Polymorphism of Fcγ RIIa May Affect the Efficacy of γ-Globulin Therapy in Kawasaki Disease

We evaluated whether there is a possible relationship between the effectiveness of γ-globulin treatment for patients with Kawasaki disease (KD) and the polymorphism of Fcγ RIIa, IIIb, and IIIa. Genomic DNA was extracted from whole blood collected from 56 patients with KD who received γ-globulin treatment. The genotypes for Fcγ RIIIb-NA(1, 2), Fcγ RIIa-H/R131, and FcγRIIIa-F/V158 were determined to investigate the association between these polymorphisms and the development of coronary lesions (CALs). Twenty-three percent of patients with the HH allele for the Fcγ RIIa polymorphism progressed to CALs, compared with 60% with the HR and RR alleles. HR and RR alleles may be a predictor of the progression of CALs in KD before the initiation of γ-globulin therapy.

[1]  T. Fujisawa,et al.  Studies of Peripheral Blood Toxic Neutrophils as a Predictor of Coronary Risk in Kawasaki Disease—the Pathogenetic Role of Hematopoietic Colony‐Stimulating Factors (GM‐CSF, G‐CSF) , 1990, Acta paediatrica Japonica : Overseas edition.

[2]  I. Sekine,et al.  Intravenous immunoglobulin therapy induces neutrophil apoptosis in Kawasaki disease. , 2002, Clinical immunology.

[3]  M. Poncz,et al.  Rapid detection of the ligand-binding polymorphism using an allele-specific restriction enzyme digestion (ASRED) , 1996 .

[4]  R. Feldman,et al.  Human immunoglobulin G (IgG) Fc receptor IIA (CD32) polymorphism and IgG2-mediated bacterial phagocytosis by neutrophils , 1995, Infection and immunity.

[5]  K. Harada Intravenous γ‐Globulin Treatment in Kawasaki Disease , 1991 .

[6]  H. Nakano,et al.  Intravenous γ‐Globulin for Kawasaki Disease , 1991 .

[7]  A. Bisno,et al.  Diagnostic guidelines for Kawasaki disease. , 2001, Circulation.

[8]  G. Cooper,et al.  A Novel Polymorphic CAAT/Enhancer-Binding Protein β Element in the FasL Gene Promoter Alters Fas Ligand Expression: A Candidate Background Gene in African American Systemic Lupus Erythematosus Patients1 , 2003, The Journal of Immunology.

[9]  H. Nakano,et al.  HIGH-DOSE INTRAVENOUS GAMMAGLOBULIN FOR KAWASAKI DISEASE , 1983, The Lancet.

[10]  M Takahashi,et al.  A single intravenous infusion of gamma globulin as compared with four infusions in the treatment of acute Kawasaki syndrome. , 1991, The New England journal of medicine.

[11]  M. Ishii,et al.  Plasma exchange in Kawasaki disease , 1995, The Lancet.

[12]  Dirk Roos,et al.  The Fc gamma RIIIA-158F allele is a risk factor for systemic lupus erythematosus , 1998 .

[13]  M. Mori,et al.  Predictors of coronary artery lesions after intravenous γ-globulin treatment in Kawasaki disease , 2000 .

[14]  M. de Haas IgG-Fc receptors and the clinical relevance of their polymorphisms. , 2001, Wiener klinische Wochenschrift.

[15]  M. Dehaas IgG-Fc receptors and the clinical relevance of their polymorphisms , 2001 .

[16]  Wen-Chuan Lee,et al.  A Swine Model of Horse Serum-Induced Coronary Vasculitis: An Implication for Kawasaki Disease , 2004, Pediatric Research.

[17]  Kei Takahashi,et al.  Kawasaki Disease With Particular Emphasis on Arterial Lesions , 1991, Acta pathologica japonica.

[18]  D. Roos,et al.  FcγRIIIa-158V/F Polymorphism Influences the Binding of IgG by Natural Killer Cell FcγRIIIa, Independently of the FcγRIIIa-48L/R/H Phenotype , 1997 .

[19]  J. Newburger,et al.  A predictive instrument for coronary artery aneurysms in Kawasaki disease. US Multicenter Kawasaki Disease Study Group. , 1998, The American journal of cardiology.

[20]  T. Huizinga,et al.  Biallelic neutrophil Na-antigen system is associated with a polymorphism on the phospho-inositol-linked Fc gamma receptor III (CD16). , 1990, Blood.