title: Antiretroviral treatment-induced dyslipidemia in HIV-infected patients is influenced by the APOC3-related rs10892151 polymorphism.
abstract: BACKGROUND
  The recently observed association between the APOC3-related rs10892151 polymorphism and serum triglyceride levels has prompted us the possibility to explore whether this genetic variant may play a major role in human immunodeficiency virus (HIV)/antiretroviral therapy-induced dyslipidemia.
  
  
  METHODS
  We determined the rs10892151 genotype distribution and serum apolipoprotein (apo) C-III concentration in a group of HIV-infected patients (n = 208) and in a group of age and sex-matched healthy volunteers (n = 200). Circulating lipid and lipoprotein levels were followed for 12 months after antiretroviral treatment initiation in the HIV-infected group.
  
  
  RESULTS
  There were no significant variations in the frequency of the A allele between the healthy and HIV-infected groups (7.5 vs. 8.6%, respectively; p = 0.7); additionally, the A allele was not related to serum apo C-III concentration. However, among patients receiving protease inhibitor (PI) treatment, carriers of the A allele had significantly increased serum triglyceride (5.76 ± 2.54 mmol/L) and total cholesterol (6.63 ± 2.85 mmol/L) concentrations together with depressed levels of HDL-cholesterol (0.75 ± 0.3 mmol/L) when compared with patients not carrying the allele (2.43 ± 1.32, 5.2 ± 2.17 and 1.24 ± 0.4 mmol/L, respectively) at the end of the study. This effect was only evident for HDL-cholesterol concentration when patients were treated with non-nucleoside reverse transcriptase inhibitors (1.05 ± 0.4 vs. 1.28 ± 0.4 mmol/L).
  
  
  CONCLUSIONS
  The A allelic variant of the rs10892151 polymorphism is not associated with serum apo C-III concentration, but predisposes HIV-infected patients to less favorable lipid profile, particularly in those patients treated with PIs.
authors.affiliation: Centre de Recerca Biomèdica, Universitat Rovira i Virgili, Institut d'Investigació Sanitària Pere Virgili, Reus, Spain.
authors.forename: Gerard
authors.initials: G
authors.lastname: Aragonès
authors.forename: Carlos
authors.initials: C
authors.lastname: Alonso-Villaverde
authors.forename: Pedro
authors.initials: P
authors.lastname: Pardo-Reche
authors.forename: Anna
authors.initials: A
authors.lastname: Rull
authors.forename: Raúl
authors.initials: R
authors.lastname: Beltrán-Debón
authors.forename: Esther
authors.initials: E
authors.lastname: Rodríguez-Gallego
authors.forename: Laura
authors.initials: L
authors.lastname: Fernández-Sender
authors.forename: Jordi
authors.initials: J
authors.lastname: Camps
authors.forename: Jorge
authors.initials: J
authors.lastname: Joven
mesh_terms: D000328:Adult; D044966:Anti-Retroviral Agents / Q000009:adverse effects* / Q000378:metabolism; D053305:Apolipoprotein C-III / Q000097:blood / Q000235:genetics*; D002784:Cholesterol / Q000097:blood; D004359:Drug Therapy, Combination; D050171:Dyslipidemias / Q000139:chemically induced* / Q000235:genetics; D005260:Female; D015658:HIV Infections / Q000188:drug therapy*; D006801:Humans; D008055:Lipids / Q000097:blood; D008074:Lipoproteins / Q000097:blood; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic / Q000187:drug effects*; D012307:Risk Factors
chemical_list: D044966:Anti-Retroviral Agents; D053305:Apolipoprotein C-III; D008055:Lipids; D008074:Lipoproteins; D002784:Cholesterol