ARTHRITIS & RHEUMATISM Vol. 50, No. 11, November 2004, pp 3610–3615 DOI 10.1002/art.20630 © 2004, American College of Rheumatology Anti–Lipoprotein Lipase Antibodies A New Player in the Complex Atherosclerotic Process in Systemic Lupus Erythematosus? Joze ´lio Freire de Carvalho, Eduardo Ferreira Borba, Vilma Santos Trindade Viana, Cleonice Bueno, Elaine Pires Leon, and Eloı ´sa Bonfa ´ Objective. The novel description of antibodies to lipoprotein lipase (anti-LPL) associated with dysli- poproteinemia 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 labo- ratory evaluation, including a fasting lipid profile, au- toantibody screening, an assessment for markers of inflammation (C-reactive protein [CRP], erythrocyte sedimentation rate [ESR]), and the SLE Disease Activ- ity 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-LPLand anti-LPL. Results. Anti-LPL antibody IgG was detected in 25 SLE patients (37.8%). Triglyceride levels were signif- icantly higher in the anti-LPLgroup (112.4 50.2 versus 89.9 54.5 mg/dl in the anti-LPLgroup; 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 ob- served in the anti-LPLgroup compared with the anti-LPLgroup (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 g/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 corre- lation was detected with total hemolytic complement activity (CH100) (r 0.34, P 0.005). Reinforcing these findings, multiple regression analysis also re- vealed 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 dyslipoproteine- mia in SLE, introducing anti-LPL as a possible new player that may ultimately help in understanding the complex events of atherogenesis in this disease. Lipoprotein lipase (LPL) is a member of the lipase family, and LPL is known to hydrolyze triglyceride molecules found in lipoprotein particles (1,2). Physio- Supported by Fundac ¸a ˜o de Amparo a ` Pesquisa do Estado de Sa ˜o Paulo grant 02/03867-0. Dr. Bonfa ´’s work was supported by Conselho Nacional de Desenvolvimento Cientı ´fico e Tecnolo ´gico, grant 304756/2003-2. Joze ´lio Freire de Carvalho, MD, Eduardo Ferreira Borba, MD, PhD, Vilma Santos Trindade Viana, PhD, Cleonice Bueno, Elaine Pires Leon, Eloı ´sa Bonfa ´, MD, PhD: Medical School, Univer- sity of Sa ˜o Paulo, Sa ˜o Paulo, Brazil. Address correspondence and reprint requests to Joze ´lio Freire de Carvalho, MD, Faculdade de Medicina USP, Reumatologia, Avenida Dr. Arnaldo, 455-3 andar, CEP:01246, Sa ˜o Paulo SP, Brazil. E-mail: reumato@edu.usp.br. Submitted for publication May 17, 2004; accepted in revised form August 16, 2004. 3610