Anti-lipoprotein lipase antibodies: a new player in the complex atherosclerotic process in systemic lupus erythematosus?
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 mug/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).


CONCLUSIONS
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.
de Carvalho
Jozélio Freire
JF
Medical School, University of São Paulo, Avenida Dr. Arnaldo, 455-3 andar, CEP:01246, São Paulo SP, Brazil. reumato@edu.usp.br
Borba
Eduardo Ferreira
EF
Viana
Vilma Santos Trindade
VS
Bueno
Cleonice
C
Leon
Elaine Pires
EP
Bonfá
Eloísa
E
D000328:Adult; D001161:Arteriosclerosis / Q000209:etiology*; D001323:Autoantibodies / Q000097:blood*; D001799:Blood Sedimentation; D002097:C-Reactive Protein / Q000032:analysis; D003165:Complement System Proteins / Q000378:metabolism; D004247:DNA / Q000097:blood; D005260:Female; D006801:Humans; D008071:Lipoprotein Lipase / Q000276:immunology*; D008180:Lupus Erythematosus, Systemic / Q000097:blood* / Q000150:complications* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D012720:Severity of Illness Index
D001323:Autoantibodies; D003165:Complement System Proteins; D002097:C-Reactive Protein; D004247:DNA; D008071:Lipoprotein Lipase