PubMed Health⌕ Search

Biomedical subjects

T Exner

Publications and source records attributed to T Exner.

At least 37 records · Page 2Linked to original sources
PubMed1994

Some recent developments with lupus anticoagulants.

Lupus anticoagulants (LA) have been defined as phospholipid-interfering antibodies. Testing for them has become a frequently requested procedure in coagulation laboratories and new methods have recently become available. Activated partial thromboplastin time (aPTT) reagents with reduced levels or different types of phospholipid provide high sensitivity. Correction procedures resistant to heparin and based on aPTT and dilute Russell's viper venom time (DRVVT) tests with added hexagonal phase phospholipids have improved the specificity of testing. Simplified tests based on venom activators of factor X and prothrombin improve the reliability of LA testing and may facilitate the further categorization of circulating anticoagulants. Recent studies on the mechanism of LA derived from various patients have confirmed their heterogeneity, principally in the protein cofactors involved in their interactions with phospholipids. Perhaps one-third of LA require beta 2-glycoprotein 1 to exert an anticoagulant effect. The remainder may require human prothrombin as suggested from studies with reconstituted clotting factor systems.

Antibodies, Antiphospholipid↗
PubMed1994

Nomenclature of quantities and units in thrombosis and haemostasis (recommendation 1993). A Collaborative project of the Scientific and Standardization Committee of the International Society on Thrombosis and Haemostasis (ISTH/SSC) and the Commission/Committee on Quantities and Units (in Clinical Chemistry) of the International Union of Pure and Applied Chemistry-International Federation of Clinical Chemistry (IUPAC-IFCC/CQU(CC)).

Explore the source record for details and available documents.

Blood Proteins↗
PubMed1993

The coagulation system in placental insufficiency: a study in the fetal circulation.

OBJECTIVE: To examine the hypothesis that Doppler-defined umbilical placental insufficiency is associated with intravascular coagulation in the fetal circulation. DESIGN: A prospective, descriptive, single centre study. SETTING: The University of Sydney, Department of Obstetrics at Westmead Hospital. SUBJECTS: Ninety-one infants were classified on the basis of the systolic:diastolic (SD) ratio of the umbilical artery flow velocity waveforms into severe (SD > 99.9th centile), moderate (SD > 95th centile) or control groups. INTERVENTION: Blood was collected from the umbilical vein at delivery. MAIN OUTCOME MEASURES: The coagulation variables measured were the plasma concentrations of thrombin-antithrombin, fibrinopeptide A and fibrinogen, the antithrombin III activity, the prothrombin time and the activated partial thromboplastin time. RESULTS: There were no differences in activated partial thromboplastin time, antithrombin III activity, fibrinopeptide A or thrombin-antithrombin complex concentrations between fetuses with placental insufficiency and those with no placental disease. Fetuses with severe and moderate placental insufficiency had a statistically significant prolongation of their mean prothrombin time compared to controls (23.7 +/- 0.8, 23.6 +/- 1.6, and 19.9 +/- 0.6 s, respectively). Infants in the severe group had a lower plasma fibrinogen concentration than control fetuses (1.66 +/- 0.09 and 1.94 +/- 0.09 g/l, respectively). The activated partial thromboplastin time and antithrombin III activity were both highly dependent on gestational age. CONCLUSIONS: These results do not support the hypothesis that Doppler-defined umbilical placental insufficiency is associated with activation of coagulation in the fetal circulation.

Antithrombin III↗
PubMed1992

Platelet aggregation and coronary heart disease risk factor variation in Australian populations with different coronary heart disease mortality.

In a cross-sectional analytic study, we examined the differences in coronary heart disease (CHD) risk factors, including coagulation factors and platelet aggregation, among males from southern European countries and those of Anglo-Celtic descent who had widely different CHD standardized mortality ratios. The participants included 169 men aged 40 to 49 years, 27% of whom were born in southern European countries. The subjects had no history of heart disease and no other clinical conditions, or were not taking medications known to affect hemostasis. Data obtained included their medical history and CHD-related risk behaviors, blood pressure, height, weight, abdominal and pelvic circumference, and coagulation, fibrinolysis, platelet activity, lipids, and lipoproteins profiles. There were significant differences between the two groups in the prevalence of a positive family history, mean apolipoprotein A1 levels, and platelet aggregation responses to ADP. Other established risk factors, including coagulation factor levels, were not significantly different.

Adenosine Diphosphate↗
PubMed1992

Heparin-induced thrombocytopenia: laboratory investigation and confirmation of diagnosis.

We report here on the usefulness of the 14C-serotonin release assay for the laboratory confirmation of the clinical diagnosis of heparin-induced thrombocytopenia syndrome (HITS). Over the past 3 yrs, some 140 individual serum samples have been tested in our laboratory for heparin-associated anti-platelet activity ('heparin antibodies'). These included sera from 54 selected (4 positive, 50 negative) controls and a group of 86 patients where the test was requested on clinical grounds. Of 20 patients derived from within our institution, 7 out of 8 patients (88%) with good clinical probability of HITS were confirmed to have heparin platelet antibodies by the serotonin release assay. In contrast, only 2 out of 9 patients (22%) with a low clinical probability of HITS were shown to be positive by this procedure, as were 2 out of 3 patients (66%) deemed to have an 'intermediate' clinical probability of HITS. In addition, screening of 50 serum samples forming a 'negative-control non-HITS' group (either patients on heparin therapy without thrombocytopenia, patients with non-heparin associated thrombocytopenia [eg. ITP*, other drug related], or normal laboratory volunteers), consistently failed to display heparin associated anti-platelet activity by the 14C-serotonin release assay. In addition to the good specificity and sensitivity described above, the 14C-serotonin release assay was found to be nearly twice as sensitive when compared to the platelet aggregation procedure, and it is therefore a useful diagnostic test for the confirmation of clinically suspected HITS.

Blood Platelets↗
PubMed1991

Development of a simple collagen based ELISA assay aids in the diagnosis of, and permits sensitive discrimination between type I and type II, von Willebrand's disease.

We have developed and evaluated an ELISA-based collagen binding assay (CBA) as an aid in the diagnosis and classification of von Willebrand's disease (vWD). The assay is simple to perform, and appears capable of differentiating Type II vWD from Type I vWD. Using plasma samples from both affected and non-affected patients, or from normal individuals, data obtained using the CBA were directly compared to data simultaneously derived from a standard von Willebrand factor antigen (protein; vWFAg) ELISA, and from a standard ristocetin cofactor (RCof) assay. Plasma derived from vWD patients (both Type I and Type II) showed overall reduced levels of vWF as detected by all three assays. Mean levels as a per cent of normal for vWFAg, CBA, RCof were 47.3, 60.7, 31.1 for Type I patients (n = 37), and 34.9, 1.6, 11.9 for Type II patients (n = 16) respectively. However despite the reduced vWF levels detected in Type I vWF binding values for both the CBA and vWFAg showed near comparability (i.e. vWFAg:CBA ratio generally less than or equal to 1.0). These ratio values were thus similar to those observed using plasma derived from either individual normal donors, or from non-vWD affected patients. On the other hand, plasma from Type II vWD affected patients showed markedly disparent values, with increased (greater than 8.0) vWFAg:CBA ratios coincident with virtually absent CBA binding in these patients. Thus, the CBA as reported here does appear to constitute a novel functional assay capable of detecting qualitative vWF differences in plasma of affected vWD patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Antigens↗
PubMed1990

Vitamin K-dependent multifactor coagulopathy in Devon Rex cats.

A coagulopathy attributable to a deficiency of vitamin K-dependent clotting factors (II, VII, IX, and X) was diagnosed in 3 Devon Rex cats. There was no evidence for exposure to vitamin-antagonist-related rodenticides. The cats did not have evidence of hepatic disease, gastrointestinal disease, or fat malassimilation. Oral treatment with vitamin K1 resulted in normalization of clotting factor concentrations. However, when treatment was discontinued in 2 cats, prothrombin and activated partial thromboplastin values became prolonged again, although the cats did not have clinical signs of a bleeding disorder.

Animals↗
PubMed1990

Comparison of test methods for the lupus anticoagulant: international survey on lupus anticoagulants-I (ISLA-1).

Six lyophilized plasma samples were sent to 20 "expert" laboratories for assessment of lupus anticoagulant (LA). Four samples contained pooled LA of graded potency mixed with aged normal plasma. One contained LA plus cephalin phospholipid and one contained a nonspecific venom anticoagulant. Sixteen methods were used overall with some participants using up to 8 methods. Results were scored in regard to the known potencies of LA in the samples and other known induced defects. Activated partial thromboplastin time (APTT) tests used by most participants for preliminary screening were relatively sensitive, but non-specific. Platelet or phospholipid neutralization procedures (PNP) appeared to be sensitive and specific but showed a non-linear response to increased LA content. Kaolin clotting time (KCT) tests showed the most sensitive response to increased LA content but the weaker LA were not scored as abnormal by most laboratories as the samples may have contained platelet fragments. Other commonly used tests such as the tissue thromboplastin inhibition (TTI) test and the dilute Russell's viper venom test (DRVVT) were carried out somewhat inconsistently. The variability in performance of tests in different laboratories indicates that standardization of methodology is urgently required. Generally it seemed that most clotting tests were "bypassed" by the addition of phospholipid to a known LA-positive sample in apparently direct proportion to their sensitivity. Sample preparation, especially prevention of contamination with activated platelets is a vital preliminary part in the assay of LA.

Autoantibodies↗
PubMed1990

Solvent extraction of test plasmas for improved recovery of lupus anticoagulant activity.

Phospholipid procoagulant material mainly derived from platelets interferes or "bypasses" the more specific tests for lupus anticoagulants. Such material in test plasmas can be inactivated with recovery of lupus anticoagulant activity by simple extraction with chloroform. This solvent treatment damages mainly factors VIII, V, VII and IX. Ether and various other solvents were less damaging to these clotting factors but not quite as effective as chloroform in the recovery of lupus anticoagulant activity.

Autoantibodies↗
PubMed1990

Use of a simplified dilute Russell's viper venom time (DRVVT) confirms heterogeneity among 'lupus anticoagulants'.

A simplified dilute Russell's viper venom time (DRVVT) test--in which the venom, trace phospholipid and calcium were combined into a single reagent--was evaluated for the detection of lupus anticoagulants (LA) in 28 plasma samples containing non-specific circulating anticoagulants. In agreement with previous studies, the DRVVT was found to be insensitive to defects in contact and haemophilic factors and was only marginally affected by antibodies directed against factor VIII. Thus, the use of a DRVVT test in investigations of anticoagulants reduces the risk of confusing a haemorrhagic inhibitor of factor VIII with a non-haemorrhagic LA. In comparisons of sensitivity against activated partial thromboplastin time tests (APTT-Actin FSL and Organon-Teknika reagents) the simplified DRVVT was prolonged slightly more than the APTT in most of the test plasmas containing various non-specific circulating anticoagulants. Three anticoagulants affecting APTTs more than the DRVVT were found to be associated with anticardiolipin IgMs. APTT-prolonging anticoagulants, whether prolonging DRVVT tests or not, showed similar 'correction' of their APTTs by the addition of platelets or phospholipid. Thus, phospholipid-dependent or LA show heterogeneity. Those affecting only the APTT and not DRVVT should perhaps be classified differently.

Adult↗
PubMed1990

Studies on an unusual von Willebrand's variant--type IID.

We describe a man and his daughter from a large New Zealand family with the extremely rare variant von Willebrand's (VW) disease type IID. These two patients had a severe bleeding history following minor surgery and displayed easy bruising. However, routine laboratory screening tests and factor VIII studies were essentially normal except for slightly reduced ristocetin cofactor activity and prolonged skin bleeding times. Although lacking higher molecular weight forms of VW antigen in common with VW type II's the patients' multimer patterns were clearly different from types IIA and IIB. Instead of showing the characteristic 'triplet' pattern in each multimer band the patients gave a single prominent band with faint satellite bands different in mobility to those in normals. Von Willebrand factor from the patients' platelets gave a similar abnormal pattern. DDAVP failed to correct the bleeding time in either patient and multimer analysis confirmed that there was no increase in the higher molecular weight VWF antigen.

Adolescent↗
PubMed1989

Endothelial cells and normal circulating haemopoietic cells share a number of surface antigens.

Human endothelial cells, cultured from umbilical cord veins, have been evaluated for expression of a large number of cell surface antigens with known haemopoietic, particularly myeloid, cell distribution. This was achieved by evaluating endothelial reactivity (using non-fixed cells) with groups of monoclonal antibodies (MAB) belonging to distinct Clusters of Differentiation (CD), as defined by the Third International Workshop on Leukocyte Differentiation Antigens (ILWS). Results indicate that many antigens known to be present on haemopoietic cells, including those on platelets, are co-expressed on endothelial cells. The most intense degree of reactivity was seen using MAB to CD-9 and CD-13, although significant reactivity was also observed using MAB to CD-31 and CD-32. Data also suggests weak binding to endothelial cells of MAB belonging to CD-14, CD-15 and CD-16. A number of unclustered MAB reactive with haemopoietic antigens can also be shown to bind to endothelial cells.

Antibodies, Monoclonal↗