Differential associations of serum amyloid A and pentraxin-3 with allele-specific lipoprotein(a) levels in African Americans and Caucasians
Tarih
2011Yazar
Zhang, Wei
Ozturk, Zeynep
Anuurad, Erdembileg
Pearson, Thomas A.
Berglund, Lars
Enkhmaa, Byambaa
Üst veri
Tüm öğe kaydını gösterÖzet
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. (Translational Research 2011;158:92-98)
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