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Association of Fcγ Receptor Polymorphisms with Adult Onset Still's Disease in Korea

JIN-HYUN WOO, YOON-KYOUNG SUNG, JIN-SOOK LEE, WON TAE CHUNG, JUNG-YOON CHOE, GWAN GYU SONG, and DAE-HYUN YOO

ABSTRACT.

Objective. Fcγ receptors (FcγR) have important functions in the regulation of immune response and clearance of immune complex. High levels of immunoglobulins have been observed in patients with the active stage of adult onset Still's disease (AOSD), and high-dose intravenous immunoglobulin treatment has decreased the disease activity of AOSD. We investigated polymorphisms of FcγR as genetic factors influencing susceptibility or disease course of AOSD in Korea.

Methods. We genotyped the FcγRIIA H/R131, IIIA F/V176, and IIIB NA1/NA2 loci in 98 patients with AOSD and 151 healthy controls. Genotyping was performed using sequence-specific PCR. Patients with AOSD were subdivided into groups according to disease course: monocyclic systemic, polycyclic systemic, or chronic articular type. Allelic, genotypic, and haplotypic associations were analyzed by chi-square test.

Results. No significant skewing in any of the 3 FcγR polymorphisms was found between Korean AOSD patients and controls. FcγRIIA R/R131 and R/H131 genotype in patients with chronic articular-type disease was more frequent than in controls (p = 0.006 and p_corr = 0.018). No differences of genotypic and allelic frequencies were found between other disease course types and controls. Haplotype IIA R131-IIIA F176-IIIB NA2 was more frequent in AOSD patients than in controls (p = 0.021).

Conclusion. Although FcγR polymorphisms are not associated with development of AOSD in Koreans, the haplotype IIA R131-IIIA F176-IIIB NA2 may be associated with AOSD. Also, the FcγRIIA polymorphism may be associated with chronic articular-type AOSD. We need to identify whether these polymorphisms are associated with a response to anti-tumor necrosis factor agents in patients with AOSD. (J Rheumatol First Release Dec 1 2008; doi:10.3899/jrheum.071254)

Key Indexing Terms:

ADULT ONSET STILL'S DISEASE
Fcγ RECEPTOR
SINGLE-NUCLEOTIDE POLYMORPHISMS

From the Division of Rheumatology, Department of Internal Medicine, Korea University College of Medicine; Department of Rheumatology, the Hospital for Rheumatic Diseases, Hanyang University College of Medicine; The Institute of Rheumatology, Hanyang University; Division of Rheumatology, Department of Internal Medicine, Dong-A University College of Medicine; Division of Rheumatology, Department of Internal Medicine, Catholic University of Daegu College of Medicine, Seoul, Korea.

J-H. Woo, MD, PhD, Instructor, Division of Rheumatology, Department of Internal Medicine, Korea University College of Medicine; Y-K. Sung, MD, PhD, Assistant Professor, Department of Rheumatology, Hospital for Rheumatic Diseases, Hanyang University College of Medicine; J-S. Lee, BS, The Institute of Rheumatology, Hanyang University; W.T. Chung, MD, PhD, Professor, Division of Rheumatology, Department of Internal Medicine, Dong-A University College of Medicine; J-Y. Choe, MD, PhD, Professor, Division of Rheumatology, Department of Internal Medicine, Catholic University of Daegu College of Medicine; G.G. Song, MD, PhD, Professor, Division of Rheumatology, Department of Internal Medicine, Korea University College of Medicine; D-H. Yoo, MD, PhD, Professor, Department of Rheumatology, Hospital for Rheumatic Diseases, Hanyang University College of Medicine.

Address reprint requests to Dr. D-H. Yoo, Division of Rheumatology, The Hospital for Rheumatic Diseases, Hanyang University College of Medicine, Seoul 133-792, Korea. E-mail: dhyoo@hanyang.ac.kr

Accepted for publication September 22, 2008.