Literature DB >> 6733279

Increased IgG molecules bound to the surface of red blood cells of patients with sickle cell anemia.

L D Petz, P Yam, L Wilkinson, G Garratty, B Lubin, W Mentzer.   

Abstract

We have used the complement-fixing antibody consumption ( CFAC ) test to detect small concentrations of IgG on red blood cells from patients with hemolytic anemias that are not thought to be caused by an immune mechanism. Although patients with hereditary spherocytosis, pyruvate kinase deficiency, and mechanical hemolytic anemias generally had normal concentrations of IgG bound to their red cells (less than 25 molecules IgG per red cell), we found that 39/62 (63%) patients with sickle cell anemia had elevated values. These 39 patients had a mean of 195 and a maximum of 890 molecules of IgG per red cell. None of the patients had been transfused within the previous 90 days, and some had never been transfused. Direct antiglobulin tests were positive in only two instances and autoantibodies were not found in the serum of any patient. However, eluates from the red cells of 6 of 23 patients demonstrated antibody activity against all of a panel of normal red cells by the indirect antiglobulin test. There was no correlation between the number of IgG molecules on patients' red cells and the severity of their anemia, the incidence of painful sickle cell crises, the reticulocyte count, or with blood transfusion history. We conclude that further study of immunohematologic abnormalities in patients with sickle cell anemia is warranted, especially in view of previous reports in this population of patients with red cell autoantibodies, autoimmune hemolytic anemia, hemolytic transfusion reactions without detectable alloantibodies, and an association of some episodes of pain crises with immunologically mediated red cell destruction.

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Year:  1984        PMID: 6733279

Source DB:  PubMed          Journal:  Blood        ISSN: 0006-4971            Impact factor:   22.113


  7 in total

1.  Co-clustering of denatured hemoglobin with band 3: its role in binding of autoantibodies against band 3 to abnormal and aged erythrocytes.

Authors:  K Schlüter; D Drenckhahn
Journal:  Proc Natl Acad Sci U S A       Date:  1986-08       Impact factor: 11.205

2.  Heinz bodies induce clustering of band 3, glycophorin, and ankyrin in sickle cell erythrocytes.

Authors:  S M Waugh; B M Willardson; R Kannan; R J Labotka; P S Low
Journal:  J Clin Invest       Date:  1986-11       Impact factor: 14.808

3.  Excessive binding of natural anti-alpha-galactosyl immunoglobin G to sickle erythrocytes may contribute to extravascular cell destruction.

Authors:  U Galili; M R Clark; S B Shohet
Journal:  J Clin Invest       Date:  1986-01       Impact factor: 14.808

4.  Potentiated adherence of sickle erythrocytes to endothelium infected by virus.

Authors:  R P Hebbel; M R Visser; J L Goodman; H S Jacob; G M Vercellotti
Journal:  J Clin Invest       Date:  1987-11       Impact factor: 14.808

5.  Molecular mapping of human band 3 aging antigenic sites and active amino acids using synthetic peptides.

Authors:  M M Kay
Journal:  J Protein Chem       Date:  1992-12

6.  Increased adherence of sickled and phosphatidylserine-enriched human erythrocytes to cultured human peripheral blood monocytes.

Authors:  R S Schwartz; Y Tanaka; I J Fidler; D T Chiu; B Lubin; A J Schroit
Journal:  J Clin Invest       Date:  1985-06       Impact factor: 14.808

7.  Oxidation as a possible mechanism of cellular aging: vitamin E deficiency causes premature aging and IgG binding to erythrocytes.

Authors:  M M Kay; G J Bosman; S S Shapiro; A Bendich; P S Bassel
Journal:  Proc Natl Acad Sci U S A       Date:  1986-04       Impact factor: 11.205

  7 in total

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