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Biomedical subjects

K Lechner

Publications and source records attributed to K Lechner.

At least 343 records · Page 19Linked to original sources
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

HTLV-I antibody status in hemophilia patients treated with factor concentrates prepared from U.S. plasma sources and in hemophilia patients with AIDS.

Serum samples from 85 Austrian hemophilia patients treated with lyophilized factor concentrates prepared from U.S. plasma sources, 24 hemophilia patients from Georgia on a home therapy program with factor concentrates, and 10 U.S. hemophilia patients with acquired immunodeficiency syndrome (AIDS) were analyzed by two different methods for the presence of antibodies to the major internal antigen of human T-cell leukemia virus I (HTLV-I) p24. All but one, a Georgia sample, were negative. The absence of antibody to HTLV-I p24 in the serum of European hemophilia patients, of U.S. hemophilia patients with no symptoms of AIDS, and of U.S. hemophilia patients with AIDS is interpreted as an indication of the lack of ready transmissibility of HTLV-I in lyophilized factor concentrates.

Acquired Immunodeficiency Syndrome↗
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

Unexpected absence of a myeloid surface antigen (3-fucosyl-N-acetyllactosamine) in promyelocytic leukemia.

According to the criteria of the FAB classification we diagnosed acute promyelocytic leukemia in 19 out of 191 AML blast cell populations. The reaction pattern with the anti-myeloid monoclonal antibodies VIM2, MCS2 and MY9 and the MHC-class II antibody VID1 in all cases showed the characteristics which were expected from the normal granulopoiesis. The monoclonal antibody VIM-D5, which recognizes the myeloid cell surface structure 3-fucosyl-N-acetyllactosamine (3-FAL), was not reactive with the majority of promyelocytic blast cells, however. In 13 cases 3-FAL was not detectable and in 6 cases only low or moderate reactivity of VIM-D5 with blast cells was observed. The phenotype of leukemic promyelocytes thus differs from the majority of normal promyelocytes in this respect.

Antibodies, Monoclonal↗
PubMed1985

Cell lineage heterogeneity in blast crisis of chronic myeloid leukaemia.

Blast cells from 45 patients with chronic myeloid leukaemia in blast crisis (CML-BC) were immunologically phenotyped with a panel of 26 monoclonal antibodies and studied for terminal deoxynucleotidyl transferase (TdT) content. Out of 45 blast-populations, 28 showed a myeloid, 14 a lymphoid, two a mixed and one an unclassifiable marker profile. In contrast to acute myeloid leukaemia (AML), we found frequent involvement of the thrombopoietic and erythropoietic systems in myeloid CML-BC. Furthermore, the marker profile on blast cells in myeloid CML-BC was different from that seen in AML. The blast cells in lymphoid blast crises of CML displayed the same lymphoid marker profile as those in acute lymphoblastic leukaemia. In three of 16 patients who were serially tested, we observed phenotypic changes in the blast cell populations. In one patient the blasts changed from lymphoid to myeloid type while remaining TdT-positive; in another case the blasts switched from granulomonocytic TdT-negative to granulomonocytic TdT-positive. In the third patient erythroid precursor cells appeared as the disease progressed. The results indicate the capacity of blast populations in CML-patients during blast crisis to differentiate along several pathways.

Adolescent↗
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↗
PubMed1985

Aplastic anemia: assessment of myeloid progenitor cells in the bone marrow and blood provides prognostic information.

15 patients with aplastic anemia were prospectively followed after having measurements of myeloid progenitor cells in bone marrow and blood. Treatment included androgens, low or high dose steroids and standardized supportive care. The median length of survival was 5.8 months. When patients were grouped according to the numbers of myeloid progenitor cells present in their blood and bone marrow, we found that the survival length of aplastic patients with higher progenitor cell numbers was prolonged when compared to that of patients with lower numbers of these cells. The prognostic information obtained from such in vitro cultures was particularly indicative when the patients were grouped according to 'growth' and 'no growth': the absence of colony-forming myeloid stem cells was associated with survival times significantly shorter than those of patients whose cells maintained their colony-forming capacity. Besides initial numbers of myeloid progenitor cells, only initial numbers of granulocytes were related to survival length. Thus, the measurement of myeloid progenitor cells in bone marrow and blood can be of prognostic value in patients with aplastic anemia.

Aged↗
PubMed1985

Lupus anticoagulants and thrombosis. A study of 25 cases and review of the literature.

25 patients with lupus anticoagulant (LA) and a history of thrombosis are described and the cases reported in the literature with this association are reviewed. From the combined data it is concluded that the prevalence of thrombosis in patients with LA is about 30%, the thrombosis sites are the leg veins in about 66%, the cerebral arteries in 25% and the peripheral arteries in 10% of the patients. High anticardiolipin levels are associated with a higher risk, while age of less than 10 years, low prothrombin activity and a platelet count of less than 50,000/microliter is associated with a lower risk of thrombosis. Heparin and oral anticoagulants are effective in the treatment and prevention of thrombosis without untoward risk of bleeding.

Adolescent↗
PubMed1985

Deficiency of the autologous mixed lymphocyte reaction in patients with classic hemophilia treated with commercial factor VIII concentrate. Correlation with T cell subset distribution, antibodies to lymphadenopathy-associated or human T lymphotropic virus, and analysis of the cellular basis of the deficiency.

14 patients with hemophilia were studied for the distribution of T cell subsets, the presence of antibody to lymphadenopathy-associated or human T lymphotropic virus type III (LAV/HTLV-III), and their responsiveness in autologous mixed lymphocyte reactions. In addition, mitogen and alloantigen responsiveness and Interleukin-2 production were investigated. Seven patients were found to have low Leu 3a/Leu 2a (T4/T8) ratios; eight patients had antibody to LAV/HTLV-III; and an additional patient had acquired immunodeficiency syndrome. Responsiveness to mitogens and alloantigens as well as Interleukin-2 production were comparable with those of healthy individuals. However, patients with low ratio, many of whom had antibodies to LAV/HTLV-III, had a highly deficient autologous mixed lymphocyte reaction. This reduced response of T cells to autologous non-T cells could not be corrected by elimination of Leu 2a/T8 cells, which indicated that there was a preferential loss of the Leu 3a cell subset(s) which responded to autologous non-T cells. Thus, these patients have a deficiency of intercellular communication within their immune system.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Lymphocytes of haemophilia patients treated with clotting factor concentrates display activation-linked cell-surface antigens.

Peripheral blood lymphocytes from 30 patients with haemophilia A were investigated for the expression of six activation-linked cell surface antigens as well as with regard to the relative proportions and total numbers of Leu-3a and Leu-2a positive cells. Twenty-nine of the haemophilia patients showed no clinical symptoms of immunodeficiency or infection whereas one patient presented the typical symptomatology of the acquired immunodeficiency syndrome (AIDS). The proportions and total numbers of circulating lymphocytes displaying Ia antigens, the p45 protein and/or the two recently defined surface antigens VIP-4 and VIP-5 were significantly increased in haemophilia patients when compared to healthy individuals of the same age group. No such increases could be observed for transferrin receptor and IL-2 receptor expression. After the observation of depressed helper/suppressor T-cell ratios in many haemophiliacs, the expression of activation linked surface antigens represents a further lymphocyte abnormality which resembles the findings in AIDS and its prodromal stages and can also be found in certain viral and parasitic diseases.

Acquired Immunodeficiency Syndrome↗
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

[Deficiency anemias in tropical countries].

Nutritional anaemias are common in tropical areas. The commonest cause is iron deficiency, which mainly arises from impaired absorption of iron from food. Substances which inhibit iron absorption in various diets play an important role in the pathogenesis of iron deficiency anaemia. Iron deficiency is further aggravated by blood loss in hook-worm infestation. Folic acid and vitamin B 12 deficiency are less important causes of nutritional anaemia. The efforts of the World Health Organization to supplement iron in food are described.

Anemia, Hypochromic↗
PubMed1984

Evidence of HLA-DR antigen biosynthesis by human keratinocytes in disease.

As opposed to normal human skin where HLA-DR expression is restricted to the Langerhans cell (LC) population, HLA-DR, but not HLA-DS antigens can be readily detected on keratinocytes (KC) in certain disease states, i.e., cutaneous T cell lymphoma (CTCL), graft-vs-host disease (GVHD), and lichen planus (LP). To clarify the cellular origin of KC-bound HLA-DR antigens, we used a monoclonal antibody directed against determinants solely expressed on the cytoplasmic HLA-DR gamma chain (VIC-Y1) and observed that, by immunofluorescence, KC displaying HLA-DR alpha/beta complexes on their surface uniformly displayed cytoplasmic VIC-Y1 reactivity. In view of the crucial role of the gamma chain for HLA-DR biosynthesis, we conclude that HLA-DR antigens on KC are actively synthesized by these cells.

Epidermis↗