Biomedical subjects
F Duckert
Publications and source records attributed to F Duckert.
Factor XII, plasma prekallikrein, alpha 2-macroglobulin and C1-inhibitor levels in renal allograft recipients during immunosuppression with cyclosporin A--sequential measurements over four months in 17 patients.
Factor XII clotting activity (F XII), plasma prekallikrein amidolytic activity (PK), alpha 2-Macroglobulin (alpha 2-M) and C1-Inhibitor (C1-Inh) antigens have been measured in 17 patients immediately before and sequentially for up to four months after kidney transplantation. Before transplantation mean F XII and PK levels were normal (99 +/- 27% and 102 +/- 21%, respectively, mean +/- S.D.) and alpha 2-M and C1-Inh levels were slightly elevated (115 +/- 55% and 129 +/- 32%, respectively, mean +/- S.D.). In the first two weeks after transplantation a significant decrease of F XII to 65 +/- 27%, of PK to 67 +/- 20% and of alpha 2-M to 88 +/- 42%, and a rise of C1-Inh to 201 +/- 44% (mean +/- S.D.) were observed (2 p less than 0.005). F XII levels four month after operation remained significantly (2 p less than 0.05) lower than preoperatively. PK and alpha 2-M values, however, were significantly higher (2 p less than 0.05) at four months as compared to the pretransplant period. Mean F XII levels in the 17 patients at various time points after transplantation correlated positively with PK, alpha 2-M and serum albumin and negatively with CyA level and dose and serum bilirubin. PK and alpha 2-M correlated positively with each other and albumin and negatively with creatinine, bilirubin and CyA (2 p less than 0.01). Whether CyA has a direct influence on production or consumption of F XII, PK, alpha 2-M and C1-Inh, or whether the changes merely reflect altered protein metabolism awaits further study.
[Persons with known alcohol problems. Screening procedures for alcohol consumption].
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Recruitment into treatment and effects of treatment for female problem drinkers.
Literature on treatment of female problem drinkers is reviewed, focusing on the following topics: Recruitment of female problem drinkers into alcoholism treatment agencies, the fate of women in traditional mixed-sex treatment institutions, special treatment approaches for women, methodological problems and needs for future research. Several studies indicate that fewer women than men are recruited into alcoholism treatment agencies and that the referral routes in many ways differ from the referral routes of men. The women also report more negative effects of treatment, and are commonly looked upon as receiving less attention and less adequate care in the mixed-treatment institutions. On the other hand, a substantial number of studies of treatment outcome have shown that women seem to do just as well in treatment in mixed-sex institutions as men do. Several reports of all-female treatment programmes have been presented. Some treatment techniques may seem to have special significance for female problem drinkers, for instance self-assertiveness training and family therapy. But very few controlled studies of such programmes have been carried out up to now.
Behavioral use of disulfiram in the treatment of problem drinking.
As part of an outpatient treatment research project alternative ways of using Antabuse (disulfiram) in the treatment of problem drinkers are developed. Instead of forced regular use, Antabuse was administered as a voluntary situational therapeutic tool. Subjects were 84 men and 51 women. Thirty percent of both men and women decided to use Antabuse. Men most often used disulfiram continuously for a longer period or to stop an ongoing drinking period. The women used Antabuse to secure shorter periods of abstinence as part of their drinking schedules and to prevent drinking in specific high-risk situations. The subjects using Antabuse reduced their ethanol consumption significantly (p less than .05) at the end of the follow-up period, compared to the nonusers.
[Determination of thromboplastin time with a new standardized thromboplastin from human placenta: results of a cooperative study].
In five centres a new sensitive standardized thromboplastin from human placenta (Thromborel S) for determination of prothrombin time (PT) was evaluated on plasmas from healthy subjects, from patients on oral anticoagulant therapy and from patients with different diseases, especially of the liver. The standardization of the human placenta thromboplastin (HPT) for prothrombin time determination was performed by comparison with a lot of the Reference Preparation British Comparative Thromboplastin (BCT). The obtained International Sensitivity Index (ISI) for 14 differents lots of the new thromboplastin varied between 1.04 and 1.29 (mean value: 1.16). The reagent is highly sensitive to the factors of the extrinsic coagulation pathway and is not affected by heparin at least up to 0.6 IU/ml. From the comparison with the British Comparative Thromboplastin lot No. 235, a therapeutical range for the stable phase of the oral anticoagulation of 2.4-4.0 prothrombin ratio or 15-27% of normal, respectively, was obtained. Comparison of prothrombin time determination using the Human Placental Thromboplastin and the British Comparative Thromboplastin lot No. 235 in 330 patients on oral anticoagulation showed good correlations either in "percent normal" or in prothrombin ratio.
Heparin cofactor II: purification and antibody production.
Heparin cofactor II (HCII) was purified from plasma to homogeneity. The procedure includes adsorption with (A1)OH3, fractionation with polyethylene glycol 6000, chromatography on QAE-Sephadex A-50, on heparin-Sepharose 4B and on Sephadex G-150. QAE-Sephadex A-50 chromatography provides a good separation of HCII from antithrombin III (AT) and most contaminants having a heparin affinity similar to that of HCII. HCII is eluted at 0.28 M NaCl from the heparin-Sepharose column. After gel filtration on G-150, contaminating AT was removed by immunoadsorption. Purified HCII shows an apparent Mr of 66,500 daltons as analyzed on SDS-polyacrylamide gel and 62,100 daltons by ultracentrifugation. Antibodies to HCII were raised in rabbits. Former antisera mostly directed to a contaminating protein were used to remove it from the HCII preparation. Antibodies to HCII were made monospecific by immunoadsorption on HCII-free plasma linked to Sepharose 4B. Since many functional AT assays have neglected the presence of HCII in plasma, antibodies to HCII using as immunoadsorbent will provide a more specific test for AT.
Heparin cofactor II and other coagulation inhibitors.
The role of the coagulation inhibitors is discussed. The importance of local reactions because of the presence in tissue of the inhibitor activators dermatan sulfate, thrombomodulin and heparin is emphasized.
The development of thrombolytic treatment in venous thrombosis. Experience with streptokinase-based regimens.
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Influence of heparin cofactor II (HCII) on the determination of antithrombin III (AT).
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[Quantitative and qualitative hemostatic changes in 373 patients with recurring venous thromboses].
Extensive haemostasis analysis in 373 patients with recurrent idiopathic venous thrombosis revealed insufficient fibrinolysis activation by the venous occlusion test in 48%. A case with antithrombin III dysfunction was the only inherited anomaly.
Association of hereditary heparin co-factor II deficiency with thrombosis.
A family was investigated for heparin co-factor II deficiency. Three of the five members examined had had thrombosis and their levels of heparin co-factor II were reduced to 50%. All five members had antithrombin III levels within the normal range. Analysis on crossed immunoelectrophoresis showed no qualitative abnormality of patient heparin co-factor II antigen. Since heparin co-factor II activity and concentration were reduced to the same extent, the deficiency was due to reduced protein synthesis.
[Fibrinolysis therapy in massive lung embolism. Experiences in 10 patients 1982-1984].
Between October 1982 and July 1984 systemic thrombolysis was carried out in 10 patients (5 males and 5 females aged 19 to 66 years) with massive pulmonary embolism (PE). Mean thrombolytic treatment duration was 77 hours. The main fibrinolytic agent used (9 cases) was streptokinase. Sequential treatment with streptokinase and urokinase was given to 2 patients and urokinase alone to one. 5 patients received porcine plasmin additionally, and one patient BRL 26921 (streptokinase-plasminogen complex) and human plasminogen. Pulmonary arterial pressures were recorded serially. Pulmonary angiograms were obtained before, occasionally during and after thrombolysis. Pulmonary arterial pressures (systolic: p less than 0.01, diastolic: p less than 0.05, mean: p less than 0.01, paired t-test, two tailed) and pulmonary angiograms (p less than 0.001, paired t-test, two tailed) all showed significant improvement. Thrombolytic treatment had to be discontinued in two patients due to side effects. Patients with the most recent PE showed the best response. Patients with recurrent PE and preexisting pulmonary hypertension showed no improvement. In PE without deep vein thrombosis (DVT), treatment duration of up to three days seems to be appropriate. In PE with concomitant DVT the treatment should be prolonged to achieve complete lysis of thrombi.
Cold promoted activation and factor XII, prekallikrein and C1-inhibitor.
During incubation of plasma in the cold an amidolytic activity due to the kallikrein-alpha 2-macroglobulin complex appears in the plasma of about 40% of the women under hormonal contraception. The factor XII and prekallikrein activity are significantly increased 151.9% and 112.4% respectively in the cold promoted activation positive plasmas (CPA pos) whereas the activity of C1-inhibitor is decreased, 76%. The quotient of the product of the C1-inhibitor and alpha 2-macroglobulin values divided by the product of the FXII and prekallikrein values is significantly lower in the CPA pos plasma 0.49 than in CPA neg plasma 0.96 (p less than 0.05). These results alone do not explain the cold promoted activation, since a patient with a C1-inhibitor as low as 9% showed no increase of the amidolytic activity after a 24 hr incubation at 4 degrees C. However, the addition of purified C1-inhibitor to a CPA pos. plasma inhibits the cold activation. Heparin at a concentration of 0.5 IU/ml delays the appearance of the amidolytic activity.
[A study on interactions between pirprofen and phenprocoumon].
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Treatment with stanozolol before thrombolysis in patients with arterial occlusions.
The administration of the anabolic steroid stanozolol during 7, 8 days as pretreatment before thrombolytic therapy of acute or subacute arterial occlusions enhances the fibrinolytic potential significantly. On average the plasminogen increased from 101% to 133%, the euglobulin lysis time after venous stasis was shortened and the alpha 2-antiplasmin remained constant. This effect could be favourable to prepare patients undergoing thrombolytic treatment.
Methodology and clinical significance of heparin cofactor II. Probable heparin cofactor II deficiency in a patient with cerebrovascular thrombosis.
HC II was functionally determined by thrombin inhibition in the presence of heparin in AT III-free plasma prepared by immunoadsorption on anti-AT III-Sepharose 4B column. HC II antigen concentration was assayed using specific antibodies to HC II. Simultaneously, AT III was measured. Plasma levels of HC II and AT III were determined in 110 patients with thrombotic tendency and two patients with obstetric complications and DIC. Highly significant correlations between activity and antigen prove the suitability of the methods. Reduced levels of HC II to about 50% with normal AT III values were repeatedly found in one patient with thrombotic tendency. The course of AT III and HC II during the process of DIC suggests that HC II may function as a thrombin inhibitor reserve when AT III becomes subnormally low.
Purification of antithrombin 'Vicenza': a molecule with normal heparin affinity and impaired reactivity to thrombin.
Antithrombin III (AT) 'Vicenza', a previously described dysfunctional AT associated with familial thrombosis, has been isolated by heparin affinity chromatography. The purified molecule has been investigated by SDS-polyacrylamide gel electrophoresis and crossed immunoelectrophoresis after incubation with different amounts of thrombin. A normal affinity for heparin has been demonstrated. However, evidence is produced that AT 'Vicenza' poorly inhibits thrombin. Present data suggest that AT 'Vicenza' consists of a population of two molecules, half of which does not form a complex with thrombin however and loses its heparin affinity upon thrombin treatment.