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H Kroll

Publications and source records attributed to H Kroll.

53 records · Page 3Linked to original sources
PubMed1994

[Immunization against a new, infrequent alloantigen (Iy) on the platelet glycoprotein Ib/IX as a cause of a serious case of neonatal alloimmune thrombocytopenia].

Neonatal alloimmune thrombocytopenia is the consequence of maternal alloimmunization against platelet-specific alloantigens, usually PIA1 or Br(a). The clinical picture is characterized by signs of haemorrhagic diathesis as a result of marked thrombocytopenia. In the last years, rare cases of immunization against 'low-frequency' or 'private' platelet alloantigens on the platelet glycoprotein (GP) complex IIb/IIIa have been found. This is the first report on NAIT due to maternal immunization against a low-frequency platelet alloantigen ('Iy') localized on platelet GP Ib/IX.

Antigens, Human Platelet↗
PubMed1994

[Prenatal substitution therapy in fetal alloimmune thrombocytopenia].

Fetal alloimmune thrombocytopenia is caused by maternofetal transfer of platelet antibodies. Since the thrombocytopenic fetus is threatened by intracranial hemorrhage, prenatal observation and, if necessary, treatment is required. However, the benefit of therapeutic options, including intravenous IgG (ivIgG) or platelet transfusions, is still controversial. In this study we have evaluated the effect of maternal ivIgG and intraumbilical platelet transfusions on fetal platelet counts in 7 cases. All patients were multiparous women who were immunized against the Zwa antigen during previous pregnancies and had given birth to at least one severely thrombocytopenic infant. First umbilical blood was sampled at the 26th week of gestation. Maternal treatment of ivIgG was given over 7 weeks, the mean number of intrauterine platelet transfusions was 5.9. In 6 of 7 cases the basal platelet count before transfusion did not rise or even further decreased during maternal ivIgG treatment. In one case the baseline platelet count increased from 18,000/microliter to 60,000/microliter during ivIgG. We conclude that, in general, ivIgG alone has no detectable effect on fetal alloimmune thrombocytopenia. Since platelet counts can be very low as early as 20 weeks of gestation, careful fetal monitoring by umbilical blood sampling is required. Platelet transfusions in short intervals appear to be the only effective regimen to increase platelet counts in extremely thrombocytopenic fetuses.

Antigens, Human Platelet↗
PubMed1993

[Detection of drug-induced antibodies to erythrocytes in the gel test].

Drug-induced immune hemolytic anemia is a serious hematological disorder which results from increased red blood cell destruction due to the production of autoantibodies, drug (metabolite)-dependent antibodies (DDAb) or both types of antibodies, even in one patient by the same drug. One of the major problems related to DDAb is that the causative drug (metabolite) usually does not bind tightly to target cells, and the antibodies are completely removed from the cells by conventional washing procedures, i.e. by the antiglobulin test. We have recently shown that the microtube geltest, by which the antiglobulin test is performed without washing the cells, is a highly sensitive and reliable alternative method for the detection of all kinds of DDAb. The results obtained with different DDAb are discussed.

Anemia, Hemolytic, Autoimmune↗
PubMed1993

[Post-transfusion purpura: clinical and immunologic studies in 38 patients].

BACKGROUND: Posttransfusion purpura (PTP) is characterized by severe thrombocytopenia and hemorrhagic diathesis about 1 week following blood transfusion. Only few studies exceed the description of single cases. MATERIALS AND METHODS: Clinical data from 38 patients were analyzed. Platelet antibodies were studied by complement binding, immunofluorescence, MAIPA assay and acid elution techniques. RESULTS: All patients were female. The mean age at onset was 60.7 years (35-78 years). 4 patients received whole blood, 28 were transfused with packed RBC. 11 of 13 patients (85%) had febrile, non hemolytic adverse reactions during the transfusion. The interval between transfusion and onset of purpura extended from 2 to 14 days, with a peak at 7 and 8 days. Hemorrhagic symptoms lasted 10.1 days. The minimal platelet count was 7.0 x 10(3)/microliters. The platelet count increased to over 50 x 10(3)/microliters after 13.9 days (n = 26), and to over 100 x 10(3)/microliters after 17.0 days (n = 22). 2 patients died of hemorrhagic complications. 24 patients were treated with glucocorticoids, 20 with intravenous immunoglobulins (ivIG), 17 of these received both therapies. 14 of 19 patients (74%) responded well to ivIG. In contrast, platelet transfusions produced no adequate increment, in 6 cases they provoked febrile reactions. 35 sera (92.1%) contained anti-Zwa, either alone or together with anti-HLA or in 1 case with anti-Bra. Anti-Baka and anti-Bakb were found in 1 case each. In 5 patients, anti-Zwa could be eluted from autologous Zwa-negative platelets. CONCLUSIONS: The broad clinical spectrum of PTP could be shown. Since 5% of the patients succumb to bleeding complications, the application of ivIG as therapy of choice is recommended. The phenomenon of elution of alloantibodies from autologous platelets is interpreted as a consequence of 'pseudo-specificity' which may play a role in the pathogenesis of PTP.

Adult↗
PubMed1992

[Detection of platelet-specific alloantigens in 400 unselected blood donors].

Antibodies against platelet specific alloantigens cause neonatal alloimmune thrombocytopenia, posttransfusion purpura, and they are sometimes found in polytransfused patients. In the last few years, new alloantigens were discovered in addition to the Zw-, Bak-, and Ko-alloantigens. In order to obtain representative data for the frequency of all platelet alloantigens in the European population, we typed 400 blood donors of our institution. No significant differences between our findings and data already published were found for the antigens of the HPA-1, -2, -3, and -5 systems; however, no HPA-4b (Yuka)-positive and no Naka-negative individual was found among the 400 blood donors tested. The Siba and HPA-2b antigens proved to be identical. The 'low-frequency' alloantigen Sra was not identified among the 400 individuals tested.

Antigens, Human Platelet↗
PubMed1992

[Clinical and serologic studies in 34 patients with post-transfusion purpura].

Posttransfusion purpura (PTP) is a rare transfusion reaction characterized by a severe bleeding tendency and thrombocytopenia which occurs approximately 1 week after transfusion of platelet-containing blood components in patients previously immunized against platelet alloantigens. 34 cases of PTP were studied. Our patients were all female with a mean age of 60.8 years (35-78 years, n = 32). The inciting blood components were whole blood (4) or red cell concentrates (28). The interval between transfusion and onset of purpura ranged from 2 to 14 days with a clear maximum at 7 and 8 days. In 11 of 13 patients (85%) transfusion was accompanied by febrile, nonhemolytic transfusion reactions. Hemorrhagic symptoms lasted 9.4 days (3-37 days, n = 16). The mean minimal platelet count was 7.1 x 10(3)/microliters [(0-28) x 10(3)/microliters, n = 29]. The platelet count rose to over 50 x 10(3)/microliters after 13.9 days (2-61 days, n = 26), over 100 x 10(3)/microliters after 17.0 days (3-75 days, n = 22). In 1 patient, PTP led to death due to intracranial hemorrhage. 22 patients were treated with corticosteroids, 20 patients with intravenous immunoglobulins (IVIG), 17 of these patients received both. Therapy with IVIG was successful in 14 of 19 patients, whereas platelet transfusions (n = 18) were not able to evaluate the platelet count. Serological analysis showed that antibodies against the HPA-1a antigen either alone (18), in combination with HLA antibodies (12) or with anti-HPA-5b (1) were responsible in 91.2%, while antibodies against other platelet antigens were rarely implicated. In elution experiments HPA-1a antibodies could be eluted from the autologous HPA-1a-negative platelets. We suppose that these antibodies had a pseudo-specificity and were involved in the destruction of the patients' own platelets.

Adult↗
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

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↗
PubMed1990

Sra, a private platelet antigen on glycoprotein IIIa associated with neonatal alloimmune thrombocytopenia.

A new platelet alloantigen, Sra, is described that was defined by an alloantibody detected in the serum of a healthy mother who delivered a child with typical clinical signs of neonatal alloimmune thrombocytopenia (NAIT). The antibody reacted strongly with the child's and father's platelets, but not with platelets of the mother or with those of a highly selected panel representing all known platelet alloantigens. Platelets from 300 unselected normal blood donors also tested negative, suggesting a phenotype frequency in the German population of less than 0.01. The antigen was present in 9 of 20 members within three generations of the paternal family, indicating autosomal codominant inheritance. By immunochemical analysis using a glycoprotein (GP)-specific immunoassay and a variety of GP IIb/IIIa-specific monoclonal antibodies for antigen immobilization (MAIPA assay), radioimmunoassay, and Western blotting, we could show that the antigen resides on a 68-Kd proteolytic fragment of GP IIIa. Immunogenetic data and gene dosage studies revealed that the Sra antigen is not related to any of the other known platelet alloantigens. In accordance with established criteria, the Sra antigen represents the first example of a "private" platelet alloantigen that bears significance in rare instances of NAIT.

Adult↗
PubMed1990

[Sr(a), a "private" thrombocyte alloantigen as a cause of neonatal alloimmune thrombocytopenia].

Neonatal alloimmune thrombocytopenia (NAIT) is caused by maternal immunization against fetal platelet antigens. In the serum of a mother who gave birth to a child with the typical clinical picture of NAIT we found an antibody directed against the new platelet antigen Sra. Anti-Sra was found to react in the immunofluorescence test and in a glycoprotein (GP) specific immunoassay (MAIPA) using a monoclonal antibody against GP IIb/IIIa for antigen immobilization with the child's and father's platelets. Radioimmunoprecipitation and immunoblot allowed to assign the Sra-antigen to GP IIIa. The phenotype frequency was estimated less than 1%, characterising the Sra-antigen as the first 'private' alloantigen on platelets.

Blood Platelets↗
PubMed1990

[219 Zw(a) positive mothers of children with clinically suspected neonatal alloimmune thrombocytopenia].

The sera of 219 Zwa-positive mothers who gave birth to children with clinically suspected neonatal alloimmune thrombocytopenia (NAIT) were tested for platelet-reactive antibodies using the platelet adhesion immunofluorescence test and a glycoprotein-specific immunoassay (MAIPA). In 102 families a serological crossmatch of maternal serum against paternal platelets was performed. 12 sera contained platelet specific antibodies: Zwb (1), Bra (4), Bra and HLA (5), Baka and HLA (1), Sra (1); three further sera contained antibodies against blood group A (1), blood group B (1), blood group B and HLA (1). Anti-Bra was the most important antibody in this cohort. There is evidence that in certain cases antibodies against blood group antigens A or B may cause NAIT. Clinical data of NAIT duo to anti-Bra suggest a less severe bleeding tendency than in NAIT due to anti-Zwa. The HLA-DRw6 antigen was identified as an immunogenetic marker for the immunization against the Bra-antigen.

Antibody Specificity↗
PubMed1989

348 cases of suspected neonatal alloimmune thrombocytopenia.

Serological and clinical data were collected in 348 cases of suspected neonatal alloimmune thrombocytopenia (NAT). Of the 144 mothers who were Zwa-negative, 107 had Zwa antibodies--alone (94); with HLA antibodies (12); or with Bra antibodies (1). Antibodies were detected in 12 of the 204 Zwa-positive mothers as follows: anti-Bra (9), anti-Zwb (1), anti-Baka with HLA antibody (1), and blood group B isoagglutinins (1). The frequency of NAT due to Bra incompatibility (19%) was second to Zwa (78%). Zwa-NAT was clinically the more severe (14% had intracranial haemorrhages) and responded well to either maternal platelet transfusions or intravenous IgG. In Bra-NAT intracranial haemorrhages were not observed and most children recovered without specific therapy.

Adolescent↗
PubMed1989

Radical neck dissection: a subjective and objective evaluation of postoperative disability.

Nearly all patients who undergo radical neck dissection note significant morbidity if the XIth cranial nerve is sacrificed. Physicians can be misled to believe in a lower morbidity because the usual physical examination is unreliable in detecting weakness and because patients rarely persist in mentioning shoulder problems during follow-up visits. Eleven patients between the ages of 55 and 70, who had undergone unilateral neck dissection with sacrifice of the XIth cranial nerve, were given questionnaires and were objectively evaluated for strength and active range of motion on a Cybex II dynamometer. Eighty-two percent of patients experienced pain, 91% experienced weakness, and 91% experienced impairment on the affected side. Peak torque for the affected side ranged between 0 to 85% of the peak torque for the normal shoulder. Gravity-free active range of motions were 20 degrees to 162 degrees with 8 of 11 at 100 degrees or less. In all but two patients, the passive range of motion was limited by pain.

Accessory Nerve↗
PubMedDate not supplied

Discovering objects in a blood recipient information system.

Application of object-oriented (OO) methodologies has been generally considered as a solution to the problem of improving the software development process and managing the so-called software crisis. Among them, object-oriented analysis (OOA) is the most essential and is a vital prerequisite for the successful use of other OO methodologies. Though there are already a good deal of OOA methods published, the most important aspect common to all these methods: discovering objects classes truly relevant to the given problem domain, has remained a subject to be intensively researched. In this paper, using the successful development of a blood recipient information system as an example, we present our approach which is based on the conceptual framework of responsibility-driven OOA. In the discussion, we also suggest that it may be inadequate to simply attribute the software crisis to the waterfall model of the software development life-cycle. We are convinced that the real causes for the failure of some software and information systems should be sought in the methodologies used in some crucial phases of the software development process. Furthermore, a software system can also fail if object classes essential to the problem domain are not discovered, implemented and visualized, so that the real-world situation cannot be faithfully traced by it.

Blood Banks↗