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Lupus
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Valine/Leucine247 polymorphism of ß2-glycoprotein I in patients with antiphospholipid syndrome: lack of association with anti-ß2-glycoprotein I antibodies

J Swadzba

Department of Medicine, Jagiellonian University School of Medicine, Krakow, Poland

M Sanak

Department of Medicine, Jagiellonian University School of Medicine, Krakow, Poland

T Iwaniec

Department of Medicine, Jagiellonian University School of Medicine, Krakow, Poland

S Dziedzina

Department of Medicine, Jagiellonian University School of Medicine, Krakow, Poland

J Musial

Department of Medicine, Jagiellonian University School of Medicine, Krakow, Poland, mmmusia{at}cyf-kr.edu.pl

In antiphospholipid syndrome (APS) the presence of anti-ß2-glycoprotein I (ß2GPI) antibodies is strongly associated with thromboembolic complications. It has been suggested that the common ß2GPI Valine/Leucine247 (Val/Leu247)polymorphism could be found more commonly in APS and might influence the generation of anti-ß2GPI antibodies. Therefore we studied ß2GPI Val/Leu247single-nucleotide polymorphism (SNP) by PCR in 338 patients with various autoimmune diseases (46 with secondary and 84 with primary APS) and 147 sex and age-matched healthy controls. In all patients lupus anticoagulant, anticardiolipin and anti-ß2GPI antibodies (both IgG and IgM) were also determined. All patients and controls were Caucasians. Frequencies of the SNP genotypes in patients did not depart from genetic equilibrum and did not differ from those found in controls. There was also no association between the presence of ß2GPI Val/Leu247genotypes and the presence or absence of lupus anticoagulant, anticardiolipin antibodies, anti-ß2GPI antibodies or clinical APS symptoms in all patients studied. In conclusion, among the exclusively Caucasian, Polish population of autoimmune patients ß2GPI Val/Leu247SNP has the same distribution as in healthy subjects and does not influence the production of anti-ß2GPI antibodies.

Key Words: antiphospholipid antibodies • APS • autoimmune diseases • ß2-glycoprotein I • genetics

Lupus, Vol. 15, No. 4, 218-222 (2006)
DOI: 10.1191/0961203306lu2288oa
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