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Biomedical subjects

A Haushofer

Publications and source records attributed to A Haushofer.

At least 19 recordsLinked to original sources
PubMed1999

Venous thromboembolism at a young age in a brother and sister with coinheritance of homozygous 20210A/A prothrombin mutation and heterozygous 1691G/A factor V Leiden mutation.

We report on members of a Turkish thrombophilic family with coinheritance of the prothrombin mutation PT20210A and the factor V Leiden mutation. The 23-year-old propositus and his elder sister both had episodes of venous theomboembolism at a young age (23 years and 26 years, respectively) and are homozygous for the PT20210A mutation and heterozygous for the factor V Leiden mutation. The 51-year-old father is suffering from coronary heart disease and is heterozygous for both thrombophilic mutations. The asymptomatic 43-year-old mother is heterozygous for the PT20210A mutation, but without activated protein C resistance. Two other children, a 20-year-old girl who is homozygous for the PT20210A mutation and a 13-year-old boy who is heterozygous for the PT20210A mutation, are both free from activated protein C resistance and thrombosis. This report provides further evidence for an early onset of thromboembolic disorders in individuals with an homozygous state of the prothrombin variant 20210A/A and coinheritance of another thrombophilic mutation. Consensus guidelines are required for the treatment and prophylaxis of patients and subjects who remain asymptomatic with homozygous or more than one heterozygous genetic defect associated with thrombophilia.

Adult↗
PubMed1995

Platelet size, fibrinogen and lipoprotein(a) in coronary heart disease.

BACKGROUND: An increase in mean platelet volume has been reported to be associated with arterial thrombosis and myocardial infarction. A larger mean platelet volume has been regarded as an independent risk factor for recurrent myocardial infarction. We therefore investigated whether it is also increased in patients with coronary heart disease examined a few days before cardiac surgery. METHODS: Four hundred and twenty-six patients with coronary heart disease who were waiting for cardiac surgery and 125 healthy individuals were included in the study. Mean platelet volume and other platelet parameters were obtained from a routine blood count procedure using a flow cytometric haematology analyser. RESULTS: Mean platelet volume did not differ significantly between patients and controls; however, as expected from the literature, patients had significantly elevated levels of fibrinogen, cholesterol, triglyceride, apolipoprotein B and apolipoprotein(a). Furthermore, we observed no significant difference in mean platelet volume between patients without myocardial infarction and those who had survived at least one myocardial infarction. CONCLUSION: Our findings suggest that, using a routine laboratory procedure, mean platelet volume cannot be used as a predictive marker for coronary heart disease or myocardial infarction.

Adult↗
PubMed1995

Quality assurance of high-dose i.v. heparin treatment exemplified by patients implanted with coronary Palmaz-Schatz stents.

The need to standardize treatment with high-dose IV standard heparin by using activated partial thromboplastin time (APTT) reagents tested for their heparin sensitivity and by establishing a standard treatment schedule led to the development of the "Lainz concept" of heparin management. The determination of heparin sensitivity of the 2 APTT reagents used (APTT Micronized Silica and APTT Actin FSL), their good agreement (r = .9977; P = .000), and their therapeutic APTT ratio of 1.5-2.5 fold of baseline APTT (therapeutic range, forty-five to seventy-five seconds) equivalent to 0.3-0.7 antifactor Xa units are presented. The "Lainz concept" was tested in 29 patients receiving high-dose heparin after coronary artery stenting. A mean dose of 1,273 U of standard heparin/hour (15.7 U/kg body weight/hour) was shown to produce APTTs in the therapeutic range. From the introduction of the "Lainz concept" 81% of the APTTs were kept within the therapeutic range by using a defined heparin-monitoring schedule based on a guideline protocol for controlling heparin treatment. Only 19% of the APTTs were below the therapeutic range. Factors underlying subtherapeutic APTTs are discussed. The reduction in the rate of subtherapeutic APTTs to less than 3% seen after the introduction of the "Lainz concept" constitutes an important contribution toward quality assurance in high-dose heparin treatment.

Aged↗
PubMed1995

[Changes in antithrombin III, prothrombin fragment 1 + 2 and thrombin-antithrombin III complex following implantation of a coronary Palmaz-Schatz stent].

To detect changes in the clotting parameters antithrombin III (AT III), prothrombin-fragment 1 + 2 (F 1 + 2) and thrombin-antithrombin-III-complex (TAT) after implantation of Palmaz Schatz stents, coagulation was monitored at standardized time points in 35 patients for 10 days. All patients were anticoagulated using a combination of heparin, phenprocoumon, and acetyl salicylic acid. Heparin therapy was guided by APTT levels (normal range 25-35 s), which were still within the therapeutic range (median 49.6 s (25%/75% percentiles 41.6/54.4) on day 10. Simultaneous oral anticoagulation was found to be effective on day 8 on average (INR median 2.24 (1.93/2.50)). The AT III activity dropped significantly (p < 0.0001) after a heparin loading dose of 15,000 IU during stenting. As the heparin dose was reduced on the following days, AT III levels increased significantly (p < 0.0001) during the observation time. There was a highly significant (p < 0.001) negative correlation between AT III and heparin levels. On days 4 and 5 F 1 + 2 values were significantly (p < 0.001 and p < 0.05) higher than on the day of stenting (median 1.07 (0.90/1.31) 1.13 nmol/l and 1.06 (0.85/1.23) nmol/l vs. 0.97 (0.69/1.15) nmol/l) and dropped during anticoagulation. F 1 + 2 levels showed a significant negative correlation (p < 0.0005) with APTT values. TAT values showed no significant changes during the observation period.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
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

[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

[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↗