title: Modest but sustained increase of serum high density lipoprotein cholesterol levels in patients with inflammatory arthritides treated with infliximab.
abstract: OBJECTIVE
  Tumor necrosis factor-a (TNF-a) is a key cytokine in the pathogenesis of chronic inflammatory arthritides, has proatherogenic effects, and may be positively correlated with impairment of the action of insulin. Patients with chronic inflammatory arthritides have an increased risk for cardiovascular diseases. We assessed whether anti-TNF-a treatment modifies the unfavorable lipid profile induced by chronic inflammatory arthritides.
  
  
  METHODS
  Sixty patients (24 with rheumatoid arthritis, 26 ankylosing spondylitis, and 10 psoriatic arthritis) receiving infliximab because of ongoing disease activity despite disease modifying drugs (DMARD) were prospectively studied for 6 months. Lipid profile, total cholesterol/high density lipoprotein cholesterol (TC/HDL-C), and low density lipoprotein cholesterol (LDL-C)/HDL-C ratios, as well as disease activity indices (DAS28 and BASDAI), were assessed.
  
  
  RESULTS
  A sustained increase of serum HDL-C was observed [mean increase (95% CI)] 5 (3-7) mg/dl, 3.5 (1-6) mg/dl, and 3 (1-5) mg/dl at 1, 3, and 6 months, respectively (p < 0.01). Compared to nonresponders, HDL-C increased significantly more in EULAR or BASDAI responders (0.8 vs 5.8 mg/dl; p = 0.05). Serum TC was significantly increased [11 (4-8) mg/dl; p = 0.001] only after the first month of treatment. TC/HDL-C and LDL-C/HDL-C decreased only after the first month [0.3 (0.1-0.4), p < 0.01, and 0.2 (0.1-0.4), p < 0.01, respectively]. For patients with baseline LDL-C > 130 mg/dl, LDL-C/HDL-C decreased (p < 0.05) during the whole study period and TC/HDL-C decreased (p < 0.05) at 1 and 3 months.
  
  
  CONCLUSIONS
  Anti-TNF-a treatment in patients with chronic inflammatory arthritides induces a modest, but sustained, increase in serum HDL-C levels, which may have a favorable effect in reducing the cardiovascular risk in these patients.
authors.affiliation: Department of Rheumatology, Clinical Immunology, and Allergy, University Hospital, Medical School, University of Crete, Heraklion, Greece.
authors.forename: Elias
authors.initials: E
authors.lastname: Spanakis
authors.forename: Prodromos
authors.initials: P
authors.lastname: Sidiropoulos
authors.forename: John
authors.initials: J
authors.lastname: Papadakis
authors.forename: Emmanuel
authors.initials: E
authors.lastname: Ganotakis
authors.forename: George
authors.initials: G
authors.lastname: Katsikas
authors.forename: Stylianos
authors.initials: S
authors.lastname: Karvounaris
authors.forename: Argyro
authors.initials: A
authors.lastname: Bizaki
authors.forename: Heraklis
authors.initials: H
authors.lastname: Kritikos
authors.forename: Dimitrios T
authors.initials: DT
authors.lastname: Boumpas
mesh_terms: D000328:Adult; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001168:Arthritis / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D015535:Arthritis, Psoriatic / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology; D008076:Cholesterol, HDL / Q000097:blood / Q000187:drug effects*; D005260:Female; D006304:Health Status; D006801:Humans; D000069285:Infliximab; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D012720:Severity of Illness Index; D013167:Spondylitis, Ankylosing / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors* / Q000276:immunology
chemical_list: D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; D008076:Cholesterol, HDL; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab