[A D-positive patient carrying anti-D].
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Biomedical subjects
Publications and source records attributed to B Habibi.
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A group AB mother (Mrs P.D.) gave birth to a group O female baby (C.D.). Extensive study of the blood group genetic markers in both the parents and the child, carried out on several occasions, showed nothing unusual outside the ABO system. Mrs P.D. then, gave birth to a second female baby who was also group O. Mrs P.D. had normal amounts of A, B, H and Lewis antigens in her saliva. The H, A and B agglutinability of her red cells was in the range of normal A2B group. This A2B blood group was characterized by very low A gene-specified glycosyltransferase activity in serum. Moreover this activity was undetectable in red blood cell membranes. These results are discussed in the light of various hypotheses in order to explain this unusual transmission of ABO blood group.
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Serum from a D--/D-- allo-immunized woman is found to contain 3 separable antibodies: anti-e, anti-Ee (Rh 17) and a third component which, in contrast to 5 other sera from people with Rh deleted phenotypes, reacts strongly with red blood cells from Mrs Nou., a DIV(C)--/DIV(C)--black woman. The latter component studied by elution and coagglutination using Nou. cells reacts with a hitherto unrecognized public antigen within the Rh system. 2750 random donors, 2Rh mod. individuals and 17 people with public minus phenotypes in other blood group systems were found to express the antigen. 2 Dc--/Dc--, 4 D--/D-- and 4 Rh nul samples were non reactive. The identity of the antibody with anti-Hr (Rh 18) was ruled out since the original anti-Hr failed to react with Nou. red blood cells.
Technical, immunological and clinical parameters of blood filtration through Erypur filters were evaluated. Red cell concentrates from which the buffy coat had not been eliminated were used throughout the study. Filtration procedure is fully automated, simple and takes about 15 minutes. 98% of leukocytes and 96% of platelets were found to be retained by the filter. Residual leukocytes were less than 3.10(7) in 68% and residual platelets less than 1.10(10) in 93% of filtered units. The incidence of lymphocyte alloantibody formation was 14.9% in the group of 67 patients who received 210 filtered units and 27.9% in the control group of 93 patients who were transfused with 298 non-filtered units. 330 filtered units were transfused to 107 carefully monitored patients and caused no reaction. 40 of these patients had polyspecific HLA antibodies and/or a documented history of non-hemolytic transfusion reactions. The clinical usefulness of Erypur filtered blood in the prevention of such reactions may thus be confirmed.
Pr antigens (Pr ags), glycoconjugates of the red blood cell surface, have been traced in stratified squamous epithelia (SSE) with homogeneous and serologically monospecific monoclonal antibodies. Pr ags were expressed either at the plasma membrane level or within the cytoplasm of the keratinocytes (associated with the cytoskeleton). Pr ags were expressed in the basal cells. The distribution within this germinative compartment was in accordance with the concept of a cellular heterogenicity in the basal cell layer. A neuraminidase resistant Pr ag was retained in the maturing compartment of epithelia undergoing parakeratotic differentiation (including psoriatic epidermis). Monoclonal cold agglutinins may serve as new markers for the study of glycoconjugates in keratinocytes during normal and pathological differentiation.
An anti-Nomifensine antibody was identified in a patient with immune hemolysis and renal failure who was under Nomifensine therapy. The anti-drug specificity of the antibody was confirmed by inhibition assays using Sepharose gel-Nomifensine conjugates. Preliminary screening tests for anti-Nomifensine antibody in a population of 104 patients treated by the drug showed no further example of such immunization.
Immunological safety of red blood cell transfusions implies both prevention of hemolytic reactions and prevention of red cell alloimmunization. A review of clinical, etiologic and immunohematological aspects of hemolytic hazards of blood transfusion is presented and the main conclusions regarding their prevention are emphasized. Appropriate measures to prevent red cell alloimmunization are outlined in the light of known variables which contribute to alloantibody formation. Prophylactic measures are suggested to be focused on the one hand on the most immunogenic red cell antigens, c, E, K. and on the other hand on the high risk individuals, young women and multitransfused patients.
Anti-red auto-antibodies were found in 69 out of 892 000 blood donors aged between 20 and 60 years, 63 of whom were followed for up to five years. This would suggest an overall incidence of 1 in 13 000 members of a "normal" population. Uncontrolled methyl-dopa treatment could be incriminated in 25% of cases. Only 10% of autoimmune subjects had slight confirmed anaemia, but 72% had biological evidence of red cell destruction (i.e. hyper-reticulocytosis, elevated serum bilirubin levels and shortened red cell life span), which demonstrates the presence of subclinical autoimmune haemolytic disease in apparently normal people. The anti-red cell auto-antibodies were of the IgG type in 97% of the subjects and were associated with various anti-tissue antibodies in 41%, thus pointing to a multisystem autoimmune disorder. In most cases the abnormality persisted or spontaneously regressed during the observation period, but long-term follow-up is required to determine whether asymptomatic red cell autoimmunization is harmless or potentially dangerous.
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Seven sera from 4 D -- --, 2 Dc -- and 1 DIV(C) -- immunized women were studied through extensive absorption-elution and coagglutination tests against a panel of common and depressed or deleted Rh phenotypes. A separable anti-e was regularly present in all sera together with an anti-Ee antibody which often showed stronger reactivity with e antigen. A possibly new anti-public Rh antibody was further separated in the serum from a D -- -- individual. The corresponding antigen is expressed on common, DIV(C) -- and depressed Rh phenotypes used, and is absent from Dc --, D -- -- and Rh null cells.
HD50 assays for the antigens Fyb and Fy3 were performed in a large number of Fyx homozygous or heterozygous individuals. A full correlation was found in quantitative expression of Fyb and Fy3 favouring the hypothesis of a Fybw Fy3w gene complex in the Duffy blood group system.
288 sera with red cell auto-antibodies and 141 control sera were investigated for cold lymphocytotoxins (CLCT). An incidence of 72% and 40% respectively was found in patients with cold haemagglutinin disease and in those with warm IgG type AHA. The absence of increased frequency in idiopathic or methyl-dopa induced asymptomatic red cell auto-immunization would suggest that CLCT might reflect an advanced degree of auto-immune disorder. No difference was observed in reaction patterns of isolated B and T lymphocytes or of those from individuals with I negative red cell phenotype.
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The study of the agglutinability of Xg(a + ) cells by several examples of anti-Xga and absorption-elution tests showed that the red blood cell antigen Xga is destroyed by proteases commonly used in blood group serology but not by neuraminidase.