Significance of complement activation in autoimmune haemolytic anaemia of "warm type". 1977

V Kretschmer, and C Mueller-Eckhardt

To study possible relationships between serum C3 and C4 levels and fixation of complement components (C) on red cells, 79 patients of autoimmune haemolytic anaemia of warm type (AIHA) and 7 patients of various diseases with positive direct antiglobulintest (DAT) but without haemolysis were investigated. 23 out of 79 patients with AIHA were analyzed repeatedly during the course of the disease. There were no significant differences of C levels between the various clinical types. However, the number of patients with reduced levels of C3 and C4 was significantly higher among cases with C fixation on the red cells than among those with fixation of immunoglobulins alone. Changes were more pronounced for C4 than C3 and mean values of serum C4 were significantly lower in the group with C fixation. If incomplete warm haemolysins were demonstrable, C4 levels were lower than in cases without warm haemolysins. During the clinical course, C3 and C4 concentrations showed a close correlation to the severity of haemolysis.

UI MeSH Term Description Entries
D003165 Complement System Proteins Serum glycoproteins participating in the host defense mechanism of COMPLEMENT ACTIVATION that creates the COMPLEMENT MEMBRANE ATTACK COMPLEX. Included are glycoproteins in the various pathways of complement activation (CLASSICAL COMPLEMENT PATHWAY; ALTERNATIVE COMPLEMENT PATHWAY; and LECTIN COMPLEMENT PATHWAY). Complement Proteins,Complement,Complement Protein,Hemolytic Complement,Complement, Hemolytic,Protein, Complement,Proteins, Complement,Proteins, Complement System
D003176 Complement C3 A glycoprotein that is central in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C3 can be cleaved into COMPLEMENT C3A and COMPLEMENT C3B, spontaneously at low level or by C3 CONVERTASE at high level. The smaller fragment C3a is an ANAPHYLATOXIN and mediator of local inflammatory process. The larger fragment C3b binds with C3 convertase to form C5 convertase. C3 Complement,C3 Precursor,Complement 3,Complement C3 Precursor,Complement Component 3,Precursor-Complement 3,Pro-C3,Pro-Complement 3,C3 Precursor, Complement,C3, Complement,Complement, C3,Component 3, Complement,Precursor Complement 3,Precursor, C3,Precursor, Complement C3,Pro C3,Pro Complement 3
D003181 Complement C4 A glycoprotein that is important in the activation of CLASSICAL COMPLEMENT PATHWAY. C4 is cleaved by the activated COMPLEMENT C1S into COMPLEMENT C4A and COMPLEMENT C4B. C4 Complement,C4 Complement Component,Complement 4,Complement C4, Precursor,Complement Component 4,Pro-C4,Pro-complement 4,C4, Complement,Complement Component, C4,Complement, C4,Component 4, Complement,Component, C4 Complement,Pro C4,Pro complement 4
D006460 Hemolysin Proteins Proteins from BACTERIA and FUNGI that are soluble enough to be secreted to target ERYTHROCYTES and insert into the membrane to form beta-barrel pores. Biosynthesis may be regulated by HEMOLYSIN FACTORS. Hemolysin,Hemolysins,Hemalysins,Proteins, Hemolysin
D006461 Hemolysis The destruction of ERYTHROCYTES by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity. Haemolysis,Extravascular Hemolysis,Intravascular Hemolysis,Extravascular Hemolyses,Haemolyses,Hemolyses, Extravascular,Hemolyses, Intravascular,Hemolysis, Extravascular,Hemolysis, Intravascular,Intravascular Hemolyses
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000744 Anemia, Hemolytic, Autoimmune Acquired hemolytic anemia due to the presence of AUTOANTIBODIES which agglutinate or lyse the patient's own RED BLOOD CELLS. Anemia, Hemolytic, Idiopathic Acquired,Autoimmune Haemolytic Anaemia,Autoimmune Hemolytic Anemia,Cold Agglutinin Disease,Hemolytic Anemia, Autoimmune,Acquired Autoimmune Hemolytic Anemia,Anemia, Hemolytic, Cold Antibody,Cold Antibody Disease,Cold Antibody Hemolytic Anemia,Idiopathic Autoimmune Hemolytic Anemia,Agglutinin Disease, Cold,Anaemia, Autoimmune Haemolytic,Anemia, Autoimmune Hemolytic,Autoimmune Haemolytic Anaemias,Autoimmune Hemolytic Anemias,Cold Agglutinin Diseases,Cold Antibody Diseases,Haemolytic Anaemia, Autoimmune

Related Publications

V Kretschmer, and C Mueller-Eckhardt
August 1969, Lancet (London, England),
V Kretschmer, and C Mueller-Eckhardt
June 1984, Blut,
V Kretschmer, and C Mueller-Eckhardt
January 1992, Lancet (London, England),
V Kretschmer, and C Mueller-Eckhardt
October 1986, British medical journal (Clinical research ed.),
V Kretschmer, and C Mueller-Eckhardt
September 1997, British journal of haematology,
V Kretschmer, and C Mueller-Eckhardt
January 1977, Vox sanguinis,
V Kretschmer, and C Mueller-Eckhardt
May 2010, BMJ case reports,
V Kretschmer, and C Mueller-Eckhardt
April 2023, British journal of haematology,
V Kretschmer, and C Mueller-Eckhardt
January 1968, Bibliotheca haematologica,
Copied contents to your clipboard!