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Biomedical subjects

W H Hitzig

Publications and source records attributed to W H Hitzig.

At least 73 records · Page 4Linked to original sources
PubMed1980

Necrotising enterocolitis and neuraminidase-producing bacteria.

In 9 out of 26 newborns with necrotising enterocolitis (NEC) exposure of the Thomsen-cryptantigen (T-antigen), probably due to the action of circulating bacterial neuraminidase, was demonstrated on red blood cells. The serological titres seemed to correlate with the clinical course of the disease. Neuraminidase-producing clostridia were isolated in two of the patients. Reaction between the exposed T-antigen and anti-T-agglutinins, normally present in human blood, may lead to difficulties during blood transfusion. This potential transfusion hazard is best avoided by routine T-antigen-tests and by transfusion of packed or washed red blood cells to T-antigen-positive patients.

Antibody Specificity↗
PubMed1980

Hemolytic-uremic syndrome associated with neuraminidase-producing microorganisms: treatment by exchange transfusion.

In two infants with pneumonia, Coombs test positive hemolytic anemia and hemolytic uremic syndrome (HUS), exposure of the Thomsen cryptantigen, probably due to the action of circulating neuraminidase, was demonstrated. Reaction between the exposed T-antigen and anti-T agglutinin, normally present in human blood, can lead to difficulties in serological testing and during blood transfusion. The place of exchange transfusions using washed RBC or heparinized whole blood in the management of this subgroup of HUS is discussed.

Antigens↗
PubMed1979

[Granulocyte dysfunction in transcobalamin II deficiency].

Granulocytes from a boy with congenital transcobalamin II (TC II) deficiency were found to have abnormally low antibacterial activity against Staphylococcus aureus. Transfusion of normal plasma supplemented with hydroxocobalamin temporarily restored granulocyte bactericidal activity to normal. Granulocyte function was also temporarily restored by oral leucovorin. The defect appears to be causally related to the patient's TC II deficiency and indirectly to an intracellular deficiency of cobalamin and folate coenzymes [1].

Blood Bactericidal Activity↗
PubMed1979

[The prognostic value of immunologic markers in juvenile acute lymphatic leukemias and non-Hodgkin lymphomas].

Prognostic factors such as T-cell markers, peripheral WBC and age at diagnosis in ALL, or B-cell markers and site of primary tumor in NHL, are used today for important therapeutic decisions. Immunologic markers are said to be the most important. A survey of 7 ALL patients diagnosed in the period 1977 to 1978 shows that 4 are in continuous remission, including 3 for more than 3 years to date (2 despite a high initial WBC). These 3 had received only standard ALL treatment. Of 7 NHL cases diagnosed in 1977/1978, 4 had abdominal primaries (3 of the B-cell type). Of 2 children with mediastinal tumors, one (with a T-cell tumor) has been disease-free for 16 months, as also the patient with a cervical reticulum cell sarcoma. These 3 patients are under intensive high dose chemotherapy. These few cases show that prognostic factors are only of relative importance and need not involve a pessimistic attitude towards treatment.

Child↗
PubMed1979

[Transcobalamine-II-polymorphism: biochemical and clinical aspects of rare variants].

Transcobalamin II(TC II) is an essential transport protein for vitamin B12 in blood. TC II can be split up into isoproteins by polyacrylamide gel electrophoresis. Family studies are compatible with a genetic polymorphism of TC II and a five allele system. Screening of TC II isoprotein patterns in about 1000 individuals yielded two unusual TC II variants: The first case was a black female with severe megaloblastic anemia since infancy. Her TC II was elevated and bound B12, but displayed markedly diminished functional capacity to transfer radioactive cyanocobalamin in cellular systems. Comparison of this patient's TC II isoprotein pattern with known variants showed a distinct difference in electrophoretic mobility, indicating the presence of a sixth allele. The second patient, also presenting with pernicious anemia-like symptoms, was found to possess an unusual TC II variant with reduced TC II serum levels. Corresponding variants were also observed in the patient's asymptomatic children. Thus, abnormal TC II variants probably causing megaloblastic anemias both correlated with unusual isoprotein patterns.

Anemia, Megaloblastic↗
PubMed1979

Bone marrow transplantation for severe combined immunodeficiency disease. Reported from 1968 to 1977.

Patients who received bone marrow transplantation (= BMT) for the treatment of severe combined immunodeficiency (= SCID), and who were reported in the medical literature from 1968 to 1977, were collected and analysed. Eighteen of these 80 children are still alive, 10 months to 9 years after transplantation. It is thus the first successful form of therapy for this otherwise invariably fatal disease. Fifteen of the 18 survivors received bone marrow cells from HLA and MLC compatible donors; the remaining 3 survivors received grafts from MLC-compatible but HLA-incompatible donors. Bone marrow transplantation is the treatment of choice for SCID when recipient and donor are HLA- and MLC-identical. All patients who received MLC-incompatible grafts died, and bone marrow transplantation for SCID from MLC-incompatible donors should be abandoned. Milt-to-severe graft-versus-host disease (= GVHD) occurred in spite of HLA- and/or MLC-compatibility, with some correlation to the number of cells transplanted. This should preferably be kept below 50 million cells per kilo body weight. Infection was the chief cause of death in all groups. Strict reverse isolation, bowel decontamination and routine pre- and post-transplant Pneumocystis carinii prophylactic treatment are recommended. The clinical picture and laboratory findings of these 80 children before BMT did not differ from non-transplanted SCID patients. Three of the 18 survivors are adenosinedeaminase deficient.

Bone Marrow Transplantation↗
PubMed1979

[Adenosine deaminase activity in blood cells; influence of cytostatic therapy in patients with acute leukemia and with renal transplants (author's transl)].

A causal relation between the enzyme, adenosine deaminase (ADA), and immune dysfunction is well known: patients with congenital inactivity of ADA invariably suffer of severe combined immunodeficiency. In contrast, we found in patients treated with immunosuppressive drugs increased ADA enzyme activity. Previous findings on ADA activity in acute leukemias are until now controversial. We found normal to increased ADA activity in children with acute lymphatic leukemia (ALL) and acute myeloid leukemia (AML) in remission as long as they were treated with cytostatic drugs. In the group of cured leukemics (in continuous remission after suspension of the therapeutic regimen) the ADA activities were normal. These findings do not exclude a heterogeneity within the leukemia group. They do not explain the signs of cellular immunodeficiencies well known in patients with acute leukemias.

Adenosine Deaminase↗
PubMed1979

[Indication for and evaluation of plasmaprotein determinations (author's transl)].

All components of the "fluid tissue" blood should be considered as functional units. This seems familiar to physicians for the blood cells. For the dissolved plasmaproteins most doctors are, however, not yet used to think in functional terms. We propose a functional classification of well-characterized plasmaproteins, and a list of correlations between clinical conditions and protein changes. The clinician and the director of the laboratory have special knowledge and accordingly different tasks. An outline of the possible distribution of their duties and for their collaboration is given. We propose the stepwise evaluation of laboratory tests requested which in its details is obviously quite subjective and debatable. Accordingly, tests are categorized for routine, for special questions, and for scientific investigation. Finally, the clinician ought to know possible sources of error and mistake. For detailed advice, he may ask the director of the laboratory. If these principles--details may be modified--are respected, doctors should be able to obtain the laboratory data they need for diagnosis and treatment with minimal inconvenience to the patient and lowest cost to the community.

Blood Protein Electrophoresis↗
PubMed1979

[Immunodeficiency syndromes--a new WHO report (author's transl)].

This short note is meant to point out the importance of a new WHO publication on immunodeficiency syndromes (IDS), which was prepared by an expert committee. For the classification of primary IDS, three different principles are useful, each for particular purposes. For the first time, the importance and frequency of secondary IDS are discussed as well. The original report should be read by clinical immunologists, pediatricians, internists and others interested in IDS.

B-Lymphocytes↗
PubMed1979

[Treatment with immunoglobulins (author's transl)].

Passive immunisation by injecting gamma-globulin prepared from a large donor pool or specific antibodies from selected single donors is of great importance in daily practice for prophylaxis. An example is given for each of the 3 most important indications: a) gamma-Globulin for viral disease (e.g. measles prophylaxis); b) Antitoxic immunoglobulins (e.g. tetanus prophylaxis); c) Rhesus-anti-D-gamma-globulin for prophylaxis of rhesus sensitization. In contrast, substitution with great amounts of gammg-globulin is of little importance for the practizing paediatrician, since such cases are rare. This is the domain of the specialist who should be consulted for planning the therapeutic procedure. Data are given on immunoglobulin preparations commercially available and their application. Side effects are listed. They are particularly severe and dangerous in patients with profound hypo-gamma-globulinemia.

Erythroblastosis, Fetal↗
PubMed1978

[Increase of unsaturated transcobalamine II in autoimmune diseases; effect of immunosuppressive therapy (proceedings)].

Transcobalamin II (TC II) is a serum protein responsible for transporting vitamin B12 to the cells. A previous observation of a child with congenital TC II deficiency and agammaglobulinemia suggested that this protein plays an important role in the immune response. Accordingly, TC II levels ere determined in 32 patients with autoimmune disease (AID) (i.e. 26 with lupus erythematosus, 4 with dermatomyositis, and 2 with autoimmune hemolytic anemia) and in 40 patients with acquired immunodeficiency due to chemotherapy. It was found that elevated TC II levels corresponded to active phases of AID. Changes in TC II levels correlated better with the clinical course of AID than complement, antinuclear antibody or native DNA binding capacity. This suggests that TC II could be a valuable parameter in following up activity of AID.

Autoimmune Diseases↗
PubMed1978

Electronic platelet counting with capillary blood samples--experiences in a paediatric clinic.

For several reasons, electronic platelet counts have not been generally adopted in paediatric routine laboratories. A method of platelet counting in capillary blood samples using an electronic counter is described. This is based on brief centrifugation of the blood sample after the addition of a diluent containing heparin/dextran and with a density of 1.050. The thrombocytes are uniformly suspended in the supernatant after 5 min of centrifugation at 250 g, so that the counting procedure in the electric unit can follow immediately. This simplified, dependable and reproducible method is also suitable for venous blood, and as a result of several years of successful trial, it can be recommended for routine use, especially in clinics with paediatric patients.

Blood↗
PubMed1978

Increased unsaturated transcobalamin II in active autoimmune disease.

Measurements of transcobalamin II (T.C. II) concentrations in 26 patients with lupus erythematosus, 4 with dermatomyositis, 2 with autoimmune haemolytic anaemia, and in 40 immunosuppressed renal-transplant patients showed that T.C. II levels were raised during active phases of autoimmune disease. Changes in T.C. II levels correlated better with the clinical course of autoimmune disease than did changes in C3, the titre of antinuclear antibody, or native D.N.A.-binding capacity.

Anemia, Hemolytic, Autoimmune↗