D-dimers, functional plasminogen, alpha 2-antiplasmin, alpha 2-macroglobulin, plasminogen tissue activator (tPA Ag), type 1 tPA plasma inhibitor (PAI), and haematocrit. Haemothorax liquid haematocrit values ranged from 13 to 35% (25 +/- 7%, with a mean peripheral venous haematocrit of 34 +/- 6%). Only three patients had some Fg C (0.05-0.13 g.l-1). The D-dimer level was very high (0.23 +/- 0.22 g.l-1). The other factors involved in fibrinolysis were also present. Moreover, there was a statistically significant inverse correlation between D-dimer and alpha 2-macroglobulin levels (r = -0.64, p less than 0.0025). These data suggest two possible mechanisms to explain the fibrinogen levels: coagulation is activated, followed by an important fibrinolytic reaction elicited by the large amounts of plasminogen and tPA present in the haemothorax liquid.

Adolescent↗
PubMed1991

[Impaired fibrinolytic response to the venous occlusion test in patients with cryptogenic colitis].

The fibrinolytic response to venous occlusion was studied in 17 patients with inflammatory bowel disease: 7 with Crohn's disease, 10 with ulcerative colitis and compared with those obtained in 20 controls. Patients with inflammatory bowel disease showed decreased tissue-type plasminogen activator antigen release (t-PA Ag), no significant Von Willebrand antigen release (vWF Ag), and a residual plasminogen activator inhibitor activity (PAI activity) after venous occlusion. These modifications were more important in the evolutive colitis group compared with the remission group. Hypofibrinolysis, as defined by a defective t-PA release, and a residual PAI activity after venous occlusion might contribute to digestive and/or extra digestive thrombotic manifestations observed during the course of inflammatory bowel diseases.

Adult↗
PubMed1990

Impact of smoking, physical training and weight reduction on FVII, PAI-1 and hemostatic markers in sedentary men.

The variations of FVII, PAI-1, TAT complexes, fibrinopeptide A, D-Dimers and beta thromboglobulin plasma levels were studied on 30 sedentary men, smokers and non-smokers, who were admitted to a 6 months' program of physical training and smoking cessation. After 3 months of intervention, sustained physical training was associated with the decrease of FVII and PAI-1 levels. Mild exercise performed during a second 3-month period could maintain normal FVII and PAI-1 activities but participants who stopped the training increased their FVII and PAI-1 plasma levels. FVII was not influenced by smoking habits. Smoking cessation seemed to slightly potentiate the decrease of PAI-1 levels associated with mild exercise. Overweight, FVII and PAI-1 levels were correlated and the weight reduction induced by training was related to the changes in the factors. In smokers, physical exercise was associated with a significant increase of hemostatic markers. This exercise-induced variation disappeared after 3 months of intervention in participants who stopped smoking and reappeared in those who smoked again after 6 months of intervention. This finding was not influenced by the physical training program.

Antithrombin III↗
PubMed1990

Impaired fibrinolytic capacity in patients with inflammatory bowel disease.

The venous occlusion test was applied to 17 patients with inflammatory bowel disease (IBD; 7 cases of Crohn's disease, 10 cases of ulcerative colitis). Results were compared to those obtained in 20 healthy matched control subjects. Patients with IBD had significantly decreased t-PA Ag release (p less than 0.001) and had no significant vWF Ag release. Residual PAI activity was evidenced after venous stasis in the IBD group but not in the control group. Hypofibrinolysis was more important in patients with an evolutive IBD than in patients with IBD in remission. Impaired systemic fibrinolytic capacity might contribute to an increased risk for thromboembolic complications and to the pathogenesis of inflammatory bowel disease.

Adult↗
PubMed1990

Study of quantitative modifications of the plasma protein S system components in non-acute inflammatory syndromes.

Thrombosis frequently accompanies inflammatory disease. There are numerous and frequent modifications of haemostasis parameters during inflammatory disease. Deficiencies in protein S, a protein C cofactor, are predisposing factors for thromboses. In 43 patients with biological inflammatory syndromes (ESR above 80 mm in the first hour found twice in a three-day period and disturbances of other biological inflammatory markers) we studied the variations of the protein S system: total antigenic protein S, free antigenic protein S, C4b BP, all antigenic fractions being assayed by electro-immuno diffusion. The results show an increase in free protein S (mean 114.3%, range 25%-180%, P less than 0.005), the biologically active fraction of protein S. They also evidence the expected increase in C4b BP (mean 188.3%, range 41%-335%, P less than 10(-5]. There is an increase in total protein S Ag (mean 145.3%, range 56%-220%, P less than 10(-5]. The results show a high positive correlation between the increased free protein S Ag and total protein S Ag (r' = 0.78, P less than 0.01), between total protein S and C4b BP (r' = 0.8, P less than 0.01) and between free protein S and C4b BP (r' = 0.73, P less than 0.01). C4b BP concentrations are correlated with haptoglobin (r' = 0.59, P less than 0.01), orosomucoid (r' = 0.53, P less than 0.01), C3 complement component (r' = 0.80, P less than 0.01), C4 (r' = 0.39, P less than 0.02) and platelet count (r' = 0.51, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Pneumocystis carinii infection of bone marrow in patients with malignant lymphoma and acquired immunodeficiency syndrome. Original report of three cases.

Pneumocystis carinii (PC) pneumonia was reported with increased frequency in patients presenting with acquired immunodeficiency syndrome (AIDS) or in patients receiving immunosuppressive chemotherapy for hemopathies. Extrapulmonary dissemination of PC is rare. In this study, three patients had PC infection of the bone marrow. Two of them presented with malignant lymphoma that had apparent immunosuppression, and the third patient presented with AIDS. In all three cases, such an infection was observed before or concomittantly with PC pneumonia. A bone marrow biopsy, bone marrow aspirate, or both can be useful, readily available tools for the diagnosis of a PC infection and especially its dissemination in patients with malignant lymphoma after intensive treatment or in patients with AIDS. The appreciation of such a dissemination may have some implications in the treatment of PC infection.

Acquired Immunodeficiency Syndrome↗