Biomedical subjects
Publications and source records attributed to G Lutze.
Patients with malignancies have an increased risk for venous thromboembolisms (VTE), but data on patients with acute leukaemia are very limited so far. We found VTE in 12% of 455 patients with acute leukaemia, half of which occurred in association with central venous catheters, with equal risk of ALL and AML.
An increased risk for thromboembolism in cancer patients has been observed in patients with solid tumours, whereas little data exist on malignant lymphoma. We found an overall thromboembolic event incidence of 7.7% in 1038 lymphoma patients treated in our institution, with a statistically significantly higher incidence in high-grade than in low-grade lymphoma.
Coumarin poisoning in dogs is not unusual and is in most cases caused by warfarin, a coumarin derivative which is used as a rodenticide. Competitive inhibition of vitamin K with an incomplete synthesis of the coagulation factors II, VII, IX and X can lead to a significant bleeding tendency. We observed a 3-year old male West Highland White Terrier with a reduced general condition and dyspnoea together with a massive haemothorax. Administration of vitamin K1 (3 mg/kg) led to a rapid improvement of the condition. Coagulation analysis revealed a prolonged activated recalcification time (ARCT), prothrombin time (PT) and aPTT with uncharacteristic thrombin time (TT); factor II, VII and X activities were reduced while factor V activity was normal, all of which are characteristic for coumarin poisoning. HPLC did not reveal the presence of warfarin but of phenoprocoumon, a drug used for thromboembolic prophylaxis in humans. This observation has not been described for dogs to date.
Today, platelet concentrates are generally produced from whole blood by differential centrifugation (buffy coat-derived platelet concentrates--PCs) or by plateletpheresis (apheresis-derived platelet concentrates--APCs). As PCs are characterized by a lower number of platelets than APCs, four to six PCs are customarily combined in order to obtain an equivalent dose. In the 1970s and 1980s, the use of PCs exceeded that of APCs by far; in contrast, since the beginning of the 1990s, APCs comprise more than half of all transfused platelets. However, the selection of PCs or APCs for transfusion to thrombocytopenic patients is still a matter of debate. The present paper compares biochemical and functional properties of both platelet preparations in vitro. Besides plasma parameters (e.g. platelet factor 4 (PF4), P-selectin, C3a-desarginin, plasma coagulation factors), platelet function was analysed by aggregometry and the PFA 100 system. APCs are characterized by a better preservation of ADP and collagen-induced platelet aggregation, and shorter closure times of the PFA 100 test system during storage. The improved primary in vitro haemostatic capacity of APCs is presumed to be owing to a lower cellular activation rate in these preparations. This hypothesis is supported by the higher plasma concentrations of PF4, beta-thromboglobulin and P-selectin found in PCs compared with APCs. The concentrations of C3a-desarginin in PCs exceed those in APCs by far. Additionally, thrombin generation is higher in PCs than in APCs. These data suggest that APCs are characterized by a superior haemostatic capacity over PCs in vitro. However, in vivo studies should be performed to confirm these findings in the patients' circulation also.
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BACKGROUND: In patients with symptomatic carotid artery stenosis, high-intensity transient signals detected by transcranial Doppler (TCD) have been related to particulate microemboli originating at the stenotic lesion. The occurrence of these microembolic events within the Doppler spectrum should be influenced by antithrombotic agents of proven efficacy in these patients mainly by reducing cerebral embolism. METHODS: Seventy-four of 192 consecutive patients with symptomatic arterial stenosis in the anterior circulation and clinical symptoms within the last 30 days underwent 1-hour bilateral TCD monitoring. Patients were selected, if they presented temporal bone windows enabling transcranial insonation, revealed normal Doppler CO2 test excluding hemodynamic impairment, had not received antithrombotic therapy other than acetylsalicylic acid (ASA) before sonographic examination, and gave informed consent to 1-hour monitoring which could be performed immediately on admission/presentation of the patient at the Department of Neurology. RESULTS: Microembolic events were detected in 38 patients (51%). The proportion of patients with events among 26 patients without antithrombotic medication was 73% as compared with 40% in 48 patients receiving ASA at the time of TCD monitoring (p = 0.023). Multivariate analysis including time from ischemia to TCD, presence and start of ASA prevention, degree and localization of stenosis, and presence of a single or recurrent ischemia revealed that absence of an ASA prevention (odds ratio OR 7.1, 95% confidence interval CI 1.6-31.4, p = 0.010), recurrent ischemic events (OR 7.1, 95% CI 1.6-32.7, p = 0.011), and extracranial localization of the stenosis (OR 3.8, 95% CI 1.1-13.2, p = 0.038) were independent predictors for microembolic events. CONCLUSION: In patients with symptomatic arterial stenosis, the absence of an ASA medication is associated with the occurrence of TCD-detected microembolic events, suggesting a relation between these events and ASA-sensitive microemboli from the stenotic lesion.
BACKGROUND AND PURPOSE: The present study investigated the influence of the antiplatelet agent acetylsalicylic acid (ASA) on cerebral microembolism as detected by transcranial Doppler sonography (TCD). METHODS: Nine patients with recent transient ischemic attack or minor stroke of arterial origin were investigated. Eight had not received an antiplatelet or anticoagulant medication before TCD, and in 1 patient a preexisting ASA medication (100 mg/d) had not been changed since the onset of stroke symptoms. An initial 1-hour TCD monitoring was extended for an additional 2.5 hours after an intravenous bolus injection of 500 mg ASA and was repeated for 1 hour on the following day. RESULTS: Microembolic signals (MES) were detected in all patients only on the symptomatic side. After the ASA bolus injection, a significant drop of the MES rate was found in 7 patients, all without previous medication, starting 30 minutes after the application (mean per hour=25.1 [range, 6 to 66] versus mean per hour=6.4 [range, 0 to 14]). In 3 of these patients, platelet aggregation tests were performed that demonstrated normal aggregation before bolus injection and inhibited aggregability as early as 30 minutes after bolus injection. The rate of MES remained unchanged in 1 patient without antiplatelet medication. The ninth patient, who had suffered an ischemic event on ASA, showed only a transient decrease of MES frequency. CONCLUSIONS: In patients with recent stroke of arterial origin, intravenous ASA can rapidly reduce cerebral microemboli as detected by TCD. Microemboli might be a useful parameter to monitor early effects of antiplatelet therapy.
The factor XII gene from 31 unrelated factor XII-deficient patients from Germany, Switzerland, and Austria was screened for mutations at the genomic level. Several novel mutations were detected and their absence in a control group of 74 healthy unrelated individuals was checked. Most changes are in the serine protease domain affecting the catalytic triad His-393-Asp-442-Ser-544; two missense mutations, R398Q (arginine 398 to glutamine; gene bank accession no. U71276) and L395M (leucine 395 to methionine; gene bank accession no. U71277), are close to the active site histidine at position 393. Another mutation detected in a cross-reacting material (CRM)-positive female with a history of three abortions affects the active site aspartic acid by changing it to asparagine (D442N; gene bank accession no. U71275). The novel mutation G570R (glycine 570 to arginine; gene bank accession no. U71274) giving rise to a CRM-positive phenotype is located next to Cys571, which forms a vital disulfide bridge. Two mutations are causing reading frame shifts: one single basepair deletion in exon 12 [exon 12: 10590(DelC); gene bank accession no. U71278] and one acceptor splice site mutation [exon 14: 11397(G --> A); gene bank accession no. L43615]. The putative regulatory mutation exon 1:-8 (g --> c) in the upstream region of the gene is associated with an aberrant Taq I restriction site allele in intron B of the gene (gene bank accession no. X80393).
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The analytical performance of the new capillary blood prothrombin time monitoring system CoaguChek was examined in a multicenter evaluation at six hospitals. The coefficients of variation of the INR obtained in the CoaguChek imprecision study were approximately 7% in the control plasma provided (within-run and day-to-day) and 4% in blood (within-run). The prothrombin times were ascertained in capillary blood (CoaguChek PT Test) and citrated venous plasma (Hepato Quick, Thromborel S) from 359 patients under oral anticoagulation therapy with phenprocoumon, acenocoumarin or warfarin. The agreement with the test results obtained with the comparison methods was acceptable versus Hepato Quick assay (n = 359; y = 1.23 x -0.49, r = 0.888) and good versus Thromborel S method (n = 359; y = 1.09 x -0.28, r = 0.895). A simplified assessment of all test results (n = 795) in a nine-field comparison table showed a concordance with the comparison methods of more than 80 (Hepato Quick: 81%, Thromborel S: 83%). The concordance between Hepato-Quick and Thromborel S was slightly higher (88%). Its good analytical performance and convenient handling recommend the CoaguChek system as a suitable system for decentralized prothrombin time testing.
Deep-frozen conventional plasma without viral inactivation [fresh frozen plasma (FFP)] and virus-inactivated plasma units [solvent/detergent (SD) procedure, methylene blue/illumination (MB) procedure] were investigated with regard to their contents of particles and their activities and concentrations, respectively, of blood clotting factors. Particles could be proved in FFP and in MB-treated plasma, but not in SD-treated plasma. Results of the global tests prothrombin time, partial thromboplastin time and thrombin time as well as the activities of blood clotting factors were located in normal range in SD-treated plasma. However, pathological results were partly found in MB-treated plasma. Activities of protein S and alpha 2-antiplasmin were lessened in SD-treated plasma. FFP and MB-treated plasma showed interindividual variations of outcomes (single-donor plasma units) in contrast to SD-treated plasma (pooled donor plasma units).
Special details of animal haemostaseological investigations are insufficiently known as yet. This concerns as well the use of standardized laboratory methods as the differences between species and the normal ranges. Global tests and determinations of activity of single blood clotting factors (II, V, VII - XII, AT III) were carried out on healthy pigs and cattle. Quantitative evaluations were performed by using human or animal reference plasmas. Special attention was paid to the determinations of single blood clotting factors.
Haemostaseological investigations of the animals need improvement. Usual methods in human medicine have to be reconsidered with regard to their qualification for veterinary medicine. A standardization of methods and accurate haemostaseological characterization of the reagents used are necessary for an appropriate interpretation of the results and interlaboratory comparative studies. Results of global tests (ARZ, PTT, TZW, TZ, RZ) and determinations of activity of single blood clotting factors (I, II, V, VII-XII) in healthy cats are presented and discussed in view of the mentioned.
A kinetic turbidity-producing method for fibrinogen determination on the basis of reptilase reagent (batroxobin) is described. The method, which is in good agreement with method by Clauss shows comparable precision, is marked out by the possibility of objective photometric measurement. Reagent stability, use of undiluted test plasma and single-point calibration are further advantages. The method is insensitive to heparin. With regards to FDP it is less disturbed than the method by Clauss. In case of adaptation to a modern photometer a clear rationalization effect can be achieved.
During a period of two years children with abacterial meningitis as well as bacterial meningitis were examined before treatment and later during disease. The new Netropsin praecipitation test according to Funke and coworkers was used to detect soluble fibrin monomer complexes. Only in a few cases of abacterial meningitis, but in the majority of cases with bacterial meningitis, a positive result had been shown. Excessive increase had been found in Waterhouse-Friderichsen syndrome. According to our results of coagulation tests we conclude 1. the ethanol gelation test is out-of-date, 2. the heparin treatment in bacterial meningitis is further indicated.
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An inhibitor against blood clotting factor IX was observed as a very rare finding in case of an eight year old boy suffering from haemophilia B. By reason of a haemarthros a replacement therapy was successful done using FEIBA (Factor Eight Inhibitor Bypassing Activity). The haemostatic characterization of the inhibitor and its influence by therapy will be presented.
The thrombin time is essential to control the fibrinolytic therapy with streptokinase. But it is not efficient to use the thrombin time to estimate the fibrinolytic activity if heparin is applied simultaneously. After addition of heparin antidote polybrene the results are comparable with the reptilase time (so-called polybrene thrombin time). In the case of a fibrinolytic therapy it is recommended to use the thrombin time according to AB-D.L. (heparin-sensitive method) and the polybrene thrombin time (heparin-insensitive method).