title: Autoantibodies to lipoprotein lipase and dyslipidemia in systemic lupus erythematosus.
abstract: OBJECTIVE
  To demonstrate the binding of bovine lipoprotein lipase (LPL) by IgG from sera obtained from patients with systemic lupus erythematosus (SLE) and other rheumatic diseases, and the relationship of anti-LPL to triglyceride levels in SLE.
  
  
  METHODS
  Binding of LPL by IgG from sera obtained from patients with SLE and other rheumatic diseases was measured by an enzyme-linked immunosorbent assay technique. Lipid profiles for fasting blood samples obtained from SLE patients and control subjects were determined.
  
  
  RESULTS
  Sera obtained from 105 patients with SLE were assessed for reactivity with LPL, and 49 (47%) of the results were positive. Sera obtained from patients with rheumatoid arthritis (RA) (n = 80), Sjögren's syndrome (n = 30), polymyositis and dermatomyositis (n = 30), and progressive systemic sclerosis (n = 31) were also studied, and 10 (13%), 3 (10%), 12 (40%), and 13 (42%), respectively, were positive for reactivity with LPL. It was determined that all affinity-purified anti-double-stranded DNA (dsDNA) antibodies and 4 of 5 monoclonal anti-dsDNA antibodies bound to LPL. The binding of IgG depleted of anti-dsDNA to LPL indicates a second anti-LPL activity in SLE. Measurements of fasting lipid levels in SLE patients with anti-LPL revealed a strong positive correlation of antibody levels and total serum triglycerides, apolipoprotein B, and apolipoprotein E concentrations.
  
  
  CONCLUSIONS
  Antibodies to LPL occurred in 47% of SLE patients and in a similar percentage of patients with polymyositis or systemic sclerosis. The prevalence of these antibodies was less in patients with RA or Sjögren's syndrome. It is hypothesized that the elevated triglyceride levels in SLE patients are in part attributable to anti-LPL, and this lipid abnormality could contribute to the premature atherosclerosis known to be present in patients with SLE.
authors.affiliation: Oklahoma Medical Research Foundation and Oklahoma University College of Medicine, Oklahoma City, OK 73104, USA. morris-reichlin@omrf.ouhsc.edu
authors.forename: Morris
authors.initials: M
authors.lastname: Reichlin
authors.forename: James
authors.initials: J
authors.lastname: Fesmire
authors.forename: Ana I
authors.initials: AI
authors.lastname: Quintero-Del-Rio
authors.forename: Marianne
authors.initials: M
authors.lastname: Wolfson-Reichlin
mesh_terms: D001055:Apolipoproteins B / Q000097:blood; D001057:Apolipoproteins E / Q000097:blood; D001172:Arthritis, Rheumatoid / Q000276:immunology; D001323:Autoantibodies / Q000097:blood*; D003882:Dermatomyositis / Q000276:immunology; D004797:Enzyme-Linked Immunosorbent Assay; D006801:Humans; D006949:Hyperlipidemias / Q000150:complications*; D007074:Immunoglobulin G / Q000276:immunology; D008071:Lipoprotein Lipase / Q000276:immunology*; D008180:Lupus Erythematosus, Systemic / Q000150:complications / Q000276:immunology*; D017285:Polymyositis / Q000276:immunology; D012595:Scleroderma, Systemic / Q000276:immunology; D012859:Sjogren's Syndrome / Q000276:immunology; D014280:Triglycerides / Q000097:blood
chemical_list: D001055:Apolipoproteins B; D001057:Apolipoproteins E; D001323:Autoantibodies; D007074:Immunoglobulin G; D014280:Triglycerides; D008071:Lipoprotein Lipase