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Biomedical subjects

A Poschmann

Publications and source records attributed to A Poschmann.

53 records · Page 3Linked to original sources
PubMed1977

[Hemolytic disease of the newborn due to ABO incompatibility (author's transl)].

Up to now, the exact diagnosis of ABO hemolytic disease of the newborn cannot be made either clinically or serologically. Affected babies are almost all either group A or group B from mothers of group O. In contrast to Rh hemolytic disease the immunological findings do not correlate well with the severity of the clinical course. Sometimes, it is impossible to differentiate between ABO hemolytic disease and non-antibody mediated hyperbilirubinemia. Pathogenetic aspects are discussed which may explain the differences between ABO and Rh hemolytic disease of the newborn. Aids to immunological and clinical diagnosis are given. Ante-natal treatment is not necessary. Indications for and technique of phototherapy and exchange transfusion are presented. Early application of these therapeutical methods prevents bilirubin encephalopathy, kernicterus with subsequent death or development of severe neurological sequelae.

ABO Blood-Group System↗
PubMed1977

"VA", a new type of erythrocyte polyagglutination characterized by depressed H receptors and associated with hemolytic anemia. I. Serological and hematological observations.

This report describes a case of persistent polyagglutinability restriced to the red blood cells, and associated with hemolytic anemia in a 20-year-old male. AIME WITH NORMAL INTERVALS. His red blood cells were weakly agglutinated by almost all adult sera. No autoagglutination was noted and the direct antihuman globulin test was negative. Polyagglutinability of his red blood cells was clearly distinguishable from T, Tn and Tk. No reaction was noted with Dolichos biflorus and peanut extracts. The cells differed from normal erythrocytes in their positive reactions with various snail agglutinins and their weak reaction with a range of anti-H reagents. There was normal aggregation by Polybrene. MN determinants were normally expressed. The symbol "VA" is roposed for this type of polyagglutination.

Adult↗
PubMed1976

[Haemolytic disease of the new-born by blood-factor incompatibility other than Rh(d) and ABO (author's transl)].

Rare forms of incompatibility were observed over a period of 20 years in 41 (2%) of 2088 new-borns with haemolytic disease. Antibodies involved were anti-c (n = 27), anti-E (n = 6) and anti-K (n = 4), as well as one case each of anti-E + Fya, -C, -Fya and -Jka. Amniotic fluid was examined during pregnancy in nine cases, three children were given intra-uterine infusions, while in the remainder the haemolytic process was mild or only moderately severe. One infant died of toxoplasmosis, another one of immaturity and respiratory distress syndrome. Kernicterus was always prevented. In haemolytic disease of the newborn caused by anti-c and anti-E, prenatal damage is markedly rarer than with D erythroblastosis, but must be considered during the pregnancy. In anti-K haemolytic disease the severity of the disease is similar to that of D erythroblastosis. All three incompatibilities may lead to kernicterus in the first few days after birth so that exchange transfusions are often necessary. In most of the other incompatibilities the course is similar to that seen with ABO erythroblastosis.

Adult↗
PubMed1976

[Neuraminidase induced hemolytic anemia. Experimental and clinical observations (author's transl)].

Recently, increasing attention has been focussed on the in vivo action of neuraminidase as possible pathogenetical factor of hemolytic anemia and even hemolytic-uremic syndrome. Neuraminidase action in red cell membranes results in the release of neuraminic acid, and thereby the uncovering of previously hidden receptors, socalled cryptantigens. With special reference to the phythemagglutinin Anti-TAh from the peanut (Arachis hypogae) and the agglutinin Anti-AHP from the albumin gland of the small Helix pomatia we describe some new methods for the detection of these cryptantigens. In addition to the screebubg genagglutination test with Anti-TAh we developed an "Anti-T-consumption test" for quantitative detection of neuraminidase action on red cells. With the purified reagents we developed an indirect fluorescnet antibody method on blood smears for the detection of cryptantigens on single cells. By animal experiments we could show that not only the membranes of red cells but the intima of renal capillaries as well are damaged by neuraminidase. With these new methods we observed 14 patients suffering from hemolytic anemia due to bacterial or viral neuraminidase. Some of these patients developed a hemolytic-uremic syndrome. We believe that the positive reaction with Anti-T Ah should lead to prophylactic heparinization to prevent dissiminated intravascular coagulation. Neuraminidase is the first identified toxin which directly acts on the membranes of red cells and the intima of renal capillaries as well, and thereby in some patients may induce hemolytic-uremic syndrome. Possibly, these results may stimulate the development of further testsystems for the detection of still unknown toxins which are not tested with our reagents, but may equally be involved in the damage of cell membranes.

Anemia, Hemolytic↗
PubMed1976

[Haemolytic disease of the newborn (fetus) (author's transl)].

Haemolytic disease of the newborn is mostly caused by Rh antibody anti-D (Rh erythroblastosis) and antibodies of the ABO system anti-A and anti-B (ABO erythroblastosis). Because of possible fetal death in utero prenatal diagnosis and treatment of Rh erythroblastosis is necessary. Prophylactic administration of anti-Rh-gammaglobulin prevents the induction of Rh antibodies. In contrast to Rh erythroblastosis prenatal diagnosis and treatment of ABO erythroblastosis is not necessary. Postnatally, however, hyperbilirubinemia due to ABO erythroblastosis should be treated to avoid Kernicterus. Our results with diagnosis and treatment of haemolytic diseases of the newborn are presented and related to the literature. Furthermore, immunofluorescence studies are reported, which could possibly explain the differences between Rh and ABO erythroblastosis.

ABO Blood-Group System↗
PubMed1975

The scope of prenatal therapy in severe rhesus hemolytic disease.

Prenatal blood transfusion of a fetus established anemia due to rhesus hemolytic disease can be life saving. In Hamburg-Eppendorf 252 transfusions in 130 babies have so far been carried out. The success rate was 51%. Out of 39 babies who had ascites at the time of the first transfusion, 13 survived. The amount of ascites aspirated at the first transfusion correlates with the prognosis: The chance of producing a living and healthy child is greater when the amount of ascites is under 5 mls than when it is over 5 mls. Babies with amniotic fluid bilirubin values from 0.4 to 0.6 still have a good chance of survival, whereas the prospects of success with values over 0.6 are very small. The technical risk of prenatal transfusion before the 27th week amounts, according to our observations, to about 6%.

Amniotic Fluid↗
PubMed1975

[Pre- and postnatal treatment of severe Rh-erythroblastosis (author's transl)].

162 children with severe Rh-erythroblastosis were treated with 326 prenatal blood transfusions. 89 (55%) survived. The indication and technique for this treatment and the postnatal intensive care of the newborn are reported. Prenatal diagnosis is extended by the author's immunofluorescence technique assessing the fetal Rh factor D even as minute contamination amongst other cells, in order to privente unnecessary treatment of Rh negative children. Checking the effectiveness of prenatal blood-transfusion this technique can demonstrate differences in the counts of HbF- and D-cells. Success of treatment appears to be, in part, determined by dexamethasone just before delivery and by immediate postnatal substitution of erythrocyte concentrates and following exchange transfusion. With increasing experience the percentage of successful treatment rose. Of 40 children treated during the last 2 years with 95 prenatal transfusions, 67,5% survived. 41 fetuses had ascites already at the first prenatal transfusion. 9 of them (22%) survived. The data of the children treated, earliest in the 21st week of pregnancy, are given: Bilirubin level in amniotic fluid, number of prenatal transfusions, gestational week at delivery, hematocrit, HbF cells, number of postnatal exchange transfusions and later transfusions. Postnatal development of successfully treated children corresponds to that of other premature children without erythroblastosis.

Amniotic Fluid↗