title: Potential role of autoantibodies belonging to the immunoglobulin G-3 subclass in cardiac dysfunction among patients with dilated cardiomyopathy.
abstract: BACKGROUND
  Immunoadsorption capable of removing circulating autoantibodies represents an additional therapeutic approach in dilated cardiomyopathy (DCM). The role played by autoantibodies belonging to the immunoglobulin (Ig) subclass G-3 in cardiac dysfunction remains to be elucidated.
  
  
  RESULTS
  Patients with DCM (left ventricular ejection fraction <30%) participated in this case-control study. Nine patients underwent immunoadsorption with protein A (low affinity to IgG-3), and 9 patients were treated with anti-IgG, which removes all IgG subclasses. Immunoadsorption was performed in 4 courses at 1-month intervals until month 3. In the 2 groups, immunoadsorption induced comparable reduction of total IgG (>80%). IgG-3 was effectively eliminated only by anti-IgG adsorption (eg, during the first immunoadsorption course; protein A, -37+/-4%; anti-IgG, -89+/-3%; P<0.001 versus protein A). The beta1-receptor autoantibody was effectively reduced only by anti-IgG (P<0.01 versus protein A). Hemodynamics did not change in the protein A group. In the anti-IgG group during the first immunoadsorption course, cardiac index increased from 2.3+/-0.1 to 3.0+/-0.1 L x min(-1) x m(-2) (P<0.01 versus protein A). After 3 months, before the last immunoadsorption course, cardiac index was 2.2+/-0.1 L x min(-1) x m(-2) in the protein A group and 3.0+/-0.2 L x min(-1) x m(-2) in the anti-IgG group (P<0.01 versus protein A). Left ventricular ejection fraction increased only in the anti-IgG group (P<0.05 versus protein A).
  
  
  CONCLUSIONS
  Autoantibodies belonging to IgG-3 may play an important role in cardiac dysfunction of DCM. The removal of antibodies of the IgG-3 subclass may represent an essential mechanism of immunoadsorption in DCM.
authors.affiliation: Klinik für Innere Medizin B, Ernst-Moritz-Arndt-Universität, Greifswald, Germany.
authors.forename: Alexander
authors.initials: A
authors.lastname: Staudt
authors.forename: Marko
authors.initials: M
authors.lastname: Böhm
authors.forename: Fabian
authors.initials: F
authors.lastname: Knebel
authors.forename: Yvonne
authors.initials: Y
authors.lastname: Grosse
authors.forename: Claudia
authors.initials: C
authors.lastname: Bischoff
authors.forename: Astrid
authors.initials: A
authors.lastname: Hummel
authors.forename: Johannes B
authors.initials: JB
authors.lastname: Dahm
authors.forename: Adrian
authors.initials: A
authors.lastname: Borges
authors.forename: Nicoline
authors.initials: N
authors.lastname: Jochmann
authors.forename: Klaus D
authors.initials: KD
authors.lastname: Wernecke
authors.forename: Gerd
authors.initials: G
authors.lastname: Wallukat
authors.forename: Gert
authors.initials: G
authors.lastname: Baumann
authors.forename: Stephan B
authors.initials: SB
authors.lastname: Felix
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D001323:Autoantibodies / Q000097:blood* / Q000302:isolation & purification / Q000494:pharmacology; D020013:Calcium Signaling / Q000187:drug effects; D002311:Cardiomyopathy, Dilated / Q000150:complications / Q000503:physiopathology* / Q000628:therapy; D016022:Case-Control Studies; D002478:Cells, Cultured; D004232:Diuretics / Q000627:therapeutic use; D004452:Echocardiography; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood* / Q000276:immunology*; D007075:Immunoglobulin M / Q000097:blood / Q000276:immunology; D007163:Immunosorbent Techniques; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000187:drug effects; D009566:Nitrates / Q000627:therapeutic use; D011485:Protein Binding / Q000276:immunology; D051381:Rats; D018342:Receptors, Adrenergic, beta-1 / Q000276:immunology; D013318:Stroke Volume / Q000187:drug effects; D016896:Treatment Outcome; D018487:Ventricular Dysfunction, Left / Q000150:complications / Q000503:physiopathology* / Q000628:therapy
chemical_list: D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D001323:Autoantibodies; D004232:Diuretics; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D009566:Nitrates; D018342:Receptors, Adrenergic, beta-1