Role of immunoglobulin G3 subclass in dilated cardiomyopathy: results from protein A immunoadsorption.
BACKGROUND
Immunoadsorption (IA) by anti-immunoglobulin G (anti-IgG) columns that effectively eliminates total IgG, including IgG3 subclass, represents an additional therapeutic approach in dilated cardiomyopathy (DCM). A recent study revealed that IA with protein A columns does not effectively remove IgG3 and does not induce hemodynamic improvement in DCM.


METHODS
Eighteen patients with DCM (left ventricular ejection fraction < or =30%) were included in this case-control study. In all patients, IA with protein A was performed in 4 courses, at 1-month intervals until month 3. Nine patients underwent protein A IA with an improved treatment regimen for IgG3 elimination. Data of these patients were compared retrospectively to existing findings for 9 comparable patients treated by protein A IA with ineffective IgG3 reduction.


RESULTS
In both groups, IA induced a comparable reduction of the total IgG level. However, reduction of the IgG3 level was different in the 2 groups (P < .001). Hemodynamics did not significantly change throughout the 3 months in the group with ineffective IgG3 reduction. In contrast, the group with improved IgG3 reduction demonstrated during the first IA course an increase in cardiac index from 2.2 +/- 0.1 to 2.8 +/- 0.2 L min(-1) m(-2) (P < .05). After 3 months before the last IA course, cardiac index was 2.2 +/- 0.1 L min(-1) m(-2) in the group with ineffective IgG3 elimination and 2.8 +/- 0.2 L min(-1) m(-2) in the group with improved IgG3 reduction (P < .01). In the group with ineffective IgG3 reduction, left ventricular ejection fraction increased after 3 months from 21.6 +/- 2% to 24.4 +/- 2% (NS), and from 24.3 +/- 2 to 34.7 +/- 4% in the group with improved IgG3 reduction (P < .05).


CONCLUSIONS
Autoantibodies belonging to IgG3 may play an important role in cardiac dysfunction of patients with DCM. Protein A IA in conjunction with an improved treatment regimen for IgG3 elimination induces hemodynamic benefit in patients suffering from DCM.
Staudt
Alexander
A
Klinik für Innere Medizin B, Ernst-Moritz-Arndt-Universität, Greifswald, Germany. staudt@uni-greifswald.de
Dörr
Markus
M
Staudt
Yvonne
Y
Böhm
Marko
M
Probst
Michael
M
Empen
Klaus
K
Plötz
Sebastian
S
Maschke
Hans E
HE
Hummel
Astrid
A
Baumann
Gert
G
Felix
Stephan B
SB
D000327:Adsorption; D001323:Autoantibodies / Q000097:blood / Q000276:immunology*; D002311:Cardiomyopathy, Dilated / Q000097:blood / Q000276:immunology*; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood / Q000276:immunology*; D007167:Immunotherapy; D008297:Male; D008875:Middle Aged; D010956:Plasmapheresis; D012189:Retrospective Studies
D001323:Autoantibodies; D007074:Immunoglobulin G