title: Dyslipidemia and changes in lipid profiles associated with rheumatoid arthritis and initiation of anti-tumor necrosis factor therapy.
abstract: OBJECTIVE
  To investigate the frequency of lipid testing in clinical practice and to explore the relationship between rheumatoid arthritis (RA), dyslipidemia, and other cardiovascular (CV) risk factors with RA treatment.
  
  
  METHODS
  Patients in this retrospective database study were ages ≥18 years and had ≥2 physician diagnoses for RA or osteoarthritis (OA; comparator group) between March 2004 and March 2008. Outcomes of interest included the percentage of RA and OA patients receiving lipid tests, lipid profiles (total cholesterol, low-density lipoprotein [LDL] cholesterol, and high-density lipoprotein [HDL] cholesterol) of RA versus OA patients, and lipid profiles of RA patients before and after initiation with a tumor necrosis factor (TNF) inhibitor. We used multivariable regression to control potential confounders between the cohorts.
  
  
  RESULTS
  Over a median ≥2-year followup, fewer RA patients than OA patients had ≥1 lipid test (62.0% [95% confidence interval (95% CI) 61.5-62.5] versus 69.8% [95% CI 69.5-70.1]). Mean total cholesterol and LDL cholesterol were each 4 mg/dl lower in the RA cohort (P < 0.0001); HDL cholesterol was similar between the cohorts. Across the RA cohort, 25.2% of patients had suboptimal LDL cholesterol levels (≥130 mg/dl). Among RA patients not receiving lipid-lowering therapy who initiated TNF inhibitor therapy (n = 96), mean total cholesterol and LDL cholesterol increased by 5.4 and 4.0 mg/dl, respectively.
  
  
  CONCLUSIONS
  Patients with RA were less likely to be tested for hyperlipidemia and had more favorable lipid profiles than patients with OA. TNF inhibitor therapy modestly increased all lipid parameters. Additional studies are needed to determine the effect of traditional CV risk factors and inflammation and the impact of biologic agents on CV outcomes in RA patients.
authors.affiliation: University of Alabama, Birmingham, USA. jcurtis@uab.edu
authors.forename: Jeffrey R
authors.initials: JR
authors.lastname: Curtis
authors.forename: Ani
authors.initials: A
authors.lastname: John
authors.forename: Onur
authors.initials: O
authors.lastname: Baser
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D018501:Antirheumatic Agents / Q000009:adverse effects / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000188:drug therapy* / Q000453:epidemiology / Q000276:immunology; D015415:Biomarkers / Q000097:blood; D050171:Dyslipidemias / Q000097:blood / Q000175:diagnosis / Q000188:drug therapy / Q000453:epidemiology*; D005260:Female; D006801:Humans; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D010003:Osteoarthritis / Q000097:blood / Q000188:drug therapy* / Q000453:epidemiology / Q000276:immunology; D011237:Predictive Value of Tests; D012189:Retrospective Studies; D018570:Risk Assessment; D012307:Risk Factors; D013997:Time Factors; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors* / Q000378:metabolism; D014481:United States / Q000453:epidemiology; D055815:Young Adult
chemical_list: D018501:Antirheumatic Agents; D015415:Biomarkers; D000960:Hypolipidemic Agents; D008055:Lipids; D014409:Tumor Necrosis Factor-alpha