FC-GAMMA RECEPTOR IIA POLYMORPHISM IN CAUCASIAN PATIENTS WITH SYSTEMIC LUPUS-ERYTHEMATOSUS - ASSOCIATION WITH CLINICAL SYMPTOMS

Objective. The class II human leukocyte Fc gamma receptor for IgG (Fc gamma RIIa) occurs in 2 codominantly expressed allelic forms (R131 and H131), Cells expressing IIa-H131 interact much more effectively with complexed IgG2 and IgG3 than do cells,vith IIa-R131, This might be lin ked to variability in immune complex handling, and therefore related t o disease pathogenesis. The present study examines these possibilities in a cohort of Caucasian patients with systemic lupus erythematosus ( SLE). Methods, One hundred eight Caucasian patients were diagnosed wit h SLE according to the American College of Rheumatology criteria. The SLE patients and 187 Caucasian controls were genotyped for the Fc gamm a RIIa polymorphism, and associations between Fc gamma RIIa genotypes, selected HLA haplotypes, and clinical as well as laboratory features were analyzed. Results. No significant skewing of the Fc gamma RIIa po lymorphism was observed in the SLE cohort. Various clinical and serolo gic parameters were found more frequently or at a younger age in patie nts homozygous for the genotype IIa-R/R131 compared with those,vith th e genotype IIa-H/H131, In patients with the genotype IIa-R/R131, signi ficantly higher frequencies of proteinuria, hemolytic anemia, anti-nuc lear RNP antibodies, and hypocomplementemia were found. The only clini cal symptom observed more frequently in patients homozygous for IIa-H/ H131 was livedo. Patients with the IIa-R/R131 genotype were significan tly younger at disease onset and had an earlier incidence of arthritis , sicca syndrome, nephritis, lymphadenitis, hematologic abnormalities, immunologic abnormalities, lupus anticoagulant, cryoglobulinemia, and hypocomplementemia. HLA-DR3 was found in 41.7% of SLE patients, but w as not associated with clinical symptoms, serologic abnormalities, or the homozygous genotypes of the Fc gamma RIIa, although an association with a significantly later onset of SLE was found. Conclusion. The Fc gamma RIIa polymorphism constitutes an additional factor that might i nfluence the clinical manifestations and course of SLE, but does not r epresent a genetic risk factor for the occurrence of SLE.