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Abstract Number: 1123

Impact of Genes Modulating Serum Low-Density Lipoprotein Cholesterol Levels on Progression of Joint Destruction in Japanese Patients with Rheumatoid Arthritis

Shinji Yoshida1, Katsunori Ikari1, Koichiro Yano1, Yoshiaki Toyama2, Atsuo Taniguchi3, Hisashi Yamanaka1 and Shigeki Momohara3, 1Institute of Rheumatology, Tokyo Women's Medical University, Tokyo, Japan, 2Department of Orthopaedic Surgery, Keio University School of Medicine, Tokyo, Japan, 3Institute of Rheumatology, Tokyo Women’s Medical University, Tokyo, Japan

Meeting: 2014 ACR/ARHP Annual Meeting

Keywords: joint destruction, Lipids, polymorphism and rheumatoid arthritis (RA)

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Session Information

Session Title: Genetics, Genomics and Proteomics II

Session Type: Abstract Submissions (ACR)

Background/Purpose

Patients with rheumatoid arthritis (RA) have a higher prevalence of dyslipidemia than healthy individuals. Since RA is a chronic inflammatory disease, an inflammatory response may be partly involved in the pathogenesis of dyslipidemia. Recently, low-density lipoprotein (LDL) cholesterolemia has been reported to be a risk factor for radiographic progression of joint destruction. Several genetic risk loci for progression of joint destruction have been identified so far. However, the genetic predisposition factors have not yet been elucidated. The purpose of this study was to evaluate impact of genetic variants modulating serum LDL cholesterol (LDL-C) levels on progression of joint destruction in Japanese patients with RA. 

Methods

This study included 1,005 Japanese patients with RA for whom Sharp/van der Heijde scores (SHS) of hands were available at a disease duration of 5 years. DNA samples of the subjects were obtained from the Institute of Rheumatology Rheumatoid Arthritis cohort study (IORRA) DNA collection. All of the patients who donated DNA samples consented to participate in this study as approved by the Tokyo Women’s Medical University Genome Ethics Committee, and satisfied the American College of Rheumatology 1987 revised criteria for the classification of RA. Thirteen single nucleotide polymorphisms (SNPs) in the 8 loci influencing serum LDL-C concentrations in the Japanese population were selected and genotyped in the DNA samples: rs611917, in SORT1; rs693, rs7575840, and rs515135, in APOB; rs3846662, in HMGCR; rs662799, in BUD13-APOA1-APOA5; rs838867, in SCARB1; rs1532624, and rs2303790, in CETP; rs688, and rs1433099, in LDLR; rs429358, and rs7412, in APOE-C1. Multivariate linear regression analyses were performed to examine the association of each SNP with radiographic progression of joint destruction in the first 5 years after onset of RA, calculated as SHS of hands at the 5-year disease duration. Adjustments were made for gender, age of onset, anti-citrullinated peptide status, and year of disease onset. All SHS were log-transformed to obtain a normal distribution. 

Results

Multivariate linear regression analyses revealed that the minor allele of rs662799 in BUD13-APOA1-APOA5 was associated with progression of joint destruction in the recessive model (P=0.04). However, the association could not reach the level of the significance after Bonferroni correction for multiple comparisons. The other SNPs showed no association (Table 1). 

Conclusion

We could not confirm the association between genes modulating serum LDL-C levels and progression of joint destruction in Japanese patients with RA. Our results indicated that rs662799 in BUD13-APOA1-APOA5 might be a risk factor for progression of joint destruction, but further studies would be required to confirm the association. 

Table 1 Multivariate linear regression analyses of each SNP associated with progression of joint destruction

Gene

SNP

Allele (minor/major)

MAF

Risk allele

Tested model

β

P value

 

 

 

 

 

 

 

 

SORT1

rs611917

G/A

0.07

A

additive

dominant

recessive

-0.01

0.02

-0.01

0.79

0.65

0.69

 

 

 

 

 

 

 

 

APOB

rs693

A/G

0.04

A

additive

dominant

recessive

0.02

0.02

-0.04

0.60

0.52

0.36

 

rs7575840

T/G

0.08

T

additive

dominant

recessive

0.03

0.03

0.01

0.37

0.39

0.65

 

rs515135

T/C

0.10

T

additive

dominant

recessive

0.02

0.02

0.01

0.57

0.59

0.77

 

 

 

 

 

 

 

 

HMGCR

rs3846662

A/G

0.48

G

additive

dominant

recessive

0.00

0.02

-0.01

0.93

0.59

0.71

 

 

 

 

 

 

 

 

BUD13-APOA1-APOA5

rs662799

G/A

0.34

G

additive

dominant

recessive

0.05

0.07

-0.00

0.14

0.04

0.95

 

 

 

 

 

 

 

 

SCARB1

rs838867

G/A

0.46

A

additive

dominant

recessive

0.03

-0.01

0.05

0.32

0.88

0.10

 

 

 

 

 

 

 

 

CETP

rs1532624

T/G

0.30

G

additive

dominant

recessive

-0.01

0.00

-0.01

0.86

0.96

0.80

 

rs2303790

G/A

0.03

A

additive

dominant

recessive

-0.04

0.02

-0.05

0.23

0.43

0.16

 

 

 

 

 

 

 

 

LDLR

 

rs688

T/C

0.12

T

additive

dominant

recessive

-0.06

-0.06

-0.04

0.05

0.08

0.16

 

rs1433099

T/C

0.29

C

additive

dominant

recessive

-0.03

-0.05

-0.01

0.40

0.11

0.85

 

 

 

 

 

 

 

 

APOE-C1

 

rs429358

C/T

0.10

C

additive

dominant

recessive

-0.03

-0.03

-0.02

0.30

0.36

0.43

 

rs7412

T/C

0.04

T

additive

dominant

recessive

0.03

-0.03

0.04

0.33

0.14

0.17


Disclosure:

S. Yoshida,
None;

K. Ikari,
None;

K. Yano,
None;

Y. Toyama,
None;

A. Taniguchi,
None;

H. Yamanaka,

Abbott, AbbVie, Asahikasei , Astellas, AstraZeneca, Bristol-Myers Squib, Chugai, Daiichi Sankyo, Eisai, GlaxoSmithKline, Janssen, Mitsubishi Tanabe, MSD, Nippon Kayaku, Pfizer, Santen, Taishotoyama, Takeda, Teijin,,

2,

Abbott, AbbVie, Astellas, AstraZeneca, Bristol-Myers Squib, Chugai, Daiichi Sankyo, Eisai, Mitsubishi Tanabe, Nippon Kayaku, Pfizer, Takeda, Teijin,

5,

Abbott, AbbVie, Astellas, Bristol-Myers Squib, Chugai, Eisai, Mitsubishi Tanabe, Pfizer, Takeda, Teijin,

8;

S. Momohara,

Abbvie Japan, Chugai Parmaceutical, Eisai, Mitsubishi Tanabe Parma, Takeda Parmaceutical,

8.

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