title: HIV disease activity as a modulator of lipoprotein(a) and allele-specific apolipoprotein(a) levels.
abstract: OBJECTIVE
  Mechanisms underlying the cardiovascular risk of lipoprotein(a) are poorly understood. We investigated the relationship of apolipoprotein(a) (apo(a)) size, lipoprotein(a), and allele-specific apo(a) levels with HIV disease activity parameters in a biethnic population.
  
  
  RESULTS
  Lipoprotein(a) and allele-specific apo(a) levels were determined in 139 white and 168 black HIV-positive patients. Plasma HIV RNA viral load and CD4+ T-cell count were used as surrogates for disease activity. Lipoprotein(a) and allele-specific apo(a) levels were higher in blacks than whites (for both P<0.001). Apo(a) allele size distribution was similar between the 2 ethnic groups, with a median apo(a) size of 28 kringle 4 repeats. Allele-specific apo(a) levels were positively associated with CD4+ T-cell count (P=0.027) and negatively with plasma HIV RNA viral load (P<0.001). Further, allele-specific apo(a) levels associated with smaller (<28 kringle 4) atherogenic apo(a) sizes were higher in subjects with CD4+ T-cell counts of ≥350 (P=0.002).
  
  
  CONCLUSIONS
  Allele-specific apo(a) levels were higher in subjects with high CD4+ T-cell count or low plasma HIV RNA viral load. The findings suggest that HIV disease activity reduced allele-specific apo(a) levels. Higher allele-specific apo(a) levels associated with atherogenic small apo(a) sizes might contribute to increased cardiovascular risk in HIV-positive subjects with improved disease status.
authors.affiliation: Department of Internal Medicine, University of California, Davis, CA, USA.
authors.forename: Byambaa
authors.initials: B
authors.lastname: Enkhmaa
authors.forename: Erdembileg
authors.initials: E
authors.lastname: Anuurad
authors.forename: Wei
authors.initials: W
authors.lastname: Zhang
authors.forename: Adnan
authors.initials: A
authors.lastname: Abbuthalha
authors.forename: Xiao-Dong
authors.initials: XD
authors.lastname: Li
authors.forename: William
authors.initials: W
authors.lastname: Dotterweich
authors.forename: Richard B
authors.initials: RB
authors.lastname: Pollard
authors.forename: David M
authors.initials: DM
authors.lastname: Asmuth
authors.forename: Lars
authors.initials: L
authors.lastname: Berglund
mesh_terms: D000328:Adult; D001741:Black or African American / Q000235:genetics; D053241:Apoprotein(a) / Q000097:blood* / Q000235:genetics; D015415:Biomarkers / Q000097:blood; D018791:CD4 Lymphocyte Count; D002140:California / Q000453:epidemiology; D002318:Cardiovascular Diseases / Q000097:blood / Q000208:ethnology / Q000821:virology; D003430:Cross-Sectional Studies; D005260:Female; D006678:HIV / Q000235:genetics / Q000276:immunology; D015658:HIV Infections / Q000097:blood* / Q000150:complications / Q000175:diagnosis / Q000208:ethnology / Q000821:virology; D006801:Humans; D017270:Lipoprotein(a) / Q000097:blood* / Q000235:genetics; D008297:Male; D008875:Middle Aged; D010316:Particle Size; D011379:Prognosis; D012367:RNA, Viral / Q000097:blood; D012307:Risk Factors; D019562:Viral Load; D044465:White People / Q000331:legislation & jurisprudence
chemical_list: D015415:Biomarkers; D017270:Lipoprotein(a); D012367:RNA, Viral; D053241:Apoprotein(a)