High Levels of Inflammatory Biomarkers Are Associated with Increased Allele-Specific Apolipoprotein(a) Levels in African-Americans

Anuurad, Erdembileg; Rubin, Jill; Chiem, Alan; Tracy, Russell P.; Pearson, Thomas A.; Berglund, Lars

doi:10.1210/jc.2007-2416

Cited by 32 publications

(38 citation statements)

References 48 publications

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“…Underlying reasons for the increase remain unresolved, but it has been pro posed that a decreased plasma albumin level and reduced oncotic pressure may contribute (160). These results un derscore the value of assessing Lp(a) concentrations con tributed by particles carrying specific apo(a) sizes, i.e., allelespecific apo(a) levels (21,105).…”

Section: Kidney Diseasementioning

confidence: 66%

“…3). Increased CRP and fibrinogen concentrations were significantly associated with higher allelespecific Lp(a) levels for smaller apo(a) size in African-Americans, while a higher plasma lipopro teinassociated phospholipase A 2 activity was associated with an elevated allelespecific Lp(a) level for smaller apo(a) size in both African-Americans and Caucasians (105,106). Further, a significant association between ele vated serum amyloid A, an HDLassociated systemic in flammatory biomarker, and a higher allelespecific Lp(a) level for smaller apo(a) size was found in African-Ameri cans (107).…”

Section: Inflammationmentioning

confidence: 94%

“…The impact of an inflammatory burden, as detected by elevated concentrations of biomarkers for systemic and vascular inflammation on Lp(a) levels associated with a defined apo(a) size, has been explored in several studies (105)(106)(107). These levels have been characterized as isoformor allelespecific apo(a) levels (Fig.…”

Section: Inflammationmentioning

confidence: 99%

See 2 more Smart Citations

Lipoprotein (a): impact by ethnicity and environmental and medical conditions

Enkhmaa

Anuurad

Berglund

2016

Journal of Lipid Research

Self Cite

184

134

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Section: Kidney Diseasementioning

confidence: 66%

Section: Inflammationmentioning

confidence: 94%

See 1 more Smart Citation

Lipoprotein (a): impact by ethnicity and environmental and medical conditions

Enkhmaa

Anuurad

Berglund

2016

Journal of Lipid Research

Self Cite

184

134

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“…Similar to LDL-C levels, Lp(a) has been identified as an independent risk factor for atherosclerotic cardiovascular events, such as myocardial infarction. 19 Lp(a) serum levels are primarily genetically determined, but other factors including inflammatory state, 20 comorbidity (e.g., kidney disease and diabetes), 21 and the use of some therapeutic agents (e.g., aspirin, niacin, proprotein convertase subtilisin/kexin type 9 inhibitors, angiotensin-converting enzyme inhibitors, tamoxifen, and thyroxin replacement therapy) may also affect plasma Lp(a) levels. 22 Although the mechanisms causing those lipid profile changes during malaria infection are not fully understood, several hypotheses have been suggested from clinical and animal studies.…”

Section: Introductionmentioning

confidence: 99%

Serum Lipids and Lipoproteins During Uncomplicated Malaria: A Cohort Study in Lambaréné, Gabon

Visser

Vries

Vingerling

et al. 2017

The American Society of Tropical Medicine and Hygiene

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Abstract. The serum lipid profile in malaria patients has been found to differ from that of healthy controls. We investigated serum lipid profile changes in malaria patients over time compared with patients with other febrile diseases. In total, 217 patients were included in the study (111 malaria patients and 106 symptomatic controls, defined as malaria-negative febrile patients). Serum lipid levels (mmol/L) were significantly lower in malaria patients compared with those with other febrile diseases (total cholesterol . No significant differences were found for apolipoprotein A1, apolipoprotein B, and lipoprotein(a). Cholesterol levels increased toward reference values on day 28 ( TC = 3.26-3.98, P < 0.001; HDL-C = 0.43-0.96, P < 0.001; LDL-C = 2.05-2.60, P < 0.001). TG levels decreased from 1.81 on admission to 1.76 (day 3) and 0.88 (day 28; P = 0.130). Lipid profile changes were not correlated with parasitemia or Plasmodium falciparum histidine-rich protein 2 levels. This study confirms characteristic temporary lipid profile changes in malaria. Lipid profile changes demonstrated a good accuracy to discriminate between malaria and other febrile diseases (area under the curve = 0.80 (95% confidence interval = 0.742-0.863, P < 0.001). Several plausible hypotheses exist regarding the pathophysiology of lipid profile changes in malaria. Further studies to elucidate the precise pathways may lead to improved understanding of the underlying pathophysiology.[

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“…Increased levels of CRP and fibrinogen were significantly associated with higher allele-specific Lp(a) levels for smaller ( < 26 K4 repeats) apo(a) sizes in African Americans. 54 Furthermore, in this cohort, higher Lp-PLA 2 activity levels were significantly associated with elevated allele-specific Lp(a) levels for smaller ( < 26 K4) apo(a) sizes in both African Americans and Caucasians. 55 A significant association between elevated SAA, an HDL-associated systemic inflammatory biomarker, and higher allele-specific Lp(a) levels for smaller apo(a) size was found in African Americans.…”

Section: Allele-specific Lp(a) Level and Inflammationmentioning

confidence: 60%

Lipoprotein(a): Genotype–Phenotype Relationship and Impact on Atherogenic Risk

Enkhmaa

Anuurad

Zhang

et al. 2011

Metabolic Syndrome and Related Disorders

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In 2010, more than 45 years after the initial discovery of lipoprotein(a) [Lp(a)] by Kare Berg, an European Atherosclerosis Society Consensus Panel recommended screening for elevated Lp(a) in people at moderate to high risk of atherosclerotic cardiovascular disease (CVD). This recommendation was based on extensive epidemiological findings demonstrating a significant association between elevated plasma Lp(a) levels and coronary heart disease, myocardial infarction, and stroke. In addition to those patients considered to be at moderate to high risk of heart disease, statin-treated patients with recurrent heart disease were also identified as targeted for screening of elevated Lp(a) levels. Taken together, recent findings have significantly strengthened the notion of Lp(a) as a causal risk factor for CVD. It is well established that Lp(a) levels are largely determined by the size of the apolipoprotein a [apo(a)] gene; however, recent studies have identified several other LPA gene polymorphisms that have significant associations with an elevated Lp(a) level and a reduced copy number of K4 repeats. In addition, the contribution of other genes in regulating Lp(a) levels has been described. Besides the strong genetic regulation, new evidence has emerged regarding the impact of inflammation as a modulator of Lp(a) risk factor properties. Thus, oxidized phospholipids that possess a strong proinflammatory potential are preferentially carried on Lp(a) particles. Collectively, these findings point to the importance of both phenotypic and genotypic factors in influencing apo(a) proatherogenic properties. Therefore, studies taking both of these factors into account determining the amount of Lp(a) associated with each individual apo(a) size allele are valuable tools when assessing a risk factor role of Lp(a). Apo(a) Gene Size Polymorphism and Lp(a)T he plasma lipoprotein(a)[Lp(a)] level is one of the most heritable quantitative traits in humans, and the high heritability of this trait has been attributed to variations at LPA locus.

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High Levels of Inflammatory Biomarkers Are Associated with Increased Allele-Specific Apolipoprotein(a) Levels in African-Americans

Cited by 32 publications

References 48 publications

Lipoprotein (a): impact by ethnicity and environmental and medical conditions

Lipoprotein (a): impact by ethnicity and environmental and medical conditions

Serum Lipids and Lipoproteins During Uncomplicated Malaria: A Cohort Study in Lambaréné, Gabon

Lipoprotein(a): Genotype–Phenotype Relationship and Impact on Atherogenic Risk

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