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Biomedical subjects

H Niessner

Publications and source records attributed to H Niessner.

At least 37 records · Page 2Linked to original sources
PubMed1986

Thromboembolism in patients with prosthetic heart valves. An adequately controlled intense anticoagulant therapy and its influence on the occurrence of thromboembolism in relation to valve type.

This study was designed to evaluate the efficacy of carefully controlled treatment with oral anticoagulants in patients with different mechanical heart valve prostheses. One hundred eighty-one patients with various types of prosthetic valves (mitral 89, aortic 87, combined 5) received oral anticoagulation aiming at Thrombotest (TT) values between 5% and 12%. Median follow-up was 46 months; 80.8% of all TT determinations were below 12%. The thromboembolic rate was 0.25%/year in patients with aortic valve replacement (AVR) and 4.87%/year in patients with mitral valve replacement (MVR). There was a strikingly lower incidence of thromboembolism with newer types of valves (Björk-Shiley convex-concave) in the mitral position under exactly the same intensity and stability of anticoagulant treatment. Clinically overt valve occlusion could be almost completely prevented (0.12%/year) in prostheses at both sites. Severe hemorrhage occurred at a rate of 1.71%/year and fatal bleeding at a rate of 0.37%/year. Our results indicate that carefully controlled anticoagulation is effective in the reduction of thromboembolic complications at a reasonable risk of bleeding.

4-Hydroxycoumarins↗
PubMed1986

Platelet-associated immunoglobulins IgG, IgM, IgA and complement C3c in chronic idiopathic autoimmune thrombocytopenia: relation to the sequestration pattern of 111indium labelled platelets.

Levels of platelet-associated immunoglobulins (PAIg) IgG, IgM, IgA and complement C3c were related to parameters of 111Indium-labelled platelet kinetics in 17 patients with chronic idiopathic autoimmune thrombocytopenia (cAITP). Elevated levels of PAIg/C3c were found in 14 patients (82%) (PAIgG n = 13, PAIgM n = 11, PAIgA n = 1, PAC3c n = 5). Only PAIgG correlated with platelet counts (RS = -0.71, p less than 0.01). Mean platelet life span (MLS) was shortened in all patients (median 12.0 h, range 0.3-45.6 h) and correlated with the platelet counts (RS = 0.49, p less than 0.05). MLS was correlated with PAIgG (RS = -0.52, p less than 0.05), but not with PAIgM, PAIgA, or PAC3c. The site of sequestration was splenic in 10 patients and splenic-hepatic in 7 patients. Although no significant correlation between either site of platelet sequestration and any of the investigated PAIg/C3c was demonstrable, platelets coated with higher PAIgG levels were more readily sequestrated in the spleen, while elevations of PAC3c were found in 4 out of 7 patients with hepatic involvement.

Adolescent↗
PubMed1986

Treatment of severe aplastic anemia with combined immunosuppression (antithymocyte globulin and high-dose methylprednisolone).

Fifteen patients with transfusion-dependent severe aplastic anemia (SAA) were treated with combined immunosuppression consisting of horse-antithymocyte globulin (ATG; Atgam, Upjohn) and high-dose 6-methylprednisolone (MP). Oxymetholone was scheduled for 2 years but was discontinued in 7 patients after 10-385 days due to liver toxicity. Serious side effects usually seen in ATG monotherapy were rare during combined immunosuppression. Currently 12 of 15 patients are alive 110-1,275 days (median 475.5) after start of treatment. One patient has received too short treatment to be evaluated. All the others are transfusion-independent. Three patients died; two from septicemia before hemopoietic recovery could be expected and one after relapse. Our results confirm that the addition of high-dose MP abrogates the side effects of ATG monotherapy, and the addition of MP does not counteract, but rather enhances the beneficial effect of ATG in SAA. We recommend combined immunosuppressive treatment with ATG and high-dose MP as a highly feasible, safe and effectful therapy for patients with transfusion-dependent SAA.

Anemia, Aplastic↗
PubMed1986

Acquired thrombasthenia due to GPIIb/IIIa-specific platelet autoantibodies.

An otherwise healthy woman developed a hemorrhagic diathesis with fluctuating clinical symptoms and laboratory findings, but without thrombocytopenia, over 8 years. In periods of bad clinical condition, a platelet defect, characteristic of thrombasthenia, was found. In contrast to classic thrombasthenia, electrophoresis of the patient's platelet membranes revealed normal amounts of glycoproteins IIb alpha, IIb beta, and IIIa in the normal positions. Monoclonal antibodies, specific for GPIIIa and GPIIb/IIIa, respectively, bound normally to the P1A1-positive platelets from the patient. Although no antibody and no platelet function inhibitor were evident in the autologous plasma, an IgG1 antibody that was bound to the patient's platelets and was directed against GPIIb/IIIa could be demonstrated. After elution from the patient's platelets, this antibody immunoprecipitated GPIIb (both subunits), IIIa, and a 200-kilodalton (kd) band (probably undissociated GPIIb/IIIa complex) from solubilized normal platelets, but did not react with thrombasthenic platelets. Adding the eluate from the patient's platelets to normal platelet-rich plasma immediately caused concentration-dependent inhibition of adenosine diphosphate (ADP)-induced and collagen-induced aggregation and also strong inhibition of ADP-stimulated fibrinogen binding. Because it was very unlikely from the patient's medical history that the antibody was caused by alloimmunization, the hemorrhagic diathesis must be interpreted as acquired thrombasthenia due to an anti-GPIIb/IIIa autoantibody.

Adult↗
PubMed1986

Increased risk of thrombosis due to abnormalities of the hemostatic system.

In recent years a number or hereditary or acquired abnormalities of the hemostatic system have been discovered which predispose to thrombosis. The type of this abnormality determines not only whether there is a tendency to venous or arterial thrombosis but also predisposes in some instances to thrombosis at a specific site. Such hemostatic abnormalities may be present in 10-30% of patients with a history of venous thrombosis. The detection of a thrombophilic state has important implications as regards the choice and the duration of antithrombotic treatment.

Blood Coagulation Disorders↗
PubMed1985

The prevalence of hereditary antithrombin-III deficiency in patients with a history of venous thromboembolism.

Antithrombin-III activity was determined in 752 patients with a history of venous thrombosis and/or pulmonary embolism. 54 patients (7.18%) had an antithrombin-III activity below the normal range. Among these were 13 patients (1.73%) with proven hereditary deficiency. 14 patients were judged to have probable hereditary antithrombin-III deficiency, because they had a positive family history, but antithrombin-III deficiency could not be verified in other members of the family. In the 27 remaining patients (most of them with only slight deficiency) hereditary antithrombin-III deficiency was unlikely. The prevalence of hereditary antithrombin-III deficiency was higher in patients with recurrent venous thrombosis.

Antithrombin III Deficiency↗
PubMed1985

Prevention of arterial and pulmonary embolism by oral anticoagulants in patients with dilated cardiomyopathy.

The incidence of arterial embolism (AE) and pulmonary embolism (PE) during treatment with oral anticoagulants (OA) or without OA therapy was studied in 38 patients with dilated cardiomyopathy (DCMP). AE/PE occurred in 17 patients (44.7%) before initiation of OA treatment. The severity of DCMP was a risk factor for AE/PE, but not the presence of atrial fibrillation or intracardial thrombi. No AE/PE episodes occurred during the period of OA therapy. No major bleeding complications were seen, probably due to the moderate intensity of OA therapy (therapeutic range 5-15% Thrombotest [TT], 2.1-4.8 International Normalized Ratio [INR], median TT value 11%, median INR 2.6). Recurrence of AE was observed in 4 of 5 patients in whom treatment with OA had been discontinued.

4-Hydroxycoumarins↗
PubMed1985

High levels of plasma protein C in nephrotic syndrome.

In patients with severe nephrotic syndrome determinations of plasma protein C: Ag levels (8 patients: 5 adults, 3 children) and protein C activity (3 out of 8 patients) revealed significantly elevated plasma protein C concentrations. Furthermore we observed a significant inverse correlation of protein C: Ag to AT III: Ag levels. No protein C: Ag could be detected in the urine of two patients studied. We conclude from our data, that changes of plasma protein C do not contribute to the high thrombotic tendency in nephrotic syndrome.

Adolescent↗
PubMed1985

[Effect of 24-day exercise therapy on induced thrombocyte aggregation in peripheral arterial occlusive disease in Fontaine stage II].

ADP and collagen induced platelet aggregation (PA) was studied in 18 patients suffering from arterial occlusive disease (stage II Fontaine) before and after a standardized treadmill test before and after 24 days of exercise training. At the beginning of this therapy collagen induced PA after treadmill testing was increased (amplitude +11.29%, p less than 0.05, maximal slope +18.57%, p less than 0.05, integrated area +15.23%, p less than 0.05), whereas ADP induced PA showed no consistent alteration. After the 24-day treatment period increase in collagen induced PA was considerably smaller (amplitude +7.48%, n.s., maximal slope +7.35%, n.s., integrated area +11.99%, p less than 0.05), whereas ADP induced PA again showed no consistent changes. Since the treadmill exercise induced PA showed a negative linear correlation with the claudication provoking walking distance the smaller increase in PA after treatment was considered to be due to the improved metabolic situation following exercise therapy.

Adenosine Diphosphate↗
PubMed1985

Deficiency of fibrinogen and factor VII following treatment of severe aplastic anaemia with anti-thymocyte globulin and high-dose methylprednisolone.

In 4 patients with SAA treated with ATG and high-dose MP, an as yet unrecognized acquired deficiency of fibrinogen and factor VII was observed. The plasma level of fibrinogen fell to 39% (34-51%) and of factor VII:C to 50% (31-55%) of the pretreatment value. The nadirs were between days 10 and 35 (fibrinogen) and d 3 and 11 (factor VII) after the 1st dose of ATG/MP. From additional clotting studies it is concluded that disseminated intravascular coagulation, fibrinolysis, liver cell damage and synthesis of abnormal clotting factors are unlikely causes of these clotting abnormalities. The most probable explanation seems to be a selective inhibition of the synthesis of fibrinogen and factor VII by an as yet unknown mechanism. These clotting abnormalities might, to some extent, increase the bleeding tendency in these patients, which up to now had been solely attributed to thrombocytopenia.

Adult↗
PubMed1985

Treatment of severe chronic idiopathic thrombocytopenic purpura in adults with high-dose intravenous gammaglobulin.

12 patients with severe chronic idiopathic thrombocytopenic purpura (ITP) were treated with i.v. polyvalent intact immunoglobulin (0.14-0.4 g/kg body weight for 5 d) because of various bleeding episodes or prior to surgery. In 9 patients a significant rise in platelet counts was noted, starting on d 2 and reaching its maximum between d 4 and 11. Thereafter, platelet counts decreased slowly, approaching pre-treatment values after 20 d in most cases. Response to immunoglobulin was reproducible, when infusions were repeated. Response to high-dose immunoglobulin was independent of age of patients and duration of disease. Platelet-associated IgG decreased in all patients tested. A pepsin-treated immunoglobulin preparation was ineffective in 3 patients.

Adult↗
PubMed1984

Impaired fibrinolytic capacity predisposes for recurrence of venous thrombosis.

The fibrinolytic capacity of 121 patients with a history of venous thrombosis and/or pulmonary embolism was studied by venous occlusion technique, at earliest 3 months after the last thromboembolic episode. After discontinuation of oral anticoagulation treatment the clinical course of the patients was followed and new thromboembolic episodes were noted. During the observation period of 56 +/- 18.8 months 45 of 121 patients experienced recurrence of thrombosis. The recurrence-rate was significantly lower in patients with a post-occlusion ELT shorter than 60 min (4.8%/year) than in patients with an ELT longer than 60 min (10.3%/year). It is concluded that the fibrinolytic capacity is a useful parameter for determining the risk of recurrence in patients with venous thrombosis.

Anticoagulants↗
PubMed1984

Efficacy of the M-2 protocol in previously untreated patients with advanced multiple myeloma.

37 consecutive, previously untreated patients with advanced multiple myeloma (16 patients Stage II, 21 patients Stage III) were treated with a five drug regimen consisting of carmustine, melphalan, vincristine, cyclophosphamide and prednisolone (M-2-protocol) in a prospective manner. Remission was achieved in 24 patients (65%). The median time to remission was 10 weeks, the median duration of remission 15,3 months. Median survival time from the onset of treatment was 24 months for all patients. Responding patients have a projected 65% three year survival. Median survival in non-responders was 10 months. 8 patients died during the first year of treatment. These results do not confirm the favourable results with this drug combination obtained in a previous trial. The discrepancy may be explained by a higher proportion of poor risk patients in the present study.

Aged↗
PubMed1984

CRM+ severe Fletcher factor deficiency associated with Graves' disease.

A 59-year-old male patient with Graves' disease and severe hereditary Fletcher factor deficiency is described. PKK clotting activity as well as the activity by a chromogenic substrate method (Chromozym PK) was less then 0.01 U/ml. In contrast to functional tests, the immunological assay (Laurell method) showed a PKK antigen concentration of 0.25 U/ml, indicating the presence of an abnormal nonfunctional PKK molecule (CRM+ variant). An inhibitor was excluded since the patient plasma did not inactivate partially purified PKK. Investigation of 11 family members revealed a reduction of the PKK clotting activity in 9 relatives of the patient. Since Graves' disease is considered an autoimmune disease, our case represents an example of an association of a severe hereditary deficiency of a contact factor and an autoimmune disease.

Cross Reactions↗
PubMed1984

Range and clinical significance of the number of myeloid-committed stem cells in the blood of patients with acute leukaemia in remission.

Circulating granulocyte/macrophage progenitor cells (CFU-GM) were assayed serially during remission in 17 patients with acute leukaemia (9 ALL, 8 AML). In patients with ALL receiving cyclophosphamide, 6-mercaptopurine and methotrexate, CFU-GM numbers were significantly lower than in normal individuals; cycles of 'reinduction' chemotherapy (vincristine, prednisolone) caused a 10-fold increase in CFU-GM per ml of blood. In 2 ALL patients a substantial increase in CFU-GM numbers preceded the morphologically detectable relapse. In patients with AML receiving repeated courses of cytosine-arabinoside and 6-mercaptopurine, circulating CFU-GM were likewise reduced. In 6 patients who relapsed, a further reduction of CFU-GM was seen. A complete absence of circulating CFU-GM was observed in 10 of the 23 investigations performed within 6 weeks prior to the morphologically detectable relapse, while such a 'zero'-growth occurred in only 1 of 54 experiments performed during stable remission. In summary, in patients with ALL in remission, circulating CFU-GM are increased following treatment with vincristine and prednisolone. In patients with AML, declining numbers of circulating CFU-GM may predict an imminent relapse.

Acute Disease↗
PubMed1983

Protein C deficiency in two Austrian families.

Protein C antigen was determined by Laurell rocket immunoelectrophoresis in 225 patients with a history of venous thrombosis. Among these patients two females with protein C deficiency were detected. Additional studies in the families of the protein C deficient patients revealed further 7 family members with protein C deficiency. In 8 not anticoagulated patients with protein C deficiency the protein C ranged from 36 to 62% (median: 45%). In one patient on oral anticoagulant treatment protein C antigen concentration was less than 10%, F II and FX were 65 and 50%, respectively. The pattern of inheritance was consistent with autosomal dominant inheritance. 5 of the 9 protein C deficient patients had severe thrombotic tendency characterized by recurrent deep venous thrombosis (n = 4), pulmonary embolism (n = 1), probable mesenteric vein thrombosis (n = 1) and superficial thrombophlebitis (n = 2). All protein C deficient patients without thrombosis were less than 17 years old.

Adult↗