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C Mueller-Eckhardt

Publications and source records attributed to C Mueller-Eckhardt.

At least 91 records · Page 5Linked to original sources
PubMed1992

[Clinical importance of granulocyte-specific antibodies].

Clinical and laboratory data of 184 patients with immune neutropenia were evaluated. They suffered from autoimmune neutropenia (n = 165), alloimmune neonatal neutropenia (n = 18) and from transfusion-associated lung injury (n = 1). Autoimmune neutropenia was predominantly found in patients below 3 years. Patients were usually affected by benign bacterial infections. The peripheral blood count showed normal or diminished leukocyte counts with median absolute neutrophil counts of 285 cells/microliters. Bone marrow examination revealed in 60% of the cases a hypercellular marrow with a shift to the left. In 36% the bone marrow was normal and in 4% a hypocellular marrow was found. Spontaneous remission occurred in all newborns and, so far, in 4 patients with autoimmune neutropenia. Symptomatic treatment of the infections was sufficient in most of the patients.

Adolescent↗
PubMed1992

[Granulocyte-specific and HLA antibodies in pregnancy: incidence and clinical value].

Postpartum sera of 1,016 unselected women were examined for granulocyte-specific and HLA antibodies. A total of 11 out of 1,016 sera (1.1%) were only reactive with neutrophils. Cytotoxic HLA antibodies were detected in 24%, noncytotoxic HLA antibodies in 4.8% of the sera. All antibodies belonged to the IgG 1 and IgG 3 subclasses. NA1 and NB1 specificity were each determined in one serum, two sera contained NA2-specific antibodies. After 1 year all antibodies were no more detectable. As none of the newborns from immunized mothers developed neutropenia, the incidence of alloimmune neonatal neutropenia seems to be lower than 0.1%.

Autoimmune Diseases↗
PubMed1992

[Neonatal isoimmune thrombocytopenia by anti-GP IIb/IIIa].

Neonatal alloimmune thrombocytopenic purpura is caused by maternal platelet-specific alloantibodies which react on fetal platelets with the corresponding antigen. We describe a 30-year-old female patient with type I Glanzmann thrombasthenia who developed an isoantibody against the platelet GP IIb/IIIa complex before or during pregnancy. The platelet count in the male newborn was 35 x 10(9)/l, but there were no signs of cerebral hemorrhage. Following infusion of 2 g/day i.v. IgG on 3 consecutive days, platelet counts rose to normal values. An isoantibody reacting with the GP IIb/IIIa complex of all platelet donors tested was found in the maternal serum using the MAIPA assay. Thus, immune-mediated neonatal thrombocytopenia may be caused by platelet isoantibodies against GP IIb/IIIa as well as by platelet-specific alloantibodies and by maternal autoantibodies.

Adult↗
PubMed1991

A rapid and sensitive test for diagnosing heparin-associated thrombocytopenia.

Heparin-associated thrombocytopenia (HAT) is a severe complication of heparin therapy. Its diagnosis is difficult. Conventional assays employ platelet aggregometry (PAA) and/or 14C-serotonin release (SRA) which are either insensitive (PAA) or require radioactive tracers (SRA). We here describe a newly developed sensitive and rapid assay based on visual evaluation of heparin-induced platelet activation (HIPA) in microtiter wells. Using sera of 34 patients with clinically suspected HAT we found the HIPA assay to be as sensitive as the SRA and superior to PAA. The HIPA assay allows investigation of crossreactivity with different types of heparins, low molecular weight (LMW) heparins and heparinoids. Three patients who required further parenteral anticoagulation and in whom the HIPA assay was negative before treatment with the LMW heparinoid Org 10172, were treated with this new heparinoid without adverse reactions. We conclude that the HIPA assay may be a useful tool for differential diagnosis and therapy in patients with HAT.

Cross Reactions↗
PubMed1991

Blood group A and B determinants are expressed on platelet glycoproteins IIa, IIIa, and Ib.

We report the localization of A, B blood group determinants on intrinsic glycoproteins using anti-A, B IgG antibodies. By radioimmunoprecipitation, anti-A and anti-B precipitated three bands with apparent molecular masses in sodium dodecylsulphate-polyacrylamide gel electrophoresis (SDS-PAGE) of 159, approximately 120 and 85 kDa under non-reduced conditions and 145, approximately 126 and 97 kDa under reduced conditions. In two-dimensional gel electrophoresis (isoelectric focussing/SDS-PAGE) these three bands could be resolved into six spots and fulfilled previously defined criteria for platelet membrane glycoprotein complexes I a/IIa, Ic/IIa, I b/IX and II b/IIIa. The results were supported by data obtained by an assay employing antibody-specific immobilization of platelet antigens (MAIPA). By this technique, blood group A, B determinants were shown to be immobilized by monoclonal antibodies specific for GPIa, Ic', IX, IIb/IIIa and strongly by mab specific GPIIa, but not by mab specific for HLA class I molecules. The more precise localization on platelet glycoproteins was achieved by immunoblotting technique by which blood group A determinants could be assigned to GPs IIa, IIIa and Ib.

ABO Blood-Group System↗
PubMed1991

Autoimmune neutropenia: clinical and laboratory studies in 143 patients.

Clinical and laboratory data of 143 patients with primary or secondary autoimmune neutropenia (AIN) were evaluated. Primary AIN was found predominantly in children below 3 years, whereas secondary AIN was more frequent in patients 40-60 years of age. Female patients with primary AIN were slightly more prevalent (54%) than male patients (46%). The peripheral blood count showed normal or diminished leukocyte counts with median absolute neutrophil counts of 250 cells/microliters. In 38% of the patients neutropenia was accompanied by monocytosis. Bone marrow examination revealed in 95% a normo- or hypercellular marrow with a marked reduction of mature neutrophils in 56% of the specimens. Twenty-three percent of the sera showed specificity for the NA1 antigen. Patients were usually affected by benign bacterial infections of the skin and of the upper respiratory tract, as well as by recurrent otitis media. Infections were treated symptomatically, and only six patients required continuous administration of antibiotics. Remission of neutropenia during treatment occurred in three of six patients treated with intravenous immunoglobulin G and in three of four patients who received steroid therapy. Except for one patient neutropenia relapsed after discontinuation of therapy. During a follow-up of 6-36 months, spontaneous remission has been observed in four patients.

Antibodies, Anti-Idiotypic↗
PubMed1991

High-dose IgG for neutropenic patients with acquired immunodeficiency syndrome (AIDS).

Leukocytopenia and bacterial infections are common and serious complications in patients with AIDS. We report here on three patients in whom the administration of high IgG doses led to gradual (two patients) or prompt (one patient) increases in circulating leukocyte counts (from 200-600 to 2500-5900/microliters), inducing definite improvement in two patients; one patient died from Pneumocystis carinii pneumonia. Although the rise in leukocyte counts lasted for only approximately 3 weeks, high-dose IgG might be a useful therapeutic adjunct in such patients.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Autoimmunization against the neutrophil-specific NA1 antigen is associated with HLA-DR2.

A significant association of autoimmune neutropenia (AIN) in infants due to NA1-specific autoantibodies and HLA-DR2 is reported. Nineteen of 26 infants presenting with AIN and NA1 autoantibodies possessed the DR2 antigen, while only one out of six children with AIN, but non-NA1-specific autoantibodies, was DR2 positive. Furthermore, one adult patient with primary biliary cirrhosis and periods of neutropenia due to NA1 autoantibodies also carried the DR2 antigen. All DR2-negative patients were positive for DRw6. These findings indicate that a close relationship exists between autoimmunization against the NA1 antigen and HLA-DR2 and possibly also DRw6.

Aged↗
PubMed1991

HPA-5b (Br(a)) neonatal alloimmune thrombocytopenia: clinical and immunological analysis of 39 cases.

Maternal alloimmunization against fetal platelets can cause fetal and neonatal thrombocytopenia (NAIT). The HPA-1a (PIA1, Zwa) antigen is by far the most common antigen implicated in NAIT. However, today another antigen often linked with that affection is HPA-5b (Br(a)). This is a report of 39 cases of NAIT involving the HPA-5b antigen. Thrombocytopenia may be of grave consequence. Three infants developed intracerebral haemorrhages (ICH). Of these, one died presumably as a consequence of ICH. Central nervous system (CNS) sequelae in the neonatal period was observed in two children. The potential hazards of death or disabling neurologic sequelae following intracerebral haemorrhage call for rapid and reliable diagnosis and effective therapy. Because there is high risk that subsequent pregnancies might be also affected by NAIT, the mothers of a previously affected child should be managed similarly to the HPA-1b mothers (PIA2, Zwb). The antenatal diagnosis of thrombocytopenia should be made and if necessary the in utero therapy instituted.

Antigens, Human Platelet↗
PubMed1991

Antigenic determinants responsible for the reactions of drug-dependent antibodies with blood cells.

In an attempt to determine the antigenic combining sites of drug-dependent antibodies in patients with drug-related immune haemolysis, we have assessed the reactivity of 35 nomifensine-induced antibodies against human red blood cells (RBC) in the presence of 11 closely related compounds: nomifensine, its three main metabolites including their methoxylated analogues and diclofensine with its three main metabolites. Three types of antibody reactivity patterns could be differentiated: Firstly, antibodies most strongly reactive with nomifensine (n = 12); secondly, antibodies primarily directed against one of its main metabolites (n = 7), and thirdly, antibodies optimally reactive with its unknown metabolites (n = 16). The antibodies preferentially directed against nomifensine showed varying cross reactions with nomifensine-related compounds and in almost all cases also with diclofensine and/or its metabolites. Those antibodies which were optimally reactive with metabolites reacted only with nomifensine-derived compounds and only one of them was non-crossreactive. The third group of antibodies showed no (n = 12) or only weak (n = 4) cross reactions with nomifensine and/or its metabolites. Although none of the substances used bound firmly to RBC, certain blood groups have been identified in previous studies to be defined. RBC antigens were required for the reaction in approximately 40% of all antibodies, independent of their reactivity with the compounds. Thus, even when the specificity of some antibodies appeared to be predominantly controlled by certain structural features of the compounds, the actual antigenic combining site of each antibody was different and seemed to comprise parts of the drug-related determinants as well as different constituents on RBC membranes. These findings indicate firstly that RBCs function as 'carrier-like' macromolecules, since they are directly involved in the reaction; secondly, that the drugs and their metabolites act as 'pseudohaptens', in as much as they do not bind tightly to the cells; and, thirdly, that the determinants which govern the immune response appear to result from an accidental attachment rather than from a predetermined selection of antigenic membrane structures, since each antibody shows a unique reaction pattern.

Anemia, Hemolytic↗
PubMed1991

Autoantibodies against platelet glycoprotein Ib/IX: a frequent finding in autoimmune thrombocytopenic purpura.

Many autoantibodies involved in the pathogenesis of autoimmune thrombocytopenic purpura (AITP) are directed against epitopes on platelet glycoproteins (GP). These autoantibodies are a specific diagnostic characteristic of patients with AITP. In this study, the relative frequency of antibodies against GPs IIb/IIIa and Ib/IX was assessed in sera from 81 AITP patients with a glycoprotein-specific enzyme immunoassay (MAIPA assay) using monoclonal antibodies against these platelet GPs. All sera contained platelet-specific antibodies which had been detected by platelet immunofluorescence. Of the 81 antibodies tested, 58 (72%) reacted with at least one of the platelet GPs studied. Autoantibodies against GPIb/IX were as common as antibodies against the GPIIb/IIIa complex. The same ratio of specificities was observed on autologous platelets of an independent cohort of 29 patients. The epitope of three autoantibodies against GPIb/IX and of mab Gi10, a monoclonal antibody, which inhibits binding of these autoantibodies, was further characterized. Severity of thrombocytopenia was not related to the GP specificity of the autoantibody. The observation that in 23 (28%) of these sera the antigenic determinants could not be assigned to the glycoproteins under investigation suggests that platelet autoantibodies may react with other GPs or other membrane constituents, e.g. glycolipids.

Antibodies, Monoclonal↗