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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 92-98 |
| Number of pages | 7 |
| Journal | Translational Research |
| Volume | 158 |
| Issue number | 2 |
| DOIs | |
| State | Published - Aug 2011 |
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ASJC Scopus subject areas
- Medicine(all)
- Biochemistry, medical
- Public Health, Environmental and Occupational Health
Cite this
Differential associations of serum amyloid A and pentraxin-3 with allele-specific lipoprotein(a) levels in African Americans and Caucasians. / Byambaa, Enkhmaa; Erdembileg, Anuurad; Ozturk, Zeynep; Zhang, Wei; Pearson, Thomas A.; Berglund, Lars.
In: Translational Research, Vol. 158, No. 2, 08.2011, p. 92-98.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Differential associations of serum amyloid A and pentraxin-3 with allele-specific lipoprotein(a) levels in African Americans and Caucasians
AU - Byambaa, Enkhmaa
AU - Erdembileg, Anuurad
AU - Ozturk, Zeynep
AU - Zhang, Wei
AU - Pearson, Thomas A.
AU - Berglund, Lars
PY - 2011/8
Y1 - 2011/8
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=79960319748&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=79960319748&partnerID=8YFLogxK
U2 - 10.1016/j.trsl.2011.01.004
DO - 10.1016/j.trsl.2011.01.004
M3 - Article
C2 - 21757153
AN - SCOPUS:79960319748
VL - 158
SP - 92
EP - 98
JO - Translational Research
JF - Translational Research
SN - 1931-5244
IS - 2
ER -