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Auto-antibodies do not influence development of atherosclerotic plaques in rheumatoid arthritis.
Joint Bone Spine 2008; 75(4):416-21JB

Abstract

BACKGROUND

Many questions remain unanswered about premature atherosclerosis in rheumatoid arthritis (RA). Besides inflammation, some studies have suggested the role of autoantibodies on its pathogenesis.

OBJECTIVE

The aim of this study was to investigate the presence of antibodies against phospholipids, beta2-glycoprotein1 (beta2-gp1), lipoprotein lipase, and heat shock proteins (Hsp) in RA patients and to evaluate their possible association with subclinical carotid atherosclerosis.

METHODS

Seventy-one RA patients and 53 age- and sex-matched controls were selected to perform anticardiolipin antibodies (aCL) (IgG and IgM), anti-beta2-gp1 (IgG, IgM, and IgA), anti-lipoprotein lipase (anti-LPL), anti-Hsp 60, and anti-Hsp 65 by ELISA tests. Intima-medial thickness (IMT) of common carotid and presence of plaques were assessed by high-resolution B-mode ultrasonography. Exclusion criteria were smoking, diabetes, and arterial hypertension. Lipoproteins, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and fibrinogen levels, as well as health assessment questionnaire (HAQ) and disease activity score (DAS) 28 were also evaluated.

RESULTS

Age (48.93+/-12.31 vs. 45.37+/-9.37 years; p=0.20) and body mass index (BMI) (p=0.69) were similar in RA and controls, as well as female gender (p=0.56). The mean IMT was similar between RA and controls (0.721+/-0.16 vs. 0.667+/-0.14 mm, p=0.07) but the frequency of plaques was higher in RA (14.1% vs. 1.9%; p=0.02). In RA patients, IMT measurements did not differ according to the presence or absence of these antibodies: IgG aCL (0.62+/-0.64 vs. 0.72+/-0.17 mm, p=0.24), IgM aCL (0.65+/-0.79 vs. 0.73+/-0.17 mm, p=0.33), anti-Hsp 60 (0.78+/-0.20 vs. 0.71+/-0.16 mm, p=0.27), anti-Hsp 65 (0.73+/-0.16 vs. 0.72+/-0.17 mm, p=0.77), IgG anti-beta2-gp1 (0.73+/-0.16 vs. 0.71+/-0.17 mm, p=0.72), and anti-CCP (0.71+/-0.16 vs. 0.76+/-0.20mm, p=0.36). In addition, IMT did not correlate with antibodies titers: IgG aCL (r=-0.09, p=0.47), IgM aCL (r=-0.15, p=0.21), anti-Hsp 60 (r=0.10, p=0.42), anti-Hsp 65 (r=0.05, p=0.69), IgG anti-beta2-gp1 (r=-0.07, p=0.57), IgM anti-beta2-gp1 (r=-0.05, p=0.69), IgA anti-beta2-gp1 (r=0.03, p=0.79), and anti-CCP (r=-0.07, p=0.57). RA patients with plaques had a significantly higher age compared to those without plaques (p=0.001), as well as higher mean IMT (p<0.001), total cholesterol (p=0.001), and LDL (p=0.003).

CONCLUSIONS

In RA a clear association between all autoantibodies studied herein and increased IMT or presence of plaques was not observed. The great prevalence of carotid atherosclerosis in RA was related to age, total and LDL cholesterol, as identified in normal population.

Authors+Show Affiliations

Rheumatology Division, University of Santa Catarina, Santa Catarina, Brazil. ivaniop@matrix.com.brNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

18457983

Citation

Pereira, Ivânio, et al. "Auto-antibodies Do Not Influence Development of Atherosclerotic Plaques in Rheumatoid Arthritis." Joint, Bone, Spine : Revue Du Rhumatisme, vol. 75, no. 4, 2008, pp. 416-21.
Pereira I, Laurindo I, Burlingame R, et al. Auto-antibodies do not influence development of atherosclerotic plaques in rheumatoid arthritis. Joint Bone Spine. 2008;75(4):416-21.
Pereira, I., Laurindo, I., Burlingame, R., Anjos, L., Viana, V., Leon, E., ... Borba, E. (2008). Auto-antibodies do not influence development of atherosclerotic plaques in rheumatoid arthritis. Joint, Bone, Spine : Revue Du Rhumatisme, 75(4), pp. 416-21. doi:10.1016/j.jbspin.2008.01.022.
Pereira I, et al. Auto-antibodies Do Not Influence Development of Atherosclerotic Plaques in Rheumatoid Arthritis. Joint Bone Spine. 2008;75(4):416-21. PubMed PMID: 18457983.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Auto-antibodies do not influence development of atherosclerotic plaques in rheumatoid arthritis. AU - Pereira,Ivânio, AU - Laurindo,Ieda, AU - Burlingame,Rufus, AU - Anjos,Lisiane, AU - Viana,Vilma, AU - Leon,Elaine, AU - Vendramini,Margareth, AU - Borba,Eduardo, Y1 - 2008/05/23/ PY - 2007/09/23/received PY - 2008/01/15/accepted PY - 2008/5/7/pubmed PY - 2008/11/7/medline PY - 2008/5/7/entrez SP - 416 EP - 21 JF - Joint, bone, spine : revue du rhumatisme JO - Joint Bone Spine VL - 75 IS - 4 N2 - BACKGROUND: Many questions remain unanswered about premature atherosclerosis in rheumatoid arthritis (RA). Besides inflammation, some studies have suggested the role of autoantibodies on its pathogenesis. OBJECTIVE: The aim of this study was to investigate the presence of antibodies against phospholipids, beta2-glycoprotein1 (beta2-gp1), lipoprotein lipase, and heat shock proteins (Hsp) in RA patients and to evaluate their possible association with subclinical carotid atherosclerosis. METHODS: Seventy-one RA patients and 53 age- and sex-matched controls were selected to perform anticardiolipin antibodies (aCL) (IgG and IgM), anti-beta2-gp1 (IgG, IgM, and IgA), anti-lipoprotein lipase (anti-LPL), anti-Hsp 60, and anti-Hsp 65 by ELISA tests. Intima-medial thickness (IMT) of common carotid and presence of plaques were assessed by high-resolution B-mode ultrasonography. Exclusion criteria were smoking, diabetes, and arterial hypertension. Lipoproteins, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and fibrinogen levels, as well as health assessment questionnaire (HAQ) and disease activity score (DAS) 28 were also evaluated. RESULTS: Age (48.93+/-12.31 vs. 45.37+/-9.37 years; p=0.20) and body mass index (BMI) (p=0.69) were similar in RA and controls, as well as female gender (p=0.56). The mean IMT was similar between RA and controls (0.721+/-0.16 vs. 0.667+/-0.14 mm, p=0.07) but the frequency of plaques was higher in RA (14.1% vs. 1.9%; p=0.02). In RA patients, IMT measurements did not differ according to the presence or absence of these antibodies: IgG aCL (0.62+/-0.64 vs. 0.72+/-0.17 mm, p=0.24), IgM aCL (0.65+/-0.79 vs. 0.73+/-0.17 mm, p=0.33), anti-Hsp 60 (0.78+/-0.20 vs. 0.71+/-0.16 mm, p=0.27), anti-Hsp 65 (0.73+/-0.16 vs. 0.72+/-0.17 mm, p=0.77), IgG anti-beta2-gp1 (0.73+/-0.16 vs. 0.71+/-0.17 mm, p=0.72), and anti-CCP (0.71+/-0.16 vs. 0.76+/-0.20mm, p=0.36). In addition, IMT did not correlate with antibodies titers: IgG aCL (r=-0.09, p=0.47), IgM aCL (r=-0.15, p=0.21), anti-Hsp 60 (r=0.10, p=0.42), anti-Hsp 65 (r=0.05, p=0.69), IgG anti-beta2-gp1 (r=-0.07, p=0.57), IgM anti-beta2-gp1 (r=-0.05, p=0.69), IgA anti-beta2-gp1 (r=0.03, p=0.79), and anti-CCP (r=-0.07, p=0.57). RA patients with plaques had a significantly higher age compared to those without plaques (p=0.001), as well as higher mean IMT (p<0.001), total cholesterol (p=0.001), and LDL (p=0.003). CONCLUSIONS: In RA a clear association between all autoantibodies studied herein and increased IMT or presence of plaques was not observed. The great prevalence of carotid atherosclerosis in RA was related to age, total and LDL cholesterol, as identified in normal population. SN - 1778-7254 UR - https://www.unboundmedicine.com/medline/citation/18457983/Auto_antibodies_do_not_influence_development_of_atherosclerotic_plaques_in_rheumatoid_arthritis_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1297-319X(08)00093-6 DB - PRIME DP - Unbound Medicine ER -