Arthritis & Rheumatism, Volume 60,
October 2009 Abstract Supplement
The 2009 ACR/ARHP Annual Scientific Meeting
Philadelphia October 16-21, 2009.
Association Between CD36 Single Nucleotide Polymorphism and Antiphospholipid Syndrome
Kato, Masaru, Horita, Tetsuya, Atsumi, Tatsuya, Amengual, Olga, Nakagawa, Hisako, Fujieda, Yuichiro, Otomo, Kotaro
CD36, known as a scavenger receptor, is a transmembrane glycoprotein expressed on monocytes, macrophages, platelets and capillary endothelial cells. CD36 recognizes multiple ligands, including phosphatidyl serine, and is a mediator of both atherogenesis and thrombosis. Some reports indicated that CD36-null mice were resistant for thrombus formation. Human CD36 deficiency was first described in 1989 as refractory to HLA-matched platelet transfusions, and is found in 4 to 10 % of Asian or African population. There has been, however, no report of the correlation between CD36 gene polymorphism and thrombotic diseases. The purpose of this study is to investigate the association between CD36 gene polymorphisms and antiphospholipid syndrome (APS).
This study comprised a total of 795 Japanese: 39 patients with primary APS, 69 with systemic lupus erythematosus (SLE) complicated with APS, 265 with SLE in the absence of APS, and 422 healthy subjects. All the APS patients fulfilled the Sydney-revised Sapporo criteria of APS, and all the SLE patients fulfilled the American College of Rheumatology classification criteria of SLE. Two following CD36 gene polymorphisms were investigated in this population using the TaqMan PCR genotyping method, the T for C allele substitution at nt478 for Pro90Ser (rs3765187), a common variation linked to CD36 deficiency, and the A for C substitution on the 5' untranslated region (rs1049654). Statistical analysis was performed by Fisher's exact test.
The allele frequency of rs3765187 in each group is presented in the Table1; The T allele at nt478 was less frequent in APS patients than in healthy subjects. There was no significant difference in the allele frequency of rs1049654 among those groups.
Table 1. The allele frequencies of CD36 SNP, nt478C/T for Pro90Ser rs3765187, in healthy subjects and patients with APS and SLE
|nt478 T frequency||p value||OR (95% CI)|
|Healthy subjects (n = 422)||10.2% (43/422)|||||
|All APS (n = 108)||2.8% (3/108)||0.024||0.25 (0.08 to 0.83)|
|All SLE (n = 334)||6.9% (23/334)||0.11||0.65 (0.38 to 1.11)|
|Primary APS (n = 39)||2.6% (1/39)||0.15||0.23 (0.03 to 1.73)|
|SLE+APS (n = 69)||2.9% (2/69)||0.085||0.26 (0.06 to 1.11)|
|SLE/non-APS (n = 265)||7.9% (21/265)||0.32||0.76 (0.44 to 1.31)|
|The p value and OR (95% CI) for each group were obtained by the comparison with healthy subjects.|
|APS, antiphospholipid syndrome; SLE, systemic lupus erythematosus; OR, odds ratio; SNP, single nucleotide polymorphism|
The single nucleotide polymorphism linked to CD 36 deficiency was less frequent in APS patients, suggesting that impaired scavenger receptor function correlates with APS-resistant. This is a first report to show the link between CD36 gene and APS.
To cite this abstract, please use the following information:
Kato, Masaru, Horita, Tetsuya, Atsumi, Tatsuya, Amengual, Olga, Nakagawa, Hisako, Fujieda, Yuichiro, et al; Association Between CD36 Single Nucleotide Polymorphism and Antiphospholipid Syndrome [abstract]. Arthritis Rheum 2009;60 Suppl 10 :1271