[Production of blood components with SAG and SAG-M blood bag system].
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Biomedical subjects
Publications and source records attributed to C Jersild.
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Successful treatment of a case of post-transfusion purpura with high-dose i.v. human immunoglobulin is reported. A 62-year-old multiparous woman developed severe thrombocytopenia in the wake of transfusions given during and after vascular surgery. A platelet alloantibody with anti-Zwa-specificity was demonstrable by an indirect immunofluorescence technique. A single infusion of Sandoglobulin 1 g/kg body weight caused an immediate platelet response with cessation of haemorrhagic manifestations within 12 h, and the platelet count became normal within 3 d. Thrombocytopenia recurred 8 d after the infusion, but one further dose of Sandoglobulin 0.5 g/kg body weight caused definitive reversal of the thrombocytopenia.
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Mitogen-stimulated lymphocytes from 8 healthy donors were exposed to interferon, and cytogenetic studies were preformed. The response of lymphocytes to the mitogens phytohemagglutinin (PHA), concanavalin A (con A) and pokeweed mitogen (PWM) was inhibited by interferon, whereas an increased number of structural chromosomal aberrations was not detected. Further investigations of the cytogenetic effects of interferon are needed.
This review describes the presently available data on HLA typing in patients with multiple sclerosis (MS). Almost 2,000 MS patients and 12,000 normal controls have been studied with HLA typing in 15 different laboratories. The combined data show remarkably homogeneous results, and are as summarized: an increased frequency of HLA-Dw2 of B7, B8, Bw18, A3, and A1. A decreased frequency of A2, A28, B12, Bw15, Bw17, Bw22, and Bw40. Analysis of data seems to indicate that the HLA linked MS susceptibility gene is linked to HLA-Dw2, and the other deviating HLA antigen frequencies, except B8, may be explained as a secondary phenomenon, due to linkage disequilibrium. The presented data do not allow any conclusions as to whether the MS susceptibility gene operates in a dominant or recessive way. The important of HLA as a marker for disease and MS in particular is discussed, and preliminary data on HLA studies of MS patients of other ethnic groups, notably American blacks, seem to indicate that genetically determined ethnic differences, notably those of HLA, may partly be responsible for the unique geographic distribution of the disease.
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A patient with severe combined immunodeficiency received seven transplants of bone marrow from an HLA-B-compatible and HLA-D-compatible unrelated donor in an attempt to provide immunologic reconstitution. The first four transplants achieved restricted engraftment with evidence of rudimentary immunologic function. A fifth transplant, given after low-dose cyclophosphamide, produced reconstituion of cell-mediated immunity. Marrow aplasia developed after recontamination with a nonpathogenic microflora. Transplantation of marrow previously stored in liquid nitrogen was ineffective. A subsequent transplant, administered after high-dose cyclophosphamide, achieved durable engraftment, with complete hematopoietic and immunologic reconstitution. Seventeen months after transplantation, full functional engraftment persists. Graft-versus-host disease has been chronic and moderately severe, but limited to the skin and oral mucosa. Transplantation of marrow from unrelated histocompatible donors may provide a useful treatment for patients with severe combined immunodeficiency or aplastic anemia who lack a matched sibling or related donor.
Twenty-five patients with a definite diagnosis of amyotrophic lateral sclerosis (ALS) were HLA-typed for the serologically detectable antigens A, B and C and MLC-typed for 7 HLA-D-determinants. No significant deviation was found neither in the A, B, and C-series nor in the HLA-D-series as compared to normal controls. The aetiological problem of ALS is discussed.
HLA typing for 27 A and B locus antigens was performed in 137 Caucasian patients with Hodgkin's disease. A and B locus antigen frequencies were compared for the entire group of patients, for 51 patients studied in a prospective manner and for 62 patients surviving with Hodgkin's disease for more than 5 years. MLC typing (HLA-D) was performed in 51 unselected Caucasian patients using 6 differend HLA-D homozygous test cells which define 3 HLA-D specificity groups (DW2, DW3, and DW4). HLA-AW33 was found in 0.0% of patients and in 5.9% of random Caucasian blood donors at the Sloan--Kettering Institute (X2 equals 7.04, p less than 0.01). HLA-A1 was found to be increased to 35.8% in the entire patient group (N = 137) as compared to 25.4% in 855 random North American Caucasians (X2 = 5.97, p less than 0.02). There was no significant deviation of any A or B locus antigen in relation to sex, histology, age of patient, or duration of survival (newly diagnosed vs 5-year survivors). No significant deviation for either of the 3 common HLA-D determinants (DW2, DW3, or DW4) was observed.
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In five patients with definite multiple sclerosis and lack of cell-mediated immunity to measles and parainfluenza virus antigens, various immunological parameters were studied before and during transfer factor treatment. The study showed that cell-mediated immunity to measles virus antigen, as evaluated by the leukocyte migration agarose test, could temporarily be restored, using repeated injections of transfer factor pooled from unselected, normal blood donors.
Close linkage between HL-A and C2 deficiency was first reported by FU and co-workers in 1974. We present here a pedigree of a 31-year-old C2-deficient individual with clinical manifestations of Hodgkins disease. The following markers were tested: C2 levels, factor B polymorphism, blood groups, and enzyme typing. In addition to close linkage between HL-A and C2 deficiency, both parents were heterozygous for Bf (HL-A linked, electrophoretic variation of B). The two HL-A haplotypes closely linked to C2 deficiency are different: 2, W18 and W24, W18. They share, however, the SD2 antigen W18 and the LD type 7a.