title: Abnormal lipoprotein particles and cholesterol efflux capacity in patients with psoriasis.
abstract: OBJECTIVE
  Psoriasis is a Th-1/17 mediated inflammatory disease associated with increased risk of cardiovascular disease (CVD). Inflammation may modulate lipoprotein particle number and directly impair HDL functions, in particular reverse cholesterol transport (RCT). We sought to study how chronic in vivo inflammation modulates lipoprotein particle composition using nuclear magnetic resonance spectroscopy (NMR) and HDL efflux in psoriasis.
  
  
  RESULTS
  We prospectively enrolled a consecutive sample of patients with psoriasis (n = 122) and compared lipoprotein and metabolic risk factors to patients without psoriasis (n = 134). Fasting lipids, insulin, glucose were measured by standard assays, and lipoprotein concentration and size were measured by NMR. In a random subset (n = 100 each group), HDL efflux capacity was quantified using a validated ex vivo system involving the incubation of macrophages with apolipoprotein B-depleted serum from patients. Traditional lipid concentrations were similar in both groups except for HDL concentration which was lower in psoriasis (43 mg/dl (36-58) vs 50 (42-62), p < 0.01). However, NMR showed an atherogenic profile in psoriasis similar to that observed in diabetes, with significant increase in LDL particle concentration [1210.5 (1002-1498) vs 1115 (935-1291), p = 0.02] with decrease in LDL size [20.6 (20.3-21.1) vs 21.3 (20.6-21.1), p < 0.001] beyond CV risk factors and HOMA-IR (p = 0.001). Finally, HDL efflux capacity was lower in psoriasis compared to controls in fully adjusted models (beta -0.14, p = 0.001).
  
  
  CONCLUSIONS
  These data support a more atherogenic lipoprotein profile by NMR and decreased HDL efflux capacity in psoriasis patients compared to controls beyond CVD risk factors. The abnormal lipoprotein particle composition and HDL efflux capacity in psoriasis may provide a link between psoriasis and CVD.
authors.affiliation: Cardiovascular Institute, University of Pennsylvania School of Medicine, USA. nehal.mehta@uphs.upenn.edu
authors.forename: Nehal N
authors.initials: NN
authors.lastname: Mehta
authors.forename: Ron
authors.initials: R
authors.lastname: Li
authors.forename: Parasuram
authors.initials: P
authors.lastname: Krishnamoorthy
authors.forename: YiDing
authors.initials: Y
authors.lastname: Yu
authors.forename: William
authors.initials: W
authors.lastname: Farver
authors.forename: Amrith
authors.initials: A
authors.lastname: Rodrigues
authors.forename: Anna
authors.initials: A
authors.lastname: Raper
authors.forename: Mackenzie
authors.initials: M
authors.lastname: Wilcox
authors.forename: Amanda
authors.initials: A
authors.lastname: Baer
authors.forename: Stephanie
authors.initials: S
authors.lastname: DerOhannesian
authors.forename: Megan
authors.initials: M
authors.lastname: Wolfe
authors.forename: Muredach P
authors.initials: MP
authors.lastname: Reilly
authors.forename: Daniel J
authors.initials: DJ
authors.lastname: Rader
authors.forename: Abby
authors.initials: A
authors.lastname: VanVoorhees
authors.forename: Joel M
authors.initials: JM
authors.lastname: Gelfand
mesh_terms: D000328:Adult; D002318:Cardiovascular Diseases / Q000209:etiology; D002784:Cholesterol / Q000097:blood*; D005260:Female; D006801:Humans; D008074:Lipoproteins / Q000097:blood*; D008075:Lipoproteins, HDL / Q000378:metabolism; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D011565:Psoriasis / Q000097:blood* / Q000150:complications; D012307:Risk Factors
chemical_list: D008074:Lipoproteins; D008075:Lipoproteins, HDL; D002784:Cholesterol