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Biomedical subjects

W M Halbmayer

Publications and source records attributed to W M Halbmayer.

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

The prevalence of poor anticoagulant response to activated protein C (APC resistance) among patients suffering from stroke or venous thrombosis and among healthy subjects.

A poor anticoagulant response to activated protein C (APC) in an activated partial thromboplastin time (aPTT) assay (APC resistance) was recently reported to be a cause of familial thrombophilia. The response to APC was measured in 30 patients suffering from juvenile or recurrent stroke, in 40 patients suffering from venous thromboembolism and in 50 healthy subjects. The prevalence of APC resistance was found to be significantly higher among patients with stroke (20%, P < 0.003) and venous thrombosis (17.5%, P < 0.02) compared with the prevalence of APC resistance among normal controls (2%). In one case of venous thrombosis, the proposita's family (A) could be investigated and in five out of nine investigated members (56%) a poor or borderline response to APC was detected. The family (B) of another APC-resistant patient revealed six subjects with poor coagulation response to APC out of eight family members studied (75%). Measuring protein S activity with an automated calcium-thromboplastin-based protein S activity assay, a significant correlation (P < 0.0001) between the results of this functional protein S assay and APC resistance (represented by the ratio (Rs value) of clotting time with and without addition of activated protein C) was observed. Nine out of 14 patients (64%) with poor APC response showed protein S activities below the normal range. Assessment of protein S activity with a second protein S clotting assay using factor Va as substrate confirmed only 47% of the decreased levels of the thromboplastin-based protein S clotting assay.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Course of thrombin activation markers in patients implanted with Palmaz-Schatz stents: first experiences with a post-interventional anticoagulation regimen.

Following implantation of coronary Palmaz-Schatz stents, 29 patients were anticoagulated with a combination of heparin, phenprocoumon and aspirin following a standard protocol. After removing the arterial and venous lines, post-interventional intravenous (i.v.) heparin treatment started with 1500 IU/h for patients > 80 kg and 1250 IU/h for patients < 80 kg. Heparin was monitored by the activated partial thromboplastin time (aPTT) and adjusted by increasing or reducing i.v. heparin by 250 IU/h to maintain the aPTT within the therapeutic range. Phenprocoumon therapy began the day after stent implantation (day 2) and lasted for 3 months. aPTT, Heptest, prothrombin fragment F1 and 2 (F1.2) and thrombin-antithrombin III complexes (TAT) were monitored at standard intervals for 10 days (mean monitoring time: 9.7 +/- 2.3 days). Anticoagulation was efficient with aPTT levels remaining within the therapeutic range on day 9 and the simultaneous, moderate-onset oral anticoagulation within the therapeutic range of the International Normalized Ratio (INR; 2.15-4.80) on day 8 on average, the mean INR being 2.43 +/- 0.76. On day 4, F1.2 levels were significantly higher than on the day of stenting (1.16 +/- 0.30 nmol/l vs 1.04 +/- 0.53 nmol/l; P < 0.005). F1.2 levels fell after day 5, the difference becoming significant from day 8 on (P < 0.05). F1.2 was negatively correlated with the Heptest (P < 0.05) and fell significantly as a function of the INR during phenprocoumon administration (P < 0.001). After phenprocoumon therapy was discontinued over 3 weeks, 25 patients were followed up by angiography. Despite adequate anticoagulation, mean F1.2 levels in patients showing restenosis at follow-up angiography were significantly higher (P < 0.005) than in those without restenosis. In one patient who developed subacute stent thrombosis, clotting factors were determined 20 min before stent occlusion. The levels of F1.2 and TAT were less than all other patients on this day (F1.2: 0.98 nmol/l vs 1.11 +/- 0.40 nmol/l; TAT: 2.7 micrograms/l vs 3.21 +/- 3.38 micrograms/l). Thus, neither F1.2 nor TAT predicted the occurrence of thrombotic stent failure in individuals. Efficient anticoagulation by a combination of anticoagulants is imperative for stent implantation. Using only current routine methods, this way of monitoring anticoagulation is effective for managing combined anticoagulation therapy.

Adult↗
PubMed1994

Prevalence of factor XII (Hageman factor) deficiency among 426 patients with coronary heart disease awaiting cardiac surgery.

BACKGROUND: Several case reports of myocardial infarction in patients with factor XII deficiency have been published. In the present study we investigated the prevalence of this condition. METHODS: Factor XII activity (one-stage clotting assay), fibrinogen (derived method), and lipoprotein (a) (enzyme-linked immunosorbent assay) were measured in the plasma of 426 consecutive patients with coronary heart disease awaiting cardiac surgery. RESULTS: Among the 426 patients, 44 (10.3%) were found to be moderately deficient in factor XII (factor XII activity 17-50%, antigen 15-57%). The prevalence of factor XII deficiency was significantly higher (P < 0.0001) among patients with coronary heart disease than among 300 healthy blood donors (2.3%). Among coronary heart disease patients with this deficiency, elevated levels of fibrinogen, lipoprotein (a), and blood pressure were no more prevalent than in those without the deficiency; nor were cigarette smoking or a positive family history of thromboembolism more prevalent. CONCLUSIONS: Coronary heart disease patients showed a 10% prevalence of factor XII deficiency. However, the pattern of atherosclerotic risk factors did not differ between patients with or without the deficiency.

Blood Coagulation Tests↗
PubMed1994

The prevalence of moderate and severe FXII (Hageman factor) deficiency among the normal population: evaluation of the incidence of FXII deficiency among 300 healthy blood donors.

Factor XII (FXII) deficiency has been reported to be a risk factor for the development of arterial and venous thromboembolism. However, no data are available on the prevalence of FXII deficiency within the normal population. Measuring APTT and FXII activity, seven FXII deficiencies could be detected among 300 healthy blood donors. This corresponds to an incidence of FXII deficiency of 2.3%. On the basis of these data the prevalence of severe and mild FXII deficiency in the normal population can be estimated to be 1.5-3.0%. Assessment of FXII antigen levels revealed, that all seven FXII deficient individuals had FXII antigen levels matching the activity. One presented a severe FXII deficiency (1/300, 0.3%) without detectable FXII activity and an APTT prolongation of more than 120 s. The remaining six FXII deficiencies (6/300, 2.0%) were moderate variations with FXII activities ranging from 20-45% and less prolonged APTTs. Among the 300 healthy donors 16 (5.3%) subjects with prolonged APTTs were identified. Causes for APTT-prolongation were FXII deficiency (7/16), lupus anticoagulant (6/16), mild FVIII deficiency (1/16) and hepatic disorder (1/16). In the remaining sample (1/16) the cause for the prolongation of the APTT remained unexplained. Although 8.7% (26/300) of the donors had a positive family-history of thromboembolism (TE-FHx), none of the FXII deficient subjects were among those with positive TE-FHx.

Adult↗
PubMed1993

[Recurrent venous thromboses in hypoplasia of the vena cava inferior and factor XII deficiency].

The cause of recurrent pelvic and leg venous thromboses in a 24-year-old man was found to be a combination of two rare anomalies, hypoplasia of the hepatic, prerenal segment of the inferior vena cava and factor XII deficiency (factor XII activity 38%, its antigen 39% of normal), the latter considered a risk factor for thromboembolism. Subsequent fibrinolysis was not successful. No thromboembolic phenomena occurred during the following 16 months of oral anticoagulation with phenprocoumon. When this treatment was discontinued at the patient's behest, there was a recurrence on the contralateral side. Anticoagulation was resumed and has continued now for 1 1/2 years without recurrence. The patient has been largely free of symptoms. Permanent anticoagulation thus seems unavoidable in this case.

Adult↗
PubMed1993

[Detection of lupus anticoagulants in the routine blood coagulation laboratory exemplified by 36 patients with systemic lupus erythematosus].

36 patients suffering from systemic lupus erythematosus (SLE) were subjected to various screening and confirmation tests for the presence of lupus anticoagulants (LA) which are a risk for thrombosis. In five out of the 36 patients (14%) lupus anticoagulants could be found. Five out of the 36 patients (14%) showed increased antiphospholipid antibody (APA) levels whereby only two of these patients were at the same time LA-positive. The specificity, sensitivity and effectiveness of various tests in respect of LA-demonstrability have been assessed and the results taken as the basis for proposal of a largely automated stepwise diagnostic procedure for LA-determination within the routine coagulation laboratory.

Adult↗
PubMed1993

Ischemic venous thrombosis caused by a distinct disturbance of the extrinsic clotting system.

Ischemic venous thrombosis that led to necrosis of four toes developed in an 81-year-old man. Despite the extensive thrombosis, results of blood clotting tests showed an extremely low prothrombin time (20%). Plasma mixing studies demonstrated an inhibitor that may have features in common with the lupus anticoagulant. Lupus anticoagulant also simulates hemorrhagic diathesis in vitro, whereas in vivo it is associated with thrombosis and thromboembolism. In contrast to the lupus anticoagulant, the inhibitor found in this patient was active within the extrinsic clotting system. Systemic steroids led to rapid clinical resolution paralleled by normalization of the prothrombin time and disappearance of the inhibitor.

Aged↗
PubMed1993

[Factor XII (Hageman factor) deficiency: a risk factor for development of thromboembolism. Incidence of factor XII deficiency in patients after recurrent venous or arterial thromboembolism and myocardial infarction].

103 patients suffering from recurrent venous thrombosis, recurrent arterial thromboembolism and/or recurrent myocardial infarction and 50 healthy subjects were tested for Hageman factor (F XII) coagulant activity and antigen. Among the 103 patients we identified 15 subjects with F XII deficiency (15%), 3 with protein C deficiency (3%) and 3 with protein S deficiency (3%). Combined F XII and protein C, protein S or antithrombin III deficiency was not observed. The 103 patients were divided into subgroups according to the type of thrombotic complication. Among patients with exclusively recurrent venous thromboembolism 8% (p = 0.153) were deficient in F XII. Among patients suffering from recurrent arterial thromboembolism and/or myocardial infarction, the incidence of F XII deficiency was significantly higher (20%, p < 0.003). In 67% of the patients with F XII deficiency a positive family history of thrombosis could be established. In contrast, only 32% (p = 0.043) of all venous and 28% (p = 0.019) of all arterial thrombosis patients had a positive family history. We believe that reduced levels of F XII should be considered as a risk factor in the development of thromboembolism. Consequently, more attention should be payed to the measurement of F XII when evaluating thromboembolic risk factors especially in cases of recurrent arterial thromboembolism and/or myocardial infarction.

Adult↗
PubMed1993

[Prothrombin fragment 1+2 (F1+2), thrombin-antithrombin III complex(TAT) and thrombophilia parameters in orally anticoagulated patients with inferior vena cava filters].

Prothrombin fragment 1 + 2 (F1 + 2) and thrombin-antithrombin-III-complex (TAT) levels were compared in 31 orally anticoagulated patients with inferior vena caval filters and a control group of 31 orally anticoagulated patients without caval filters and the incidence of markers of thrombophilia (deficiency of antithrombin-III, protein C, protein S and factor XII, presence of lupus anticoagulants) was determined. 8 of 31 patients (26%) from the group of caval filter carriers showed markers of thrombophilia (3 protein S deficiencies, 1 protein C deficiency, 2 factor XII deficiencies and 2 patients with lupus anticoagulants). In all orally anticoagulated patients a significant interdependence (p < 0.05) between F1 + 2- and TAT-levels and intensity (INR) of the oral anticoagulation could be observed. Comparison of F1 + 2- and TAT-levels of caval filter carriers and controls revealed no significant difference which leads to the conclusion that inferior vena caval filters do not induce detectable systemic activation of prothrombin under adequate oral anticoagulation therapy.

Administration, Oral↗
PubMed1993

[Preoperative monitoring of blood coagulation in urologic operations: diagnosis of familial factor XI deficiency within the scope of preoperative blood coagulation studies].

Presurgical coagulation diagnosis should--apart from coagulation monitoring in the laboratory based on a stepwise diagnosis for detection of coagulations disorders, starting with global tests (NT/APTT) followed by appropriate specific investigation in case of pathological findings--consist of an adequate hemostaseological anamnesis and physical checkup of the patient. This would allow detection of important signs of hemostaseological impairment during the pre-analytical phase already and permit subsequent initiation of more specific coagulation tests. The casuistics of a patient with factor XI-deficiency ("Minor Form"), a condition which is extremely infrequent in our country, demonstrates the coagulation diagnostic procedure which led to detection of his inherited factor XI-deficiency. In addition the pre-, peri- and postsurgical therapeutical management of this particular patient using an antifibrinolytic drug (tranexamic acid) is presented.

Blood Coagulation Tests↗
PubMed1992

The prevalence of factor XII deficiency in 103 orally anticoagulated outpatients suffering from recurrent venous and/or arterial thromboembolism.

One hundred and three patients suffering from recurrent venous thrombosis, recurrent arterial thromboembolism and/or recurrent myocardial infarction and 50 healthy subjects were tested for Hageman factor (FXII) coagulant activity and antigen. Among the 103 patients we identified 15 subjects with FXII deficiency (15%), 3 with protein C deficiency (3%) and 3 with protein S deficiency (3%). Combined FXII and protein C, protein S or antithrombin III deficiency was not observed. The 103 patients were divided into subgroups according to the type of thrombotic complication. Among patients with exclusively recurrent venous thromboembolism 8% (p = 0.153) were deficient in FXII. Among patients suffering from recurrent arterial thromboembolism and/or myocardial infarction, the incidence of FXII deficiency was significantly higher (20%, p less than 0.003). In 67% of the patients with FXII deficiency a positive family history of thrombosis could be established. In contrast, only 32% of all venous and 28% of all arterial thrombosis patients had a positive family history. We believe that reduced levels of FXII should be considered as a risk factor in the development of thromboembolism. Consequently, more attention should be payed to the measurement of FXII when evaluating thromboembolic risk factors especially in cases of recurrent arterial thromboembolism and/or myocardial infarction.

Acenocoumarol↗
PubMed1992

[Functional protein S in 77 patients treated with anticoagulants and in 32 probands with normal coagulation parameters].

We determined functional protein S with a new automated clotting assay, total protein S antigen with the Laurell technique and free protein S antigen with an ELISA test and calculated the ratio of total protein S antigen and prothrombin antigen (Laurell) of plasmas of 77 patients oral anticoagulant therapy and of 32 normals. The correlation of total protein S antigen with protein S activity was found to be r = 0.857. The normal range of the tests was calculated for orally anticoagulated patients and for normals and was compared with the analytical data from 4 orally anticoagulated, congenital protein S deficiency patients. We believe that the automated functional protein S clotting assay is a quick and easily performed test, which now allows even for protein S the use of a functional assay as the first step for the screening of coagulation inhibitor deficiencies.

Arterial Occlusive Diseases↗
PubMed1991

C1-esterase inhibitor in uncomplicated pregnancy and mild and moderate preeclampsia.

Routine coagulation tests and measurement of the plasma levels of C1-esterase inhibitor (C1-INH) and antithrombin III were performed in 17 women with mild preeclampsia, 10 women with moderate preeclampsia and 20 women with uncomplicated pregnancy. All pregnant probands were within the third trimester of pregnancy. 20 non-pregnant women were used as controls. The groups were matched in age and the pregnant ones were also matched in gestational age. C1-INH activity and antigen were significantly reduced (p less than 0.002) in normally pregnant women as compared with non-pregnant ones. Further, C1-INH activity was lower in women with mild preeclampsia and significantly lower in women with moderate preeclampsia (p less than 0.05) as compared with normally pregnant women. None of the plasmatic coagulation tests was indicative of a consumption reaction. We conclude that C1-INH activity and antigen reductions are commonly associated with pregnancy. Furthermore, as markedly lower values can be found in mild and moderate preeclampsia, measurement of the C1-INH activity in pregnant women within the third trimester might proof useful to establish the diagnosis of a preeclamptic condition.

Adult↗
PubMed1991

[Automation in the modern coagulation laboratory. Exemplified by the integration of the Microanalyser ACL 300].

We report on the organisation of our coagulation laboratory which had to meet the requirements of both, the large routine operations and those of a special laboratory for specific blood coagulation problems. A valuable support for the routine activities of our coagulation laboratory was the installation of 2 automated coagulation analysers, type ACL 300. Due to the selective (diagnosis/therapy) patient-related allotment of samples and the establishment of a final diagnosis according to a step-wise method it was possible to integrate the 2 ACL 300 analysers into our existing system and consequently to take full advantage of the savings in staff time. Moreover we report on the evaluation of the 1st ACL 300 (810) analyser and the specific characteristics of the ACL series.

Autoanalysis↗
PubMed1990

[A simple test for the monitoring of plasma anti-XA activity of patients following subcutaneous administration of enoxaparin].

Since low molecular weight heparin is used for the prevention of thromboembolism, the coagulation laboratories are in need of a simple, reliable and practicable test for factor Xa inhibition in order to monitor the effect of low molecular heparin in plasma. Effects of subcutaneous administration of 20 mg or 40 mg enoxaparin were studied in blood samples drawn from 20 patients before and 1, 2, 3, 4, 6, 12 and 24 hours after injection. Thrombin time, aPTT, Heptest and the anti-Xa activity (amidolytic assay) were measured. Subcutaneous administration of 20 mg or 40 mg enoxaparin was followed by a barely significant (p less than 0.05) rise in aPTT (only at the higher dosage) and thrombin time four hours after injection. Heptest and amidolytic assay (S-2222) correlated well and significant (p less than 0.01) increases, with maximum values 4 hours after injection, were seen after administration of 20 mg as well as of 40 mg enoxaparin. Higher mean values were achieved after injection of 40 mg than 20 mg enoxaparin. We believe the Heptest to be a quick and easily performed test, giving results which agree well with those of the amidolytic anti-Xa activity reference method.

Aged↗