Double role of mannose-binding lectin in relation to carotid intima-media thickness in patients with rheumatoid arthritis

TY - JOUR

T1 - Double role of mannose-binding lectin in relation to carotid intima-media thickness in patients with rheumatoid arthritis

AU - Troelsen, Lone N

AU - Garred, Peter

AU - Christiansen, Buris

AU - Torp-Pedersen, Christian

AU - Christensen, Ib J

AU - Narvestad, Eva

AU - Jacobsen, Søren

AU - Troelsen, Lone N

AU - Garred, Peter

AU - Christiansen, Buris

AU - Torp-Pedersen, Christian

AU - Christensen, Ib J

AU - Narvestad, Eva

AU - Jacobsen, Søren

N1 - Keywords: Adult; Aged; Arthritis, Rheumatoid; Cardiovascular Diseases; Carotid Artery, Common; Denmark; Female; Genotype; Humans; Linear Models; Male; Mannose-Binding Lectin; Middle Aged; Risk Factors; Statistics, Nonparametric; Tunica Intima; Tunica Media

PY - 2010/1/1

Y1 - 2010/1/1

N2 - Background: Patients with rheumatoid arthritis (RA) have increased risk of atherosclerosis and cardiovascular disease (CVD) that cannot be explained by excess of traditional risk factors. Several studies indicate that mannose-binding lectin (MBL) may modify the development of atherosclerosis; both high and low serum levels of MBL are reported to be associated with CVD. Intima-media thickness of the common carotid artery (ccIMT) is a validated non-invasive anatomic measure of subclinical CVD. We examined the relation between ccIMT and MBL in 114 RA patients. Methods: In a cross-sectional study MBL2 genotypes and serum concentrations of MBL were assessed; ccIMT was determined by means of ultrasonography; traditional and RA related cardiovascular risk modifiers were measured. Results: The median ccIMT was 0.67 mm. The investigated MBL2 genotypes were not significantly associated with ccIMT. Using a general linear model, ccIMT was not linearly associated with serum MBL but was highly associated with the quadratic term of serum MBL (MBL2) (P = 0.001) reflecting a U-shaped relation. MBL2 was also significantly associated with ccIMT in a multivariable analysis adjusting for traditional and RA related cardiovascular risk modifiers (P = 0.025). Conclusion: In RA patients, a quadratic U-shaped relation between serum MBL and ccIMT was observed independently of the effects of traditional and RA related risk factors for CVD. These results provide further support to the notion that both high and low levels of MBL may be associated with CVD.

AB - Background: Patients with rheumatoid arthritis (RA) have increased risk of atherosclerosis and cardiovascular disease (CVD) that cannot be explained by excess of traditional risk factors. Several studies indicate that mannose-binding lectin (MBL) may modify the development of atherosclerosis; both high and low serum levels of MBL are reported to be associated with CVD. Intima-media thickness of the common carotid artery (ccIMT) is a validated non-invasive anatomic measure of subclinical CVD. We examined the relation between ccIMT and MBL in 114 RA patients. Methods: In a cross-sectional study MBL2 genotypes and serum concentrations of MBL were assessed; ccIMT was determined by means of ultrasonography; traditional and RA related cardiovascular risk modifiers were measured. Results: The median ccIMT was 0.67 mm. The investigated MBL2 genotypes were not significantly associated with ccIMT. Using a general linear model, ccIMT was not linearly associated with serum MBL but was highly associated with the quadratic term of serum MBL (MBL2) (P = 0.001) reflecting a U-shaped relation. MBL2 was also significantly associated with ccIMT in a multivariable analysis adjusting for traditional and RA related cardiovascular risk modifiers (P = 0.025). Conclusion: In RA patients, a quadratic U-shaped relation between serum MBL and ccIMT was observed independently of the effects of traditional and RA related risk factors for CVD. These results provide further support to the notion that both high and low levels of MBL may be associated with CVD.

U2 - 10.1016/j.molimm.2009.10.021

DO - 10.1016/j.molimm.2009.10.021

M3 - Journal article

C2 - 19939454

SN - 0161-5890

VL - 47

SP - 713

EP - 718

JO - Molecular Immunology

JF - Molecular Immunology

IS - 4

ER -