ROMATOİD ARTRİT’TE FC GAMA RESEPTÖR IIIA V/158/F GEN POLİMORFİZMİNİN SIKLIĞININ ARAŞTIRILMASI VE HASTA KLİNİK VE LABORATUAR BULGULARIYLA KARŞILAŞTIRILMASI

Abstract

DOI: 10.26650/IUITFD.426162

Amaç: Romatoid Artrit (RA), nedeni bilinmeyen, esas olarak periferik eklemleri progresif olarak tutan kronik multisistemik bir hastalıktır. Hümoral ve hücresel immün yanıtları arasında bir bağ olan, IgG‘ nin Fc reseptörleri otoimün hastalıkların etyoloji ve patogenezinde oldukça ilgi çekmektedir. Geniş genetik varyasyon sergileyen bu bölge Romatoid artrit de dahil olmak üzere çeşitli kronik inflamatuvar hastalıklara yatkınlık ile ilişkilidir. Bu çalışmasında Romatoid Artrit‘ te FcγRIIIA V158F gen polimorfizminin sıklığının araştırılması ve hasta klinik ve laboratuar bulgularıyla karşılastırılması amaçlanmıştır.

Gereç ve Yöntem: Çukurova Üniversitesi Tıp Fakültesi Romatoloji Bilim Dalı polikliniğine Nisan 2010-Haziran 2011 tarihleri arasında başvuran ve Amerikan Romatizma Derneği‘ nin tanı kriterlerine göre RA tanısı almış 105 RA‘lı hasta ve 110 sağlıklı kontrol çalışmaya dahil edildi. Hasta ve kontrollerden öyküsünde diyabet, tiroid fonksiyon bozuklukları, geçirilmiş veya mevcut kalp hastalıkları, malignite, nörolojik hastalıklar ile kronik inflamatvuar hastalıklardan bir ya da daha fazlası olanlar çalışma dışı bırakıldı. RA‘ lı hastaların hastalıkla ilgili semptomları, sistemik hastalık varlığı, ilaç kullanımı, hastalık süreleri ve aile öyküsü sorgulandı. Tüm olgulara genel fizik muayene ve romatolojik muayeneleri yapıldı ve rutin laboratuvar tetkikleri ile CRP, RF, ESR, ANA, Anti-DNA düzeyleri istendi. Hasta grubu ARA‘nın fonksiyonel sınıflandırması kullanılarak evrelere ayrıldı. Alınan kan örneklerinde real time PCR yöntemi ile FcγRIIIA V158F gen polimorfizmleri araştırıldı.

Bulgular: Hasta ve kontrol grubunun Fc γ RIIIA gen polimorfizm dağılımları arasında anlamlı fark saptanmadı (p=0,106). Hastaların tanı aldıkları yaş dağılımları ile gen polimorfizmi arasında anlamlı fark saptanmadı (p=0,919). Hastaların cinsiyet dağılımlarına göre de gen polimorfizmi açısından anlamlı fark saptanmadı (p=0,552). Hastalığın klinik bulgularından olan akciğer ve göz tutulumları, romatoid nodül varlığı ile gen polimorfizmi arasında ilişki saptanmadı. RF ve ANA sonuçları ile gen polimorfizmi arasında da anlamlı fark saptanmadı (p=0,625, p=0,716). Hastaların anti-CCP sonuçları ile gen polimorfizmi arasında anlamlı fark saptanmadı (p=0,136).

Sonuç: Çalışmamızda RA patogenezi ile Fc γ RIIIA 158 gen polimorfizmi arasında anlamlı bir ilişki saptanmamıştır. 

Keywords

• FcγRIIIA gen polimorfizmi,romatoid artrit

INVESTIGATION OF THE FREQUENCY OF FC GAMMA RECEPTOR IIIA V/158/F GENE POLYMORPHISM AND COMPARISON OF CLINICAL AND LABORATORY FINDINGS IN RHEUMATOID ARTHRITIS (RA)

Abstract

DOI: 10.26650/IUITFD.426162

Objective: Rheumatoid Arthritis (RA) is a chronic multisystem disease with unknown etiology that progressively affects peripheral joints. Receptors, which serve as links between humoral and cellular immune responses, recognize the Fc region of immunoglobulin G (FcR) and have become the focus of many research studies concerning the etiology and pathogenesis of autoimmune diseases. This region displays extensive genetic variation, which has been associated with susceptibility to various chronic inflammatory disorders including RA. This study aimed to investigate the frequency of the FcγRIIIA V158F genetic polymorphism and compare clinical and laboratory findings in RA.

Materials and Methods: Between April 2010 and June 2011, 105 patients, who had been diagnosed with RA according to the American Rheumatology Association (ARA) diagnostic criteria, were admitted to the Cukurova University Department of Rheumatology outpatient clinic and 110 healthy controls were included in this study. Patient groups were divided into stages using the ARA functional classification. The FcγRIIIA V158F gene polymorphism of patients was investigated from blood samples using the real-time Polymerase Chain Reaction (PCR) method.

Results: There was no significant difference in the distribution of the FcγRIIIA polymorphism between patients and controls (p=.106). There were no significant differences between the distribution of age at diagnosis of patients with the gene polymorphism (p=.919) or in the gene polymorphism (p=.552). No association was found between the gene polymorphism and clinical signs of disease such as eye involvement and the presence of rheumatoid nodules. There was also no significant association between the gene polymorphism with rheumatoid factor, anticyclic citrullinated peptide, and antinuclear antibodies (p=.625, p=.136, p=.716, respectively).

Conclusion: In our study, no significant relationship was found between the FcγRIIIA V158F gene polymorphism and the pathogenesis of RA.

Keywords

• FcγRIIIA V158F gene polymorphism,rheumatoid arthritis

References

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