TransfusionVolume 25, Issue 2 p. 182-183 The foregoing letter was sent to Drs. Salama and Mueller-Eckhardt, who replied as follows A. Salama MD, A. Salama MD Institute of Clinical Immunology and Blood Transfusion Justus Liebig University Langhansstr. 7 D-6300 Giessen, FRGSearch for more papers by this authorC. Mueller-Eckhardt MD, C. Mueller-Eckhardt MD Institute of Clinical Immunology and Blood Transfusion Justus Liebig University Langhansstr. 7 D-6300 Giessen, FRGSearch for more papers by this author A. Salama MD, A. Salama MD Institute of Clinical Immunology and Blood Transfusion Justus Liebig University Langhansstr. 7 D-6300 Giessen, FRGSearch for more papers by this authorC. Mueller-Eckhardt MD, C. Mueller-Eckhardt MD Institute of Clinical Immunology and Blood Transfusion Justus Liebig University Langhansstr. 7 D-6300 Giessen, FRGSearch for more papers by this author First published: March‐April 1985 https://doi.org/10.1111/j.1537-2995.1985.tb02326.xCitations: 3AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume25, Issue2March‐April 1985Pages 182-183 RelatedInformation

Drug Prescribing for Patients with Chronic Kidney Disease in General Practice: a Cross-Sectional Study

Two patients with acute immune haemolytic anaemia caused by diclofenac are described. Both patients had developed IgG drug-independent autoantibodies and drug-dependent antibodies. The drug-dependent antibodies in one patient reacted with red blood cells (RBC) only in the presence of urine from patients receiving diclofenac (ex vivo antigen) but not in the presence of the drug itself or its known metabolites. This antibody appeared to recognize a trace metabolite which has not yet been identified. The drug-dependent antibodies in the second patient reacted with RBC in the presence of urine as ex vivo antigen as well as in the presence of the drug itself and its main metabolites. Incorrect diagnosis of such cases often is due to the occurrence of autoantibodies and/or unusual drug metabolism and excretion.

In two patients, a 50-year-old woman (case 1) and a 2-year-old girl (case 2) acute shortness of breath requiring artificial ventilation developed 3-5 hours after infusion of two erythrocyte concentrates in case 1 and unfiltered platelet-enriched plasma (20 ml/kg) in case 2. The chest radiograph showed diffuse infiltrations in the lungs of both patients. After administration of catecholamines and respirator therapy, extubation was possible in the first patient after two days, in the second after five days. In neither case had there been any evidence of hypervolaemia, heart failure or infection to explain the lung findings. However, the serum of case 1 and the serum of the platelet donor had antibodies against granulocytes. The granulocyte-compatibility test (between patient serum and donor granulocytes) was positive. This confirmed the clinical suspicion of transfusion-related acute lung injury (TRALI). However, demonstration of antibodies was not only important for the diagnosis, but made it possible to recognize a blood donor whose serum contained antibodies against granulocytes which can provoke TRALI.

Drug Prescribing for Patients with Chronic Kidney Disease in General Practice: a Cross-Sectional Study

Fetal alloimmune thrombocytopenia is caused by maternal immunization against a fetal platelet antigen and transplacental transfer of the antibody into the fetal circulation. Since 10-20% of the fetuses or newborns are threatened by intracranial hemorrhages, early management is required. Fetal blood sampling should be started between the 20th and 22nd week of gestation to assess fetal phenotype and platelet count. Different concepts to elevate the fetal platelet count have been discussed: maternal intravenous immunoglobulins, fetal intravenous immunoglobulins, or only repeated fetal platelet transfusions. Our investigations suggested that platelet transfusions in short intervals appear to be the only effective regimen to increase platelet counts in thrombocytopenic fetuses at risk.

Fetal alloimmune thrombocytopenia is caused by maternal immunization against a fetal platelet alloantigen and transplacental transfer of the antibody into the fetal circulation. Since 10-20% of the fetuses or newborns are threatened by intracranial hemorrhages (ICH) early management is required. Intensive prenatal monitoring should be performed if a maternal HPA-1a antibody is known and a previous infant suffered from thrombocytopenia and/or ICH. Fetal blood sampling (FBS) should be started at 20th to 22nd weeks of gestation to assess fetal phenotype and platelet count. Different concepts to elevate the fetal platelet count have been discussed: corticosteroids, maternal intravenous immunoglobulins (ivIgG), fetal ivIgG and repeated fetal platelet transfusions. In a European survey with data from five centres maternal corticoid treatment and ivIgG infusion were accompanied by increasing fetal platelet counts in only 20 and 24% of the cases, respectively. In fetuses with very low platelet counts only transfusions of compatible platelets in short intervals are able to sustain a safe platelet count. Fetuses with mild thrombocytopenia should be monitored by subsequent FBS since it could be shown that platelet counts tend to decline during gestation. To avoid bleeding complications during and after FBS which was observed in about 5% of the cases every cord vessel puncture should be covered by a platelet transfusion. As no safe and non-invasive therapy exists for fetal alloimmune thrombocytopenia the value of prenatal screening programs in unaffected pregnancies is questionable.

Fetal alloimmune thrombocytopenia is caused by materno-fetal 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), platelet transfusions or fetal IgG transfusions is still controversial. In this study we have evaluated the effect of intrauterine IgG and intraumbilical platelet transfusions on fetal platelet counts. 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 20th week of gestation. Fetal treatment of IgG was given, on av erage, over 9 weeks. In all cases, fetal IgG levels rose significantly whereas platelet counts did not increase following fetal IgG treatment. We conclude that fetal IgG infusions have no detectable effect on fetal allo-immune thrombocytopenia. Since platelet counts can be very low as early as 20 weeks of gestation, careful fetal monitoring by umbilical blood sampling is essential. Platelet transfusions in short intervals appear to be the only effective regimen to increase platelet counts in thrombocytopenic fetuses at risk.

We have evaluated the effect of maternal intravenous immunoglobulin G (ivIgG) treatment on platelet counts in fetal alloimmune thrombocytopenia. Seven patients were studied. All of them were multiparous women who had been immunized against the HPA-la antigen during previous pregnancies and had given birth to al least one severely thrombocytopenic infant. In this study, umbilical blood collection was performed first at the 20th week of gestation and repeated 2-13 times (mean 6 times), depending on the degree of fetal thrombocytopenia. Fetal platelet counting was combined with intrauterine transfusion of 20-30 ml of HPA-la-negative platelet concentrates to prevent bleeding following umbilical cord puncture. Initial fetal platelet counts ranged from 10 000 to 91 000 per mu l. Maternal treatment with ivIgG (1 g per kg body weight; mean dose 70 g) was given once a week over 7 weeks. In five of seven cases, the basal platelet count did not rise and in two of these cases, it decreased during maternal ivIgG treatment. In one fetus, the baseline platelet count increased from 10 000 to 35 000 pet mu l during ivIpG. and in another fetus from 23 000 to 64 000 per mu l. Our observations suggest that ivIgG has no definite benefit for fetal alloimmune thrombocytopenia. Since platelet counts can be very low, careful fetal monitoring by umbilical blood sampling is required. Frequent platelet transfusions in short intervals may be necessary to increase platelet counts in extremely thrombocytopenic fetuses.

During developing a blood recipient information system, we have applied a special OOA method to discover objects and elicit user requirements. We find that not only those objects that are indispensable from the point of information-technical view but also those that are more familiar to the user and more interesting from the user's viewpoint should be discovered and dealt with because most of the important user requirements cluster round the latter kind of objects. In our practice, such objects are series of serological examinations and series of crossmatching tests, and the most important functions in the system have been also implemented on the basis of these objects so that the real-world situation and dynamics the system is intended to model can be tracked faithfully.

The neutrophil-specific antigen NC1 is defined by an antibody in the serum of a mother who gave birth to a child with alloimmune neonatal neutropenia. NC1 has been reported to be associated with the neutrophil-specific antigen NA2, but the precise relation of NC1 and NA2 remained unclear. Therefore, we investigated the serum using the antigen capture assay MAIGA and the granulocyte (GIFT) and lymphocyte (LIFT) immunofluorescence tests. In GIFT, no NA association was observed. In LIFT, serum antibodies bound preferably to lymphocytes with the HLA antigens HLA-B7 and cross-reacting antigens. In MAIGA, an antibody specific for the NA2 variant of the granulocyte Fc gamma-receptor III was observed. The NA2 specificity was confirmed by testing granulocytes from 40 further different donors. This indicates that the NC1 and NA2 antigens are identical. A positive GIFT result but a negative one in LIFT using cells of an NA2-negative typed individual suggest the presence of an additional, non-NA2-specific granulocyte antibody.

Neonatal alloimmune thrombocytopenia (NAIT) is usually induced by platelet‐specific antibodies against HPA‐la (Zw a ) or HPA‐5b (Br a ). Recently, low‐frequency alloantigens on the platelet glycoprotein (GP) IIb/IIIa complex have been discovered as a cause for NAIT. In this report, a new low‐frequency platelet‐specific alloantigen, ly, is described which induced severe NAIT. The corresponding antigen was detected in 1/249 unrelated German blood donors. Antibody binding assays with trypsin‐digested platelets (ELISA, immunoprecipitation with biotin‐labelled platelets) indicate that the antigen is not localized on the glycocalicin moiety of GP Ibα, but may be situated on the remnant moiety of GP Ibα, GP IX or GPIbβ. Apparently, ly is not related to the HPA‐2 (Ko) antigen system.

To avoid the well-known shortcomings of phenotyping granulocytes for the NA antigens using NA-specific human sera, a DNA-based method to determine the NA genotype was developed. Genomic DNA was isolated from blood cells or serum, amplified by polymerase chain reaction (PCR), immobilized on nylon membrane and genotyped using digoxigenin-labeled, sequence-specific oligonucleotides (SSO). The genotyping results of whole blood samples from 54 and of serum from 20 individuals correlated perfectly with our phenotyping using the antigen capture assay MAIGA. In three cases with the phenotype ''NA-null'' no hybridization of the NA-specific oligonucleotides occurred. These data show that SSO is a reliable method for NA genotyping especially if only small volumes of blood or even only serum probes are available.

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.