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J C Gris

Publications and source records attributed to J C Gris.

69 records · Page 4Linked to original sources
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

Biocompatibility of blood tubings.

We studied hemocompatibility of various blood tubings with C3a anaphylatoxin measurement and comparative electron scanning microscopy. The following tubing materials were tested: polyvinylchloride (PVC) plasticised with phthalate (PVC), pvc plasticised with phthalate coextruded with polyurethane (PIV), and two phthalate-free lines: pvc plasticised with trimellitate coextruded with polyurethane (TRI) and pvc plasticised with LT 360 (LTP). Results of C3a generation rate showed a significant activation by all blood tubings, with a reduced rate with PIV when compared to all others. Electron scanning microscopy showed marked alterations of PIV surface on tubings stored for 6 months. Protein deposits on internal surfaces after dialysis were similar whatever tubing material was tested, but adhesive cell number was greater with TRI when compared to PVC and LTP. Hemocompatibility is unchanged with phthalate-free tubings when compared to phthalate plasticised ones. In contrast with phthalate plasticised PVC there is no beneficial effect of polyurethane coextrusion with trimellitate plasticised PVC in regard to C3a generation.

Anaphylatoxins↗
PubMed1988

[Comparison of thawing of plasma by microwave or water bath: preliminary longitudinal biological study of hemostatic parameters].

Exploration of haemostasis was performed on plasmas thawed in an experimental microwave oven comparatively to a 37 degrees C water bath. Factor VIII:R:Ag, procoagulant and antigenic fibrinogen, and Fg:C/Fg:Ag ratio were found to be significantly, slightly decreased with microwave thawing. Factor VIII:C and VIII:C/VIII:R:Ag ratio were found to be increased with microwaves. Antigenic fractions were decreased because of partial precipitation. In addition, Fibrinogen slightly lost its activity; on the contrary, factor VIIIC was activated by micro-waves. All this allows to select parameters for new experimental microwave ovens development.

Blood Coagulation Factors↗
PubMed1988

Anti-idiotypic antibodies against anti-phospholipid autoantibodies which suppress lupus-like anticoagulant activity.

We have studied IgG F(ab')2 fractions in the plasma from a patient during spontaneous remission from lupus anticoagulant (LAC). Fractions from the remission period inhibited the LAC activity of preremission fractions, as evaluated by in vitro coagulation tests. Idiotypic/anti-idiotypic interactions were demonstrated by affinity chromatography. The same results were obtained with IgG F(ab')2 from pooled normal plasma. This enables us to treat the LAC relapse in this patient with purified recurrent anti-idiotypic determinant antibodies extracted from normal plasma.

Adult↗
PubMed1987

[Is protein C deficiency responsible for portal thrombosis after neonatal exchange transfusion?].

The authors report the case of a 12-year old boy admitted to hospital for cerebral ischaemic accident and in whom laboratory examinations revealed a 40% deficiency of protein C. Other investigations showed that the child, who had undergone exchange transfusion by the umbilical route at birth, had portal vein thrombosis. It is suggested that protein C deficiency might be responsible for some cases of portal vein thrombosis occurring after umbilical catheterization performed in the neonatal period.

Catheterization↗
PubMed1987

Present results of the treatment of myelodysplastic syndromes with low-dose cytosine arabinoside. Preliminary results of a cooperative protocol (38 patients) and review of the literature.

In vitro differentiating agents causing little bone marrow aplasia have been proposed as a specific therapy of myelodysplastic syndromes with excess of blasts. A critical review of the published data is presented. The preliminary results of a cooperative protocol using very low dosage of cytosine arabinoside (3mg/m2/twice daily) with or without androgens are given.

Aged↗
PubMedDate not supplied

[Treatment of deep venous thrombosis in congenital antithrombin III deficiency with low molecular weight heparin].

A 19-year old male patient with hereditary antithrombin III type I deficiency was admitted for thrombosis of the right iliac, femoral and popliteal veins. Treatment with a low molecular weight heparin resulted in recanalization of the veins confirmed by phlebography. After two weeks of treatment, the drug was replaced by another low molecular weight heparin and this was followed, 3 weeks later, by a documented relapse of thrombosis.

Adult↗
PubMedDate not supplied

Acquired isolated factor VII deficiency during sepsis.

Isolated acquired factor VII deficiency is uncommon. We report 11 cases of acquired factor VII deficiency associated with severe systemic sepsis. All patients initially displayed a heterozygous-like factor VII deficiency confirmed by both clotting and amidolytic assays, associated with low factor VII antigen levels, and increased haemostasis markers (D-dimers, prothrombin fragments 1.2, thrombin-antithrombin complexes). After sepsis recovery, normal factor VII levels were evidenced. Isolated factor VII consumption or proteolytic degradation by leucocyte proteases can be evoked, but the mechanism of acquired factor VII deficiency during sepsis remains to be elucidated. The knowledge of this syndrome should avoid false diagnosis of congenital factor VII deficiency.

Adult↗
PubMedDate not supplied

[Recurrent venous thromboembolism caused by heparin cofactor II deficiency. A case].

We report the case of a 28-year-old man who was admitted in an emergency because of severe abdominal pain with gastrointestinal haemorrhage and shock. Laparotomy showed infarction of the small intestine with mesenteric veins thrombosis. Severe thromboembolic complications occurred during the post-operative period: bilateral femoral deep vein thrombosis with pulmonary embolism, axillary and subclavian vein thrombosis associated with an intravenous catheter, portal hypertension related to portal vein thrombosis and cavernoma, thrombosis of the superior longitudinal sinus. Laboratory investigations performed after thrombotic episodes and repeated 5 years later evidenced a type 1 Heparin Cofactor II deficiency (HCII Ag by EID: 40 percent; functional Tollefsen's method: 60 percent). This heterozygous deficiency was also found in one of the patient's sons. This is the first reported case of HCII deficiency associated with mesenteric infarction and cerebral thrombophlebitis. The relationship between these severe venous thrombotic episodes and the HCII deficiency is discussed in relation to the dermatan sulphate-HCII couple physiology. Vascular injury may act as a triggering factor in patients with HCII deficiency.

Adult↗