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Biomedical subjects

M Hanss

Publications and source records attributed to M Hanss.

At least 19 recordsLinked to original sources
PubMed2002

Human plasma fibrinogen measurement derived from activated partial thromboplastin time clot formation.

Prothrombin time-derived measurement of fibrinogen (PTd) has already been described. Activated partial thromboplastin time-derived measurement of fibrinogen (aPTTd) has not yet been clearly defined. Using an MDA II coagulometer (Organon Teknika, Durham, North Carolina, USA), we have therefore compared fibrinogen levels determined with Clauss, PTd, and aPTTd assays and an enzyme immunoassay (EIA) in 172 samples. Of these, 47 were from pre-operative controls, 18 from patients with liver disease, 28 from patients with hyperfibrinogenaemia, 33 from patients treated with vitamin K antagonists, 22 from patients treated with unfractionated heparin and 24 from haemophilic patients. Within the normal range, interassay and intra-assay variations were comparable. For control samples, PTd, aPTTd and Clauss assays were well correlated, without any systematic error. EIA was also correlated but values were slightly higher (mean of difference = 0.24). Pathological samples showed an overestimation of fibrinogen when using PTd measurements in patients treated with vitamin K antagonists, as well as when using aPTTd measurements in patients presenting with factor VIII and factor IX deficiencies. These results indicate that, despite expected financial savings, aPTTd fibrinogen measurements should not be used without restriction. PTd and aPTTd fibrinogen determinations are provided without any additional cost. Their comparison with Clauss fibrinogen results may constitute a validation tool or have additional diagnostic utility (e.g. identifying polymerization abnormalities in case of dissimilar results).

Adult↗
PubMed2001

Cardiac surgery with cardiopulmonary bypass in patients with type II heparin-induced thrombocytopenia.

BACKGROUND: The use of cardiopulmonary bypass (CPB) in patients with a history of type II heparin-induced thrombocytopenia (HIT) may be associated with complications related to their anticoagulation management. METHODS: Between January 1997 and December 1999, among 4,850 adults patients who underwent cardiac surgery in our institution, 10 patients presented with preoperative type II HIT. In 4 patients, anticoagulation during CPB was achieved with danaparoid sodium. In 6 other patients, heparin sodium was used after pretreatment with epoprostenol sodium. RESULTS: No significant change in platelet count occurred in any patient. No intraoperative thrombotic complication was encountered. Total postoperative chest drainage ranged from 250 to 1,100 ml in patients pretreated with epoprostenol and 1,700 to 2,470 ml in patients who received danaparoid sodium during CPB (p < 0.05, Mann-Whitney U test). CONCLUSIONS: During CPB, inhibition of platelet aggregation by prostacyclin may be a safe anticoagulation approach in patients with type II HIT.

Aged↗
PubMed2001

A database for human fibrinogen variants.

Identifying and studying abnormal human fibrinogens is a source of much information, and helps in taking care of the affected patients. To permit exhaustive numbering and easy updates, an extensive register has been compiled and made available on the internet. Known molecular abnormalities are mentioned with the essential clinical features.

Database Management Systems↗
PubMed1996

[Diagnosis of venous thrombosis and/or pulmonary embolism by determination of d-dimers using ELISA. Review based on a study of 80 consecutive patients hospitalized in an emergency unit].

The sensitivity and specificity of an ELISA method (Fibrinostika Fbdp Organon Teknika) for assay of D-dimers in the diagnosis of deep vein thrombosis and/or pulmonary embolism was studied in 80 consecutive patients seen at an emergency unit. Fifty-six of the patients presented clinical signs of deep vein thrombosis. Diagnosis was confirmed in 26 of the 56 patients with a D-dimer level above 370 ng/ml (sensitivity 92.3%) and 370 ng/ml for 13 of 30 patients with a negative venous ultrasound Doppler examination (specificity 43.3%). The positive predictive value was 58.5% and the negative predictive value was 87%. There was a significant difference in the level of D-dimers between distal and proximal deep vein thrombosis. In 40 cases with suspected pulmonary embolis, either alone or with suspected deep vein thrombosis, diagnosis was made in only 4 of 9 with a highly or intermediately probable ventilation/perfusion scan. D-dimer level was always above 3,000 ng/ml. Coupling the ELISA dimer test with noninvasive explorations improves negative predictive value but can also avoid invasive explorations (venography, pulmonary angiography) in certain patients. A D-dimer test as sensitive as the ELISA test and as rapid as the latex test remains to be described.

Adolescent↗
PubMed1994

Increased plasma free gamma carboxyglutamic acid levels during deep vein thrombosis and intravascular disseminated coagulation.

Gammacarboxyglutamic acid (gla) is a non essential amino acid synthesized in presence of vitamin K, predominantly found in coagulation and bone proteins. In 14 cases of deep vein thrombosis and in 11 cases of disseminated intravascular coagulation, compared to 19 normal subjects and 9 patients hospitalized for leg pain, free plasma gla levels were found significantly elevated (respectively 372 +/- 244 and 559 +/- 361 versus 146 +/- 34 and 120 +/- 40 pmol/mL). In six paired plasma and serum, gla levels were similar. These results suggest an involvement of blood coagulation in gla generation with need of a catabolism of the activated factors. A significant decrease was noticed during vitamin K antagonist therapy and liver disease, both instances in which the synthesis of gla containing coagulation factors is affected. During hepatocellular carcinoma with elevated desgamma carboxyprothrombin, gla was found normal, denying an global impairement of the vitamin K metabolism.

1-Carboxyglutamic Acid↗
PubMed1993

Role of platelet membrane glycoproteins Ib/IX and IIb/IIIa, and of platelet alpha-granule proteins in platelet aggregation induced by human osteosarcoma cells.

We have previously shown that the platelet-aggregating activity of human MG-63 and HOS osteosarcoma cells depends at least in part upon tumor cell surface-associated thrombospondin, and suggested that platelet-osteosarcoma cell interactions could occur through interactions with specific platelet membrane receptors. In this study, the platelet-aggregating activity of MG-63 and HOS cells was studied by using a variety of platelet disorders. Both osteosarcoma cell lines induced a biphasic platelet aggregation response when added to normal platelet-rich plasma, while the second phase of aggregation was absent when added to gray platelets (deficiency in alpha-granule proteins) and to aspirin-treated platelets. Platelets from two unrelated patients with type I Glanzmann's thrombasthenia (deficiency in glycoprotein (GP) GPIIb/IIIa) did not aggregate at all with osteosarcoma cells. Using giant platelets from three patients with Bernard-Soulier syndrome (deficiency in GPIb/IX), the aggregation response induced by MG-63 and HOS cells was monophasic and reversible when compared to normal-sized platelets and to giant platelets from a patient with May-Hegglin anomaly (no membrane GP defect). Because GPIb serves as a receptor for von Willebrand factor during hemostasis, aggregation experiments were also conducted with the platelet-rich plasma of two patients with a low plasma von Willebrand factor concentration (type I von Willebrand's disease) before and after the infusion of deamino-D-arginine vasopressin. MG-63 and HOS cells induced biphasic platelet aggregation both before and after deamino-D-arginine vasopressin treatment, while the ristocetin-dependent binding of von Willebrand factor to platelets only occurred after deamino-D-arginine vasopressin treatment. Preincubation of normal platelet-rich plasma with monoclonal antibody SZ-2 directed against the von Willebrand binding domain of GPIb did not inhibit the platelet-aggregation activity of osteosarcoma cells, whereas anti-GPIb antibody SZ-2 did inhibit ristocetin-induced platelet agglutination. In addition, anti-GPIX antibodies did not affect platelet-osteosarcoma cell interactions. In conclusion, our data demonstrate that the first phase of the platelet-aggregating activity of human osteosarcoma cells is initiated by the interaction of these tumor cells with platelet membrane GPIIb/IIIa, whereas the second phase, even if plasma von Willebrand factor is deficient, involves platelet membrane GPIb and the participation of platelet alpha-granule proteins in membrane-mediated events, making aggregation irreversible.

Antibodies, Monoclonal↗
PubMed1993

Substitution of cysteine for phenylalanine 751 in mature von Willebrand factor is a novel candidate mutation in a family with type IIA von Willebrand disease.

Type IIA is a variant form of von Willebrand disease (vWD) characterized by the absence of von Willebrand factor (vWF) high molecular weight multimers in plasma. Most of the candidate missense mutations potentially responsible for type IIA vWD have been found clustered within a short segment of vWF, lying between Gly742 and Glu875 of the mature subunit. The present work reports a single heterozygous T-->G transversion in eight patients from a large type IIA vWD family, resulting in the substitution Phe751-->Cys. The absence of this mutation in 100 normal vWF genes as well as the lack, in these patients, of any other abnormality within the whole exon 28 encoding amino acids 463-921 of mature vWF, provide a strong support that this non-conservative mutation may be at the origin of the disease in this family. The presence of an additional cysteine at position 751 may induce a conformational change of the vWF subunit affecting either its 'in vivo' sensitivity to proteolytic cleavage or, more likely, its intracellular transport as suggested by the abnormal multimeric pattern of platelet vWF observed in these patients.

Cysteine↗
PubMed1993

Plasma erythropoietin in essential thrombocythaemia.

Plasma erythropoietin levels were frequently decreased in patients with essential thrombocythaemia (14/31 cases), as in polycythaemia vera. These two diseases or some forms of them might be two facets of a single disease process.

Erythropoietin↗
PubMed1991

Des-gamma-carboxyprothrombin detection by immunoblotting after polyacrylamide gel affinoelectrophoresis in human plasmas.

In the absence of vitamin K or in the presence of the vitamin K antagonists, abnormal nonfunctional forms of prothrombin circulate in the blood. A reliable and reproducible technique, derived from traditional crossed affinoimmunoelectrophoresis in presence of calcium lactate, was developed and optimized. The technique is based on nondenaturing polyacrylamide gel affinoelectrophoresis, with calcium lactate, of plasma samples, followed by immunoblotting with rabbit anti-human prothrombin serum and detection with an anti-rabbit immunoglobulin peroxidase conjugate. Depending on the plasmas, one or two bands were visualized and quantified by densitometry of the immunoblots. The technique was able to detect abnormal des-gamma-carboxylated prothrombins at concentration of 0.1 microgram/mL.

Adsorption↗
PubMed1990

Functions and tocopherol content of blood platelets from elderly people after low intake of purified eicosapentaenoic acid.

Elderly people present an increased incidence of atherosclerosis and vascular cerebral damages, associated with blood platelet hyperactivity and a stimulation of arachidonic acid metabolism in vivo. The effects of a low intake of purified eicosapentaenoic acid (EPA) on platelet hyperactivity in old human subjects has been investigated. In a randomized, double blind study, 8 people took during 2 months a daily intake of 100 mg of eicosapentaenoic acid (EPA) given as a triglyceride (1,3-dioctanoyl,2-eicosapentaenoyl-glycerol), and 8 other subjects ingested a placebo. A slight, but significant reduction of platelet-rich plasma aggregation in response to epinephrine and arachidonic acid occurred after EPA intake, as well as a decreased aggregation of washed platelets induced by thrombin, although collagen- and U-46619-induced aggregations were not significantly modified. EPA intake failed to affect arachidonic acid metabolism in thrombin-stimulated platelets or in clotted venous blood. The urinary excretion of thromboxane, 6-keto-PGF1 alpha and their 2,3-dinor-metabolites was also not modified. Similarly, no change in the plasma and platelet lipid fatty acid compositions could be observed. Platelet, but not plasma, alpha- and gamma-tocopherol were enhanced by EPA intake. An increase of platelet vitamin E has been associated with a decrease of aggregation, especially in vitamin E-deficient subjects, like elderly people. Therefore, low intake of EPA might have contributed to inhibit platelet aggregation by increasing cellular vitamin E.

Administration, Oral↗
PubMed1990

Increased plasma tissue-type plasminogen activator levels in patients with chronic thrombocytopenia.

Plasma fibrinolytic factors were measured in 14 patients with chronic idiopathic thrombocytopenic purpura (ITP), in 5 patients with chronic central thrombocytopenia and in 16 healthy volunteers. The von Willebrand factor (vWF), tissue-type plasminogen activator (t-PA) and D-dimer (DD) antigens were found to be significantly higher in both patient groups than in the control group. No difference appeared in euglobulin fibrinolytic activity and plasminogen activator inhibitor activity. The increases in both t-PA and vWF suggest the occurrence of an endothelial cell stimulation, associated with the reduction of circulating platelet number. The correlation of increased DD and t-PA levels during ITP can be the proof of a fibrinolysis activation and suggest an antifibrinolytic role of platelets at physiological concentrations. These results can justify antifibrinolytic therapy in bleeding thrombocytopenic patients.

Adult↗
PubMed1989

Aggregation to thrombin and collagen of platelets from a Glanzmann thrombasthenic patient lacking glycoproteins IIb and IIIa.

The aim of this study was to investigate the platelets of a Glanzmann thrombasthenic patient, which in citrated PRP failed to respond to various agonists, but aggregated and secreted to high concentrations of thrombin (0.36, 0.72 and 1 U/ml) and collagen (4, 10 and 20 micrograms/ml) when washed and resuspended in a Tyrode-albumin solution (containing 2 mM Ca2+). Aggregation of the patient platelets was not affected by anti-IIb/IIIa monoclonal antibody (P18) which strongly inhibits thrombin or collagen induced aggregation of normal platelets. Washed platelets of this patient did not aggregate to ADP (10-100 microM) in the presence of added fibrinogen (2 mg/ml) nor bind 125I-labelled fibrinogen (40 to 320 micrograms/ml) when thrombin-stimulated. Different anti-IIb/IIIa monoclonal antibodies (P2, P18) when used in binding or crossed immunoelectrophoretic studies showed a complete absence of the IIb-IIIa glycoprotein complex on the patient platelets. Moreover, glycoproteins IIb or IIIa were absent on silver-stained two-dimensional (non-reduced/reduced) polyacrylamide gel separations of the patient platelets and were not detected by Western blots used in combination with anti-PLA1 (antigen present on IIIa), anti-Leka (antigen present on IIb). This study shows that platelets lacking glycoproteins IIb or IIIa can aggregate in response to high concentrations of collagen or thrombin when resuspended in the presence of physiological concentrations of calcium. Results obtained in this study could indicate the existence of other mechanisms (other than the IIb-IIIa glycoprotein complex) involving glycolipids, heparans, proteoglycans, and/or unknown membrane glycoproteins to mediate platelet aggregation of stimulated thrombasthenic platelets.

Adult↗
PubMed1987

Secretion of tissue-type plasminogen activator and plasminogen activator inhibitor by cultured human endothelial cells: modulation by thrombin, endotoxin, and histamine.

Primary cultures of pooled endothelial cells obtained from four to six human umbilical cord veins were grown to confluency in M 199 cell culture medium containing 20% human serum. The secretion of tissue-type plasminogen activator antigen (t-PA Ag) and fast-acting plasminogen activator inhibitor activity (PA-I activity) was measured in the conditioned medium after incubation of confluent cultures with serum-free medium for 24 hours (1.5 ml/25 cm2 cell surface). The baseline production of t-PA Ag was 2.7 +/- 1.4 ng/ml (mean +/- SD) and of PA-I activity 36 +/- 18 IU/ml. Stimulation with thrombin resulted in a dose-dependent and time-dependent increase of the secretion of both components. At 1 NIH U thrombin per milliliter, a fourfold increase of t-PA Ag and a twofold increase of PA-I activity were observed. This effect was dependent on a free active site in thrombin and specific protein synthesis (inhibited by cycloheximide and dactinomycin) but unrelated to prostacyclin synthesis (no effect of aspirin or indomethacin). No free t-PA activity could be demonstrated on fibrin plates in conditioned medium from either stimulated or nonstimulated endothelial cell cultures. Endotoxin stimulation resulted in a specific secretion of PA-I activity but not of t-PA Ag, whereas histamine stimulation at concentrations of 0.1 to 1 mumol/L caused a specific secretion of t-PA Ag but not of PA-I. These findings indicate that the secretion of t-PA Ag and PA-I activity are not necessarily coupled.(ABSTRACT TRUNCATED AT 250 WORDS)

Cells, Cultured↗