title: Oxidative stress and psoriasis: the effect of antitumour necrosis factor-α inhibitor treatment.
abstract: BACKGROUND
  Psoriasis is a chronic, inflammatory skin condition associated with a high frequency of cardiovascular events. Modifications of plasma lipids, and an increase in the levels of biochemical markers of inflammation and lipid peroxidation have been reported in subjects with psoriasis, suggesting a relationship between psoriasis, inflammation and oxidative damage.
  
  
  OBJECTIVE
  To investigate whether modulation of inflammatory activity by tumour necrosis factor-α inhibitors in patients with psoriasis is associated with modification of lipid profiles, oxidative stress and paraoxonase (PON)1 activity.
  
  
  METHODS
  The levels of plasma lipids and lipoprotein(a), and the levels of the markers of inflammation and lipid peroxidation were evaluated in subjects with psoriasis (n=23) before and after 24 weeks of treatment with etanercept. In the same subjects plasma total antioxidant capacity and the activity of PON1, an antioxidant and anti-inflammatory enzyme associated with the high-density lipoproteins (HDLs), were investigated.
  
  
  RESULTS
  The results showed that clinical improvement in patients with psoriasis treated with etanercept is associated with a reduction in the levels of inflammatory markers [C-reactive protein (CRP)] and lipid peroxidation, and also with increased antioxidant capacity in the serum of patients with psoriasis. These modifications are associated with a significant increase in the activity of PON1. A significant increase in the PON1/CRP ratio has also been observed in patients with psoriasis after treatment. The significant inverse correlation between CRP and PON1 activity suggests a relationship between PON1 activity and inflammation.
  
  
  CONCLUSIONS
  Treatment with etanercept is associated with a reduction in lipid peroxidation and an improvement in HDL antioxidant and anti-inflammatory properties.
authors.affiliation: Department of Life and Environmental Sciences, Polytechnic University of Marche, Ancona, Italy.
authors.forename: T
authors.initials: T
authors.lastname: Bacchetti
authors.forename: A
authors.initials: A
authors.lastname: Campanati
authors.forename: G
authors.initials: G
authors.lastname: Ferretti
authors.forename: O
authors.initials: O
authors.lastname: Simonetti
authors.forename: G
authors.initials: G
authors.lastname: Liberati
authors.forename: A M
authors.initials: AM
authors.lastname: Offidani
mesh_terms: D000328:Adult; D043303:Aryldialkylphosphatase / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism; D000068800:Etanercept; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use*; D007166:Immunosuppressive Agents / Q000627:therapeutic use*; D015227:Lipid Peroxidation / Q000187:drug effects; D008055:Lipids / Q000097:blood; D017270:Lipoprotein(a) / Q000097:blood; D008075:Lipoproteins, HDL / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010084:Oxidation-Reduction / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects*; D011565:Psoriasis / Q000097:blood / Q000188:drug therapy*; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use*; D012720:Severity of Illness Index; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D015415:Biomarkers; D007074:Immunoglobulin G; D007166:Immunosuppressive Agents; D008055:Lipids; D017270:Lipoprotein(a); D008075:Lipoproteins, HDL; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D043303:Aryldialkylphosphatase; C468406:PON1 protein, human; D000068800:Etanercept