title: Anti-lipoprotein lipase antibody in systemic sclerosis: association with elevated serum triglyceride concentrations.
abstract: OBJECTIVE
  The vascular damage systemic sclerosis (SSc) consists mainly of microvascular changes, but recently macrovascular changes with dyslipidemia were recognized. In systemic lupus erythematosus (SLE), autoantibody to lipoprotein lipase (LPL), a key enzyme that hydrolyzes triglycerides, suggested a role of autoimmunity for elevated serum triglyceride levels and atherosclerosis. We investigated the prevalence and levels of anti-LPL antibodies, their clinical correlation, and their functional significance in patients with SSc.
  
  
  METHODS
  Serum samples from patients with diffuse cutaneous SSc (dSSc; n = 55), limited cutaneous SSc (lSSc; n = 75), SLE (n = 21), and dermatomyositis (DM; n = 21) and healthy controls (n = 41) were examined by ELISA. The presence of anti-LPL antibody was evaluated by immunoblotting analysis using purified LPL. To determine the functional relevance of anti-LPL antibody in vivo, we assessed whether anti-LPL autoantibody was able to inhibit LPL activity using the LPL activity kit.
  
  
  RESULTS
  ELISA revealed that IgG or IgM anti-LPL antibodies were detected in 35% of SSc patients, while they were also positive in 67% of SLE patients and 43% of DM patients. The presence of IgG anti-LPL antibody was associated with elevated serum triglyceride levels, greater extent of skin fibrosis, and more frequent presence of lung fibrosis, heart involvement, and anti-topoisomerase I antibodies. The presence of anti-LPL autoantibody was confirmed by immunoblotting analysis. LPL activity was inhibited by IgG anti-LPL antibodies in sera from SSc patients with elevated serum triglyceride levels.
  
  
  CONCLUSIONS
  Our results suggest that anti-LPL autoantibody contributes to elevated serum triglyceride levels by inhibiting LPL enzyme activity in patients with SSc.
authors.affiliation: Department of Dermatology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.
authors.forename: Masanari
authors.initials: M
authors.lastname: Kodera
authors.forename: Ikuko
authors.initials: I
authors.lastname: Hayakawa
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Komura
authors.forename: Koichi
authors.initials: K
authors.lastname: Yanaba
authors.forename: Minoru
authors.initials: M
authors.lastname: Hasegawa
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Takehara
authors.forename: Shinichi
authors.initials: S
authors.lastname: Sato
mesh_terms: D001323:Autoantibodies / Q000097:blood*; D003882:Dermatomyositis / Q000150:complications / Q000276:immunology / Q000473:pathology; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D006949:Hyperlipidemias / Q000150:complications* / Q000473:pathology; D008071:Lipoprotein Lipase / Q000276:immunology*; D008180:Lupus Erythematosus, Systemic / Q000150:complications / Q000276:immunology / Q000473:pathology; D008297:Male; D008875:Middle Aged; D012595:Scleroderma, Systemic / Q000150:complications / Q000276:immunology / Q000473:pathology; D014280:Triglycerides / Q000097:blood*
chemical_list: D001323:Autoantibodies; D014280:Triglycerides; D008071:Lipoprotein Lipase