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Biomedical subjects

E Grau

Publications and source records attributed to E Grau.

At least 73 records · Page 4Linked to original sources
PubMed1990

[Importance of antiphosphatidylserine antibodies in patients with lupus anticoagulant. Analysis of 30 cases].

Anti-phosphatidylserine (APS) and anticardiolipin (ACL) antibodies were measured in 30 patients with lupus anticoagulant. In 17 cases there were clinical features of thrombosis (56.7%). The number of patients with IgG APS and ACL levels higher than seven standard deviations from the normal mean was significantly higher in the group with thrombosis (p less than 0.017 and p less than 0.02, respectively). The IgG APS level was higher in the group without systemic lupus erythematosus (p less than 0.029). There was a positive correlation between IgG APS and the activated thromboplastin time (r = 0.654, p less than 0.001). The correlation between IgG APS and IgG ACL was rho = 0.61. Two of the 5 patients with increased IgG APS and normal IgG ACL had thrombosis. We think that, in this group of patients, IgG APS titer may be, like IgG ACL, a biological marker of thrombosis risk.

Adult↗
PubMed1990

Detection of both type 1 and type 2 plasminogen activator inhibitors in human monocytes.

Increasing evidence suggests the involvement of leukocytes in the fibrinolytic system. Monocytes secrete pro-urokinase (Grau, Thromb Res 1989; 53: 145) and it has been shown that these cells have specific receptors for urokinase and plasminogen (Miles, Thromb Haemostas 1987; 58: 936). The aim of this study was to analyse the presence of plasminogen activator inhibitor(s) in platelet-free suspensions of human peripheral blood monocytes and polymorphonuclear leukocytes (PMN). SDS-PAGE and reverse fibrin autography showed an inhibitory band of 50 kDa in the monocyte extracts (Triton X-100) but not in the PMN extracts. Urokinase (u-PA) was mixed with increasing amounts of monocyte extract for 10 min and the mixtures were added to 125I-fibrin coated wells containing plasminogen. A dose-dependent decrease in the u-PA fibrinolytic activity was observed. The amount of inhibition increased when the monocyte releasates were preincubated with u-PA (40% inhibition after 5 min preincubation and 80% after 15 min), indicating a direct interaction between this activator and an inhibitor(s). After SDS-PAGE of monocyte extracts, immunoblotting and peroxidase staining identified both PAI1 and PAI2, with an apparent molecular weight of 47-50 kDa. Monocyte-associated PAI1 formed complexes with single chain t-PA with a molecular mass 50 kDa higher than the molecular mass of the free PAI1. However, a significant amount of PAI1 remained unbound to t-PA. This inactive PAI1 could have come from a rapid inactivation of the primary active PAI1. These PAI1 and PAI2 detected in human monocytes may be transcendent in the regulation of the fibrinolytic system.

Electrophoresis, Polyacrylamide Gel↗
PubMed1990

[Intracranial hemorrhage in patients undergoing anticoagulant treatment with acenocoumarol].

Between 1980 and 1985, 2,012 patients treated with acenocoumarol were followed up. 31 of them had intracranial hemorrhage (ICH), representing an incidence of 1.54%. Its mortality rate was as high as 45%. The most common indication of anticoagulant therapy was cardiac valvular disease. No precipitating factors or concomitant hemorrhages in other sites were detected. Most patients with ICH were, at the time of the accident, within the therapeutic anticoagulant range. The most common localization of ICH was intraparenchymal; most of them developed after one year of anticoagulant therapy. In 32% of instances there was previous hypertension and previous stroke in 26%. ICH had a three times greater incidence in patients over 65 years. The patients who died showed larger hematomas than survivors in computed tomography.

Acenocoumarol↗
PubMed1989

[Association of acute leukemia with disseminated intravascular coagulation in adults. Analysis of 14 cases].

The association of acute leukemia (AL) and disseminated intravascular coagulation (DIC) in 89 patients with a de novo diagnosis of AL made in our center during the last 8 years was retrospectively evaluated. DIC was demonstrated in 14 patients (15.7%) (7 AML-M3, 1 AML-M3, 1 AML-M2, 1 AML-M4, 2 AML-M5, and 2 ALL-L1). In 5 of them ICD was diagnosed after the beginning of chemotherapy. The factors predisposing to the development of DIC were: 1) the type of AL (p less than 0.01), as 70% of AML-M3 had DIC; 2) the intensity of granulation in leukemia cells (p less than 0.004); 3) the presence of Auer's rods and/or splinters in these cells, and 4) the presence of hemorrhagic diathesis (p less than 0.007). Eight of the 14 patients with DIC received heparin at a prophylactic dosage. No significant differences in the clinical course were in the group of patients with DIC who received heparin and in those who did not, excepting that in the former the platelet requirements were higher (p less than 0.005). Mortality rate during the first month was higher in the group of AL with DIC than in AL without DIC (p less than 0.025). Long term mortality was similar in both groups. The control of hemostasis is fundamental in AL, even in those patients without DIC at the time of diagnosis. The administration of blood derivatives has a high priority in AL with DIC. The role of heparin is still controversial.

Adult↗
PubMed1989

Molecular characterization of antithrombin Barcelona-2: 47 arginine to cysteine.

The molecular characterization of antithrombin Barcelona-2 is reported. The abnormal antithrombin was isolated from plasma by chromatography on heparin-Sepharose at pH 6.0, and ion exchange on DEAE-Sephadex at pH 8.6 and 6.0. The tryptic peptides were mapped by reverse-phase HPLC and amino acid sequencing and mass spectrometry showed arginine-47 to be replaced by cysteine. The affinity of Barcelona-2 for heparin is dramatically decreased. The new cysteine does not form a mixed disulphide with DTNB, implying it is present as a disulphide with some other available thiol molecule such as cysteine. This extra bulk at position 47 accounts for the low heparin affinity compared with two other mutations (Rouen-1 47 His; Rouen-2 47 Ser) at this residue. These results confirm the view that Arg-47 is an important residue in heparin binding. No dimers of Barcelona-2 were observed suggesting that steric hindrance of the new cysteine at residue 47 prevents dimerisation.

Amino Acid Sequence↗
PubMed1989

Fibrinolytic activity of normal human blood monocytes.

Neutrophils (PMN) are important in the cellular phase of blood fibrino lytic activity (FA). The contribution of monocytes (MC), which have FA, is unclear. To determine the relative roles of these cells to activity in normal blood, we examined, by solid phase radiofibrin assay, FA of normal blood and plasma, and of purified PMN and MC, with and without plasminogen (PLG), mini-plasminogen (mPLG), the other major elastase fragment of PLG, or autologous plasma. PMN alone (0.5 x 10(6)/ml) had striking activity (292 +/- 25 SEM ng fibrin lysed/h; n = 10 normal subjects) while MC alone (0.5 x 10(6)/ml) had mean FA of 32 +/- 4 ng/h, which could be accounted for by contaminating PMN (36 +/- 8 ng/h). Thus, in a 1 h assay (when cellular FA accounts for 70-80% of FA in whole blood), normal numbers of MC (0.5 x 10(6)/ml) had no detectable FA when assayed with PLG or normal plasma. With longer assay times (2-6 h), PLG-dependent (plasminogen activator, PA) activity was demonstrated with mixtures of MC and PLG or plasma. This PA activity was released into the medium and required prior contact of MC and an intact, soluble PLG molecule for PA activity to be detected in medium (suggesting a PLG-MC triggering mechanism), since activity was reduced or absent when MC were exposed to mPLG, the other major elastase fragment of PLG, or solid phase PLG. Exposure of MC to solid phase fibrin did not result in PA release. MC PA activity was little affected by cycloheximide pretreatment, indicating preformed rather than newly synthesized PA. By SDS-PAGE and fibrin zymography, MC extracts revealed a single PA band with features of pro-urokinase (single chain urinary-type PA): Mr 55,000, inhibition by antiurokinase antibody (but not by anti-tPA), and resistance to inhibition by DFP. By ELISA assay, approximate normal monocyte content of this PA (as Mr 55,000 urokinase) was 0.03 fg (3.3 x 10(8) molecules) per cell.

Cycloheximide↗
PubMed1988

Plasma and urinary heparin cofactor II levels in patients with nephrotic syndrome.

Heparin cofactor II (HC II) levels were measured by electroimmunoassay in plasmas and urines from 68 patients with nephrotic syndrome. In addition, antithrombin III (AT III) and protein C (PC) activities and antigens were measured also in the same group of patients. Seven of these patients had histories of thrombosis. Plasma HC II levels (mean +/- SD 105 +/- 43) were not different from levels in healthy subjects (94 +/- 17). Only 5 patients had low plasma levels of HC II. None of the patients with thrombosis had low HC II levels. Even though measurable amounts of HC II were found in 25 urines from 50 patients. There was a relationship in the urinary excretion between HC II and AT III and their urinary clearances were quite similar. However, no correlation was found between plasma HC II and AT III levels, and levels of AT III activity and antigen were significantly lower than in healthy subjects. Three patients with histories of thrombosis had low AT III levels. Most patients (including those with thrombosis histories) had high plasma PC levels and increased urinary loss. It is suggested that HC II does not play an important role in the pathogenesis of thrombosis in nephrotic syndrome.

Adolescent↗
PubMed1988

Quantitative and qualitative congenital deficiency of antithrombin III: a new molecular variant called ATIII-Barcelona 2.

A Spanish family with a quantitative-qualitative antithrombin III (ATIII) deficiency and thrombotic tendency is reported. The qualitative defect was suggested by the crossed immunoelectrophoresis (CIE) in the presence of heparin in plasma of all those affected. However, the crossed immunoelectrofocusing (CIEF) showed the same ATIII pattern in controls and affected members. Two populations of ATIII were detected by affinity chromatography on heparin-sepharose from affected members' plasma. The ATIII unbound to sepharose beads was devoid of heparin cofactor activity and showed a lack of anodal migration in CIE in the presence of heparin. The ATIII eluted corresponded to normal ATIII. Our data supports the view that an abnormal ATIII molecule is present in all affected family members in the heterozygous state. This is the first reported ATIII variant in which a molecular abnormality produces a lack of affinity for heparin but no changes in its isoelectric point. This familial ATIII deficiency was named ATIII- Barcelona 2.

Antithrombin III↗
PubMed1988

AT III Barcelona: a familial quantitative-qualitative AT III deficiency.

A quantitative and qualitative deficiency of antithrombin III (ATIII) was found in four members of a Spanish family with thrombotic tendency. In all affected members, levels of ATIII antigen and activity (heparin cofactor activity) were reduced to 50% of the normal range. When crossed immunoelectrophoresis (CIE) was performed in the presence of heparin, an abnormal slow-moving peak was found. Crossed immunoelectrofocusing (CIEF) from normal and affected individuals showed that normal ATIII migrated between pH 4.9-5.3 while the ATIII under study was asymmetrically distributed between two pH ranges: 4.9-5.3 and 4.6-4.8. Affinity adsorption of affected members' plasma to heparin-sepharose beads revealed one population of ATIII in the supernatant corresponding to the abnormal ATIII, devoid of heparin cofactor activity and showing a peak between pH range: 4.6-4.8 in CIEF. Our data supports the view that a quantitative-qualitative deficiency was present in the heterozygous state in all the affected family members. Both normal and abnormal ATIII were present in plasma of the affected individuals. This abnormal ATIII was characterized by a lack of affinity for heparin. This familial ATIII deficiency was named ATIII Barcelona.

Adult↗
PubMed1986

Coincident multiple myeloma and non-Hodgkin's lymphoma with 2 serum monoclonal immunoglobulins.

A case with features of both multiple myeloma and non-Hodgkin's lymphoma at the moment of diagnosis is presented. The patient had lytic bone lesions and biclonal gammopathy, IgM kappa and IgA kappa. In the bone marrow biopsy, there was a diffuse infiltration by atypical plasma cells coexisting with an interstitial and nodular infiltration by poorly differentiated lymphoid cells. Immunofluorescence studies showed positive staining with alpha and kappa antisera in the cytoplasm of plasma cells and with mu and kappa antisera on the surface of lymphoid cells. After the beginning of chemotherapy, the IgA kappa monoclonal protein disappeared and the IgM kappa monoclonal protein remained constant.

Aged↗
PubMed1986

Massive pulmonary embolism: short-term effects of thrombolytic treatment.

This study assessed the short-term effects of thrombolytic treatment in 38 patients with massive pulmonary embolism. Thirty-two were treated with streptokinase and six with urokinase. Intrapulmonary artery instillation of fibrinolytic agents was utilized except in 3 patients. There was a marked hemodynamic and arteriographic improvement (p less than 0.0005) in 33 patients (86.8%). Four patients (10.5%) died because of treatment failure. In these cases the fibrinogen concentration remained above 1 gr/liter during therapy. Bleeding was detected in 22 patients (57.8%) but was most often related to puncture or cut-down sites, and only 2 patients (5.2%) had major bleeding. One patient (2.6%) had cerebral hemorrhage. It is concluded that "classic" thrombolytic treatment is to be chosen in life-threatening pulmonary embolism. However, the difficulties sometimes encountered in producing an intense lytic effect and its low fibrinolytic specificity for the thrombus do not permit the obtainment of better results.

Acute Disease↗