skip to main content

Anti–lipoprotein lipase antibodies: A new player in the complex atherosclerotic process in systemic lupus erythematosus?

de Carvalho, Jozélio Freire ; Borba, Eduardo Ferreira ; Viana, Vilma Santos Trindade ; Bueno, Cleonice ; Leon, Elaine Pires ; Bonfá, Eloísa

Arthritis and rheumatism, 2004-11, Vol.50 (11), p.3610-3615

Hoboken: Wiley Subscription Services, Inc., A Wiley Company

Texto completo disponível

Citações Citado por
  • Título:
    Anti–lipoprotein lipase antibodies: A new player in the complex atherosclerotic process in systemic lupus erythematosus?
  • Autor: de Carvalho, Jozélio Freire ; Borba, Eduardo Ferreira ; Viana, Vilma Santos Trindade ; Bueno, Cleonice ; Leon, Elaine Pires ; Bonfá, Eloísa
  • Assuntos: Adult ; Arteriosclerosis - etiology ; Atherosclerosis (general aspects, experimental research) ; Autoantibodies - blood ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood Sedimentation ; C-Reactive Protein - analysis ; Cardiology. Vascular system ; Complement System Proteins - metabolism ; Diseases of the osteoarticular system ; DNA - blood ; Female ; Humans ; Lipoprotein Lipase - immunology ; Lupus Erythematosus, Systemic - blood ; Lupus Erythematosus, Systemic - complications ; Lupus Erythematosus, Systemic - physiopathology ; Male ; Medical sciences ; Middle Aged ; Severity of Illness Index
  • É parte de: Arthritis and rheumatism, 2004-11, Vol.50 (11), p.3610-3615
  • Notas: ObjectType-Article-1
    SourceType-Scholarly Journals-1
    ObjectType-Feature-2
    content type line 23
  • Descrição: Objective The novel description of antibodies to lipoprotein lipase (anti‐LPL) associated with dyslipoproteinemia prompted us to analyze the association of anti‐LPL with clinical and serologic features in patients with systemic lupus erythematosus (SLE) and its link to markers of inflammation that are known to be involved in atherogenesis. Methods Enzyme‐linked immunosorbent assay was used to test for the presence of anti‐LPL antibodies in 66 consecutive patients with SLE. Clinical and laboratory evaluation, including a fasting lipid profile, autoantibody screening, an assessment for markers of inflammation (C‐reactive protein [CRP], erythrocyte sedimentation rate [ESR]), and the SLE Disease Activity Index (SLEDAI) were performed at the time of inclusion in the study. Exclusion criteria were any conditions that affect the lipid profile. SLE patients were categorized into 2 groups according to detection of these anti‐LPL antibodies, as follows: anti‐LPL+ and anti‐LPL−. Results Anti‐LPL antibody IgG was detected in 25 SLE patients (37.8%). Triglyceride levels were significantly higher in the anti‐LPL+ group (112.4 ± 50.2 versus 89.9 ± 54.5 mg/dl in the anti‐LPL− group; P = 0.033), but no significant differences between the 2 groups were detected for total, high‐density lipoprotein, and low‐density lipoprotein cholesterol levels. A higher frequency of elevated CRP levels and ESRs was observed in the anti‐LPL+ group compared with the anti‐LPL− group (44% and 17.1%, respectively [P = 0.023] and 52% and 19.5%, respectively [P = 0.013]). Moreover, SLE patients with anti‐LPL antibodies also had significantly higher levels of CRP (11.1 ± 16.4 versus 2.4 ± 2.6 μg/ml; P = 0.036) and higher ESRs (33.4 ± 29.8 versus 16.5 ± 11.8 mm/hour; P = 0.020). Anti‐LPL titers had a significant positive correlation with the CRP level (r = 0.56, P < 0.001), the ESR (r = 0.55, P < 0.001), the SLEDAI score (r = 0.45, P < 0.001), anti–double‐stranded DNA (anti‐dsDNA; r = 0.52, P < 0.001), and anticardiolipin IgG antibodies (r = 0.25, P = 0.04), and a significant negative correlation was detected with total hemolytic complement activity (CH100) (r = −0.34, P = 0.005). Reinforcing these findings, multiple regression analysis also revealed a significant association of anti‐LPL with the CRP level (P = 0.025) and anti‐dsDNA (P < 0.001). Importantly, a comparison of positive and negative anti‐dsDNA sera revealed similar mean CRP levels (P = 0.56) and ESRs (P = 0.102), contrasting with the SLEDAI score (P = 0.004) and CH100 (P = 0.008). Conclusion These data support the link between inflammation, immune response, and dyslipoproteinemia in SLE, introducing anti‐LPL as a possible new player that may ultimately help in understanding the complex events of atherogenesis in this disease.
  • Editor: Hoboken: Wiley Subscription Services, Inc., A Wiley Company
  • Idioma: Inglês

Buscando em bases de dados remotas. Favor aguardar.