title: Differential associations of serum amyloid A and pentraxin-3 with allele-specific lipoprotein(a) levels in African Americans and Caucasians.
abstract: Lipoprotein(a) [Lp(a)] is a cardiovascular disease (CVD) risk factor, where inflammation impacts levels differentially across ethnicity. We investigated the effect of systemic [serum amyloid A (SAA)] and vascular [pentraxin-3 (PTX-3)] inflammation on Lp(a) levels across different apolipoprotein(a) [apo(a)] sizes in a biethnic population. Lp(a) and allele-specific apo(a) levels, apo(a) sizes, SAA, and PTX-3 levels were determined in 336 Caucasians and 224 African Americans. We dichotomized subjects into 2 groups using the respective median SAA (29.8 and 41.5 mg/dL for Caucasians and African Americans, respectively) or PTX-3 levels (1.6 and 1.1 ng/mL for Caucasians and African Americans, respectively). Among African Americans, but not in Caucasians, Lp(a) levels were increased (146 vs 117 nmol/L, P = 0.024) in the high versus low SAA group. No difference was observed across PTX-3 groups. Furthermore, among African Americans with smaller (<26 K4 repeats) apo(a) sizes, allele-specific apo(a) levels (111 vs 79 nmol/L, P = 0.020) were increased in the high versus low SAA group. Again, no difference was observed for PTX-3. We did not find any significant associations between allele-specific apo(a) and SAA or PTX-3 levels among Caucasians with smaller (<26 K4) apo(a) sizes. In conclusion, increased levels of SAA, but not PTX-3, were associated significantly with higher Lp(a) levels for smaller (<26 K4) apo(a) sizes in African Americans. Our results implicate that a proinflammatory stimulus may result in an increased cardiovascular risk through a selective increase in Lp(a) levels among African Americans who carry a smaller apo(a) size.
authors.affiliation: Department of Medicine, University of California, Davis, CA 95817, USA.
authors.forename: Byambaa
authors.initials: B
authors.lastname: Enkhmaa
authors.forename: Erdembileg
authors.initials: E
authors.lastname: Anuurad
authors.forename: Zeynep
authors.initials: Z
authors.lastname: Ozturk
authors.forename: Wei
authors.initials: W
authors.lastname: Zhang
authors.forename: Thomas A
authors.initials: TA
authors.lastname: Pearson
authors.forename: Lars
authors.initials: L
authors.lastname: Berglund
mesh_terms: D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase / Q000097:blood; D001741:Black or African American; D000483:Alleles; D002097:C-Reactive Protein / Q000032:analysis*; D002318:Cardiovascular Diseases / Q000209:etiology; D005260:Female; D006801:Humans; D053583:Interleukin-1beta / Q000494:pharmacology; D015850:Interleukin-6 / Q000502:physiology; D017270:Lipoprotein(a) / Q000097:blood* / Q000235:genetics; D008297:Male; D000685:Serum Amyloid A Protein / Q000032:analysis*; D000683:Serum Amyloid P-Component / Q000032:analysis*; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology; D044465:White People; D000099153:Pentraxins
chemical_list: D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase; D002097:C-Reactive Protein; D053583:Interleukin-1beta; D015850:Interleukin-6; D017270:Lipoprotein(a); D000685:Serum Amyloid A Protein; D000683:Serum Amyloid P-Component; D014409:Tumor Necrosis Factor-alpha; D000099153:Pentraxins