Case-control study of serum lipoprotein(a) and apolipoproteins A-I and B in stroke in the young

Abstract Background: Lipoprotein(a) [Lp(a)] is a plasma lipoprotein that has been implicated in both atherogenesis and thrombophilia. A few reports in recent years, principally in European populations, have suggested that elevated plasma Lp(a) level may constitute a risk factor for ischemic arterial stroke (IAS) in children. However, the ELISA assays used in these studies are technically limited by their ability to provide accurate Lp(a) values independently of apo(a) size. Objective: To determine the prevalence of elevated plasma Lp(a) concentration among children with non-neonatal IAS and healthy children in a U.S. population using the current gold-standard laboratory methodology, toward the evaluation of Lp(a) as a risk factor for pediatric IAS. Methods: In a case-control study, children from 1 month to 21 years of age with a history of radiologically-confirmed IAS (case group, n=22) and healthy children (contemporaneous control group, n=41) were consecutively recruited from The Children’s Hospital, Denver, and the Mountain States Regional Hemophilia and Thrombosis Center (Aurora, CO). Children with IAS who were receiving drugs that affect Lp(a) level, such as niacin or statins, were excluded. Fasting plasma samples were obtained by peripheral venipuncture into EDTA with susequent centrifugation to yield platelet-poor plasma. Lp(a) assay was performed in the Northwest Lipid Metabolism and Diabetes Research Laboratories at the University of Washington, Seattle, using a double monoclonal antibody-based ELISA validated to be sensitive to apo(a) size heterogeneity. Results were expressed in nmol/L of Lp(a) protein, with corresponding race-appropriate percentiles. In accordance with NHLBI recommendations, values above the 75th percentile were considered to indicate increased risk, and were hence designated as elevated. Results: Median Lp(a) concentration did not significantly differ between the two groups (cases: 16.9 nmol/L, controls: 24.7 nmol/L; P=0.96). While the prevalence of elevated Lp(a) levels was increased among children with IAS (cases: 36%, controls: 24%), this difference did not reach statistical significance (P=0.32). The odds of having elevated Lp(a) were nearly two times that of healthy controls (OR=1.8, 95% CI=0.50–6.3); however, this also was not statistically significant. Conclusions: The present study demonstrates a qualitatively increased prevalence of elevated plasma Lp(a) concentration among children with non-neonatal IAS when compared to healthy children, using the gold-standard methodology for Lp(a) assessment. Expansion of the study to a larger population via multicenter collaboration will be necessary to definitively determine whether Lp(a) is a risk factor for IAS in children. Furthermore, given that genetic variation in the apo(a) gene is the major determinant of plasma Lp(a) concentration, apo(a) phenotyping may be useful to better define risk strata. These efforts are an important precursor to interventional studies evaluating Lp(a) management strategies in the secondary prevention of IAS in children.

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Study on serum Lipoprotein (a) level in preeclamptic Bangladeshi women

University Heart Journal ◽

10.3329/uhj.v4i2.2073 ◽

2009 ◽

Vol 4 (2) ◽

pp. 32-35

Author(s):

Noor E-Ferdous ◽

Mahmuda Khatun ◽

Md Abu Siddique ◽

Asma Ul Hosna ◽

Shirin Akter Begum ◽

...

Keyword(s):

Case Control Study ◽

Serum Lipoprotein ◽

Severe Preeclampsia ◽

College Hospital ◽

Lipoprotein A ◽

Medical College ◽

Mild Preeclampsia ◽

The Mean ◽

Average Serum ◽

Control Study

It is a case control study which was design to know the association of serum Lipoprotein (a) level in preeclamptic (PE) in women. This study was carried out in department of Obstetrics and Gynecology, Sir Salimullah Medical College Hospital, Mitford, Dhaka. Total number of subjects was 100. Out of which 50 were cases and 50 were controls. Cases were physically and clinically proved PE patients. Controls were age, parity and gestational age matched. Three ml of blood were collected from each subjects, serum fasting LP(a) level were measured The mean age of study group was 24.49 Â± 6.48 years. Serum Lipoprotein(a) level was 51.51 Â± 29.38mg/dl Vs 17.40 Â± 7.89 mg/dl in cases and controls respectively. This difference was statistically significant (p < 0.001). Mean serum Lipoprotein(a) level was found to be raised in severe preeclampsia (74.87mg/dl) and lowest in control subject Severe preeclampsia was found to be associated with higher level of lipoprotein (a) than both control (p < 0.01) and mild preeclamptic (p < 0.01) subjects. Mild preeclampsia was also found to have higher average serum Lipoprotein (a) than the normal (P < 0.01) subjects. Key Words: Lipoprotein(a), Preeclampsia, Bangladeshi women. doi:10.3329/uhj.v4i2.2073 University Heart Journal Vol. 4 No. 2 July 2008 p32-35

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Association between lipoprotein(a) concentration and the risk of stroke in the Chinese Han population: a retrospective case-control study

Annals of Translational Medicine ◽

10.21037/atm.2020.01.38 ◽

2020 ◽

Vol 8 (5) ◽

pp. 212-212 ◽

Cited By ~ 1

Author(s):

Hanhui Fu ◽

Dingding Zhang ◽

Rui Zhu ◽

Liying Cui ◽

Ling Qiu ◽

...

Keyword(s):

Case Control Study ◽

Case Control ◽

Chinese Han Population ◽

Retrospective Case ◽

Chinese Han ◽

Han Population ◽

Lipoprotein A ◽

Control Study

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Abstract 5093: Genetically Elevated Lipoprotein(a) and Risk of Myocardial Infarction - a Positive Mendelian Randomization Study

Circulation ◽

10.1161/circ.118.suppl_18.s_1144-a ◽

2008 ◽

Vol 118 (suppl_18) ◽

Author(s):

Pia Kamstrup ◽

Anne Tybjærg-Hansen ◽

Rolf Steffensen ◽

Børge G Nordestgaard

Keyword(s):

Myocardial Infarction ◽

Plasma Levels ◽

Case Control Study ◽

Mendelian Randomization ◽

Causal Effect ◽

Case Control ◽

Lipoprotein A ◽

Increased Risk ◽

Disease Study ◽

Control Study

Background: High levels of lipoprotein(a) (Lp(a)) associate with increased risk of myocardial infarction (MI). We tested whether this is a causal effect using a Mendelian randomization design. Methods: We genotyped for the Lp(a) kringle IV type 2 (KIV-2) size polymorphism, which explains 21% of variation in plasma levels of Lp(a). We used a cohort study of the Danish general population, The Copenhagen City Heart Study, including 9867 individuals followed for up to 16 years during which time 599 developed MI, and a case-control study, The Copenhagen Ischemic Heart Disease Study, including 1118 MI patients and 2234 controls. Results: First, increased plasma levels of Lp(a) associated with increased risk of MI (Lp(a) tertiles, trend: p<0.001). Second, number of KIV-2 repeats inversely associated with Lp(a) levels: mean Lp(a) levels were 56, 31, 20, and 15 mg/dL for the 1 st , 2 nd , 3 rd , and 4 th quartile of KIV-2 repeats, respectively (trend, p<0.001, Figure ). Third, multifactorially adjusted hazard ratios for MI were 1.6(95% CI:1.3–.2.0), 1.3(1.0 –1.7), and 1.1(0.9 –1.4) for individuals in the 1 st , 2 nd , and 3 rd quartile, respectively, as compared to individuals in the 4 th quartile of KIV-2 repeats (Figure ). Finally, in the case-control study, multifactorially adjusted odds ratios for MI were 1.5(1.2–1.9), 1.3(1.0 –1.6), and 1.2(1.0 –1.5) for individuals in the 1 st , 2 nd , and 3 rd quartile, respectively, as compared to individuals in the 4 th quartile of KIV-2 repeats. Conclusion: Since Lp(a) levels predict MI, and since Lp(a) KIV-2 genotype predicts both life-long increased Lp(a) levels and MI, increased Lp(a) levels appear to directly cause MI. Figure. Levels of lipoprotein (a) and risk of myocardial infarction by KIV-2

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