Dissociation-Enhanced Lanthanide Fluorescence Immunoassay of Lipoprotein(a) in Serum

1992 ◽  
Vol 38 (6) ◽  
pp. 853-859 ◽  
Author(s):  
G Jürgens ◽  
A Hermann ◽  
D Aktuna ◽  
W Petek
Keyword(s):  
Human Serum ◽  
Large Scale ◽  
Solid Phase ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Serum Lipoprotein ◽  
Polyclonal Antiserum ◽  
Apo B ◽  
Lipoprotein A ◽  
Ischemic Cerebrovascular Disease

Abstract Lipoprotein(a), a human serum lipoprotein structurally related to low-density lipoprotein (LDL), contains in addition to apolipoprotein B (apo B) apolipoprotein(a) [apo(a)], a glycoprotein with a strong homology to plasminogen. Lp(a) is a risk factor for coronary heart disease and ischemic cerebrovascular disease. Several immunological techniques are used to quantify Lp(a) in human serum, including radioimmunoassays, rocket immunoelectrophoresis, and enzyme-linked immunosorbent assays. Only the last method is suitable for large-scale clinical studies. We describe another solid-phase immunoassay, based on the dissociation-enhanced lanthanide fluorescence system Delfia (Wallac Oy), and outline the technical details. A polyclonal antiserum directed against Lp(a) was used as the capture antibody. Two kinds of detection antibodies were applied, a polyclonal antiserum against apo B and the polyclonal antiserum against Lp(a). The results agree excellently with the values estimated by rocket immunoelectrophoresis. This assay is easily established, measures Lp(a) in a wide concentration range, and is suitable for screening large populations.

Changes in serum lipoprotein(a) and lipids during treatment of hyperthyroidism

1995 ◽  
Vol 41 (2) ◽  
pp. 226-231 ◽  
Author(s):  
A W Kung ◽  
R W Pang ◽  
I Lauder ◽  
K S Lam ◽  
E D Janus
Keyword(s):  
Thyroid Hormones ◽  
Geometric Mean ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Serum Lipoprotein ◽  
Transitional Period ◽  
Lipoprotein Cholesterol ◽  
Apo B ◽  
Lipoprotein A ◽  
Free Thyroxine Index

Abstract Because of suggestions that thyroid hormones modulate serum lipoprotein(a) [Lp(a)] concentration, we evaluated prospectively the serial changes of serum Lp(a), measured as apolipoprotein(a) [apo(a)], and other lipoproteins in 40 subjects with hyperthyroidism treated with radioactive iodine (RAI) therapy. Hyperthyroid patients had lower (P < 0.001) concentrations of apo(a), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and apo B, but higher apo A-I concentrations compared with age-matched controls [geometric mean (range)]; apo(a) 81 (17-614) vs 187 (17-1808 IU/L): TC 4.07 +/- 0.8 vs 5.22 +/- 1.00 mmol/L (mean +/- SD); LDL-C 2.47 +/- 0.89 vs 3.40 +/- 0.88 mmol/L; HDL-C 1.05 +/- 0.33 vs 1.24 +/- 0.34 mmol/L; apo B 0.66 +/- 0.23 vs 1.13 +/- 0.34 g/L, and apo A-I 2.07 +/- 0.42 vs 1.46 +/- 0.28 g/L, respectively. Euthyroidism was associated with normalization of serum TC, LDL-C, and apo B within 1 month of treatment. However, apo(a) required 4 months to normalize, and HDL-C and apo A-I were still abnormal 6 months after RAI. Serum apo(a), TC, LDL-C, and apo B were negatively correlated with serum thyroxine (T4), free thyroxine index, and triiodothyronine (T3) and positively correlated with thyrotropin during the transitional period from hyperthyroidism to euthyroidism. Parallel changes of these lipoproteins and thyroid hormones were also observed after treatment of hyperthyroidism. In conclusion, thyroid hormones do modulate lipoproteins, particularly Lp(a). The delay in normalization of apo(a) but not LDL suggests an effect on apo(a) production rather than on LDL removal.

Biological variability of cholesterol, triglyceride, low- and high-density lipoprotein cholesterol, lipoprotein(a), and apolipoproteins A-I and B

1994 ◽  
Vol 40 (4) ◽  
pp. 574-578 ◽  
Author(s):  
S M Marcovina ◽  
V P Gaur ◽  
J J Albers
Keyword(s):  
High Density Lipoprotein ◽  
Ldl Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Hdl Cholesterol ◽  
High Density ◽  
Biological Variability ◽  
Apo B ◽  
Lipoprotein A ◽  
The Individual

Abstract Biological variability is a major contributor to the inaccuracy of cardiovascular risk assessments based on measurement of lipids, lipoproteins, or apolipoproteins. We obtained estimates of biological variation (CVb) for 20 healthy adults and calculated the percentiles of CVb as an expression of the variability of CVb among individuals for cholesterol, triglyceride, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, apolipoprotein (apo) A-I, apo B, and lipoprotein(a) [Lp(a)] by four biweekly measurements of these analytes. The CVb for the group was approximately 6-7% for cholesterol, HDL cholesterol, apo A-I, and apo B; approximately 9% for LDL cholesterol; and 28% for triglyceride. However, for each analyte, there was a considerable variation of CVb among individuals. For all analytes except Lp(a), there was no relation between the individual's CVb and the analyte concentration. Lp(a) was inversely related to CVb, and there was a very wide variation in the CVb for Lp(a) among the participants, ranging from 1% to 51%. The number of independent analyses to perform to accurately assess an individual's risk for coronary artery disease should be determined on the basis of the individual CVb for a given analyte rather than the average CVb.

Relation of lipoprotein(a) in 11- to 19-year-old adolescents to parental cardiovascular heart disease

1993 ◽  
Vol 39 (3) ◽  
pp. 477-480 ◽  
Author(s):  
J C Vella ◽  
E Jover
Keyword(s):  
Heart Disease ◽  
Ldl Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Hdl Cholesterol ◽  
Young Population ◽  
Serum Samples ◽  
Apo B ◽  
Lipoprotein A ◽  
Cardiovascular Heart Disease

Abstract We studied several risk factors in relation to parental cardiovascular heart disease: total cholesterol, triglycerides, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, apolipoprotein (apo) A-I, apo B, and lipoprotein(a) [Lp(a)] were determined in 322 serum samples (43 from subjects with and 279 without parental cardiovascular heart disease). The distribution of Lp(a) concentrations in our young population was similar to that of other white populations, i.e., markedly skewed, with higher frequencies at low values. As compared with children whose parents did not report cardiovascular heart disease, those with affected parents had a higher mean Lp(a) (0.23 vs 0.18 g/L; P < 0.05). Moreover, 42% of the children with parental cardiovascular heart disease, but only 19% of those with no parental cardiovascular heart disease, exhibited Lp(a) values > 0.30 g/L. These results suggest not only that Lp(a) is an important risk factor for cardiovascular heart disease, but also that Lp(a) is more strongly related to the risk of cardiovascular heart disease than are HDL- and LDL-cholesterol and apo A-I and B.

A monoclonal-antibody-based enzyme-linked immunosorbent assay of lipoprotein(a)

1990 ◽  
Vol 36 (2) ◽  
pp. 192-197 ◽  
Author(s):  
W L Wong ◽  
D L Eaton ◽  
A Berloui ◽  
B Fendly ◽  
P E Hass
Keyword(s):  
Monoclonal Antibody ◽  
Immunosorbent Assay ◽  
Clinical Laboratory ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Enzyme Linked Immunosorbent Assay ◽  
Apo B ◽  
Lipoprotein A ◽  
Premature Coronary Heart Disease ◽  
Large Populations

Abstract Lipoprotein(a) [Lp(a)] is a low-density lipoprotein (LDL)-like lipoprotein particle recently described as a risk factor for premature coronary heart disease, stroke, and atherosclerosis. Structurally, Lp(a) is similar to LDL in that it has comparable lipid composition and contains apolipoprotein B-100 (apo B-100). In addition, Lp(a) contains the glycoprotein apolipoprotein(a) [apo(a)], which is disulfide-linked to apo B-100. The recent awareness of a striking correlation between atherosclerosis and concentrations of Lp(a) in plasma prompted our development of an accurate quantitative assay for plasma Lp(a), a monoclonal-antibody-based enzyme-linked immunosorbent assay for Lp(a) that is shown to be sensitive, precise, and highly specific. The response to several isoforms of Lp(a) is linear, and as many as 80 samples can be quantified on one plate. This easily performed assay is suitable for use in the clinical laboratory and for screening large populations.

scholarly journals Characterization of apolipoprotein B from human serum low density lipoprotein in n-dodecyl octaethyleneglycol monoether: an electron microscope study.

1980 ◽  
Vol 87 (3) ◽  
pp. 555-561 ◽  
Author(s):  
G Zampighi ◽  
J A Reynolds ◽  
R M Watt
Keyword(s):  
Apolipoprotein B ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Serum Lipoprotein ◽  
Low Density ◽  
Apo B ◽  
Shaped Particle ◽  
Orderly Fashion ◽  
High Degree

We have studied the structure of the totally delipidated polypeptide (apolipoprotein B [apo B]) present in low-density serum lipoprotein in detergent (n-dodecyl octaethyleneglycol monoether) solution by electron microscopy. The protein-detergent complex appears as a rod-shaped particle, 75-80 nm long and 4.5-5.5 nm wide. The volume of this particle is consistent with the previously published composition reported by Watt and Reynolds (1980, Biochemistry 19:1593-1598) of two copies of apo B and five to six equivalent micelles of detergent. The asymmetric particle possesses a high degree of flexibility and a strong tendency to self-associate in an orderly fashion. The extent of this association is pH dependent.

Two new monoclonal antibody-based enzyme-linked assays of apolipoprotein B.

1986 ◽  
Vol 32 (8) ◽  
pp. 1484-1490 ◽  
Author(s):  
S G Young ◽  
R S Smith ◽  
D M Hogle ◽  
L K Curtiss ◽  
J L Witztum
Keyword(s):  
Monoclonal Antibody ◽  
Solid Phase ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Apo B ◽  
Competitive Assay ◽  
Microtiter Plates ◽  
Ldl Particles ◽  
Direct Assay

Abstract We describe two new monoclonal antibody-based, solid-phase immunoenzymometric assays for the quantification of apolipoprotein (apo) B in plasma: a competitive assay and a direct assay. For both, we utilize 96-well microtiter plates and native low-density lipoprotein (LDL) for preparing the standard curve. A single monoclonal antibody, MB24, is used in the competitive assay. The direct assay involves use of two monoclonal antibodies, MB24 and MB47. These two antibodies bind to distinct, unrelated apo B epitopes expressed by all LDL particles, and both antibodies detect apo B in very low-density and intermediate-density lipoproteins as well as LDL. With the two-step competitive assay, which involves use of LDL-coated microtiter plates, the intra- and interassay reproducibility in plasma apo B measurements averaged 6% and 12%, respectively. In the one-step direct assay, which takes less than 2 h for completion, plasma samples and peroxidase-labeled MB24 are incubated simultaneously on MB47-coated microtiter wells. The amount of labeled MB24 bound to lipoproteins trapped by MB47 is proportional to apo B concentration. With the direct assay, intra- and interassay CVs averaged 7% and 12%, respectively. These assays are simple, reproducible, involve convenient incubation intervals, and do not require radioisotopes; thus they can be widely applied in clinical laboratories.

scholarly journals Increased Serum Lipoprotein(a) Concentrations after Growth Hormone (GH) Treatment in Patients with Isolated GH Deficiency

1996 ◽  
Vol 33 (4) ◽  
pp. 330-334 ◽  
Author(s):  
Domhnall J O'Halloran ◽  
Gilbert Wieringa ◽  
Agathocles Tsatsoulis ◽  
Stephen M Shalet
Keyword(s):  
Growth Hormone ◽  
Gh Deficiency ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Serum Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Low Density Lipoprotein Cholesterol ◽  
Gh Treatment ◽  
Lipoprotein A ◽  
Lipid Fractions

Fourteen post-pubertal subjects (11 male, 3 female) with isolated growth hormone (GH) deficiency were treated with a low dose (0·125 U/kg for the first 4 weeks and thereafter 0·025 U/kg/week) daily sc GH injection for 1 year. Fasting blood samples were collected at entry into the study and subsequently at 3 monthly intervals for estimation of serum cholesterol, high-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol and lipoprotein(a) [Lp(a)]. Serum Lp(a) increased progressively during the treatment period (by analysis of variance) and was 41% higher at 12 months ( P < 0·02) despite the fact that five patients showed little or no change. There was no significant change in any of the other lipid fractions. These observations are of concern as Lp(a) is an independent risk factor for cardiovascular disease and should introduce a cautionary note into the enthusiastic efforts to offer GH replacement to all GH deficient adults.

Decreases in Apolipoprotein(a) after Renal Transplantation: Implications for Lipoprotein(a) Metabolism

1992 ◽  
Vol 38 (3) ◽  
pp. 353-357 ◽  
Author(s):  
I W Black ◽  
D E Wilcken
Keyword(s):  
Renal Transplantation ◽  
Creatinine Clearance ◽  
Ldl Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Apo B ◽  
Lipoprotein A ◽  
Patients Âgés ◽  
Apolipoprotein A ◽  
End Stage

Abstract Serum concentrations of apolipoprotein(a) [apo(a)], the unique glycoprotein of lipoprotein(a), are increased in patients with end-stage renal failure. We prospectively studied serum apo(a) and other lipoproteins in 20 consecutive patients, ages 46 +/- 11 years, before and for six months after successful renal transplantation. All patients received cyclosporine, and no patient was treated for hyperlipidemia. The mean creatinine clearance increased from 7.5 mL/min before transplant surgery to 40.9 mL/min six months afterwards (P less than 0.001). Apo(a) decreased from a median of 403 units/L before transplantation to 184 units/L at one week (P less than 0.001) and was 170 units/L (P less than 0.001) at six months. For the assay used, 1 unit of apo(a) is equivalent to 1 mg of lipoprotein(a). In contrast, from baseline to six months, increases were found for low-density lipoprotein (LDL) cholesterol (P = 0.03), high-density lipoprotein cholesterol (P = 0.06), apo B (P = 0.07), and apo A-I (P = 0.01). The decrease in apo(a) in individual patients was significantly correlated with the increase in creatinine clearance (r = -0.48, P less than 0.001). The single patient who developed nephrotic syndrome after renal transplantation had marked increases in apo(a) (693-1595 units/L), apo B, and LDL cholesterol, which paralleled the degree of proteinuria. These findings suggest that abnormal renal function affects the regulation of lipoprotein(a) metabolism.

Effect of weight loss on serum lipoprotein(a) concentrations in an obese population

1991 ◽  
Vol 37 (7) ◽  
pp. 1191-1195 ◽  
Author(s):  
James P Corsetti ◽  
Judith A Sterry ◽  
Janet D Sparks ◽  
Charles E Sparks ◽  
Michael Weintraub
Keyword(s):  
Weight Loss ◽  
Weight Reduction ◽  
Density Lipoprotein ◽  
Serum Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Double Blind Study ◽  
Double Blind ◽  
Apo B ◽  
Lipoprotein A ◽  
Obese Population

Abstract To assess the distribution of serum concentrations of the atherogenic lipoprotein(a) [Lp(a)] in an obese population and the possible effects of weight reduction, we determined Lp(a) in 52 white, moderately obese subjects (16 men and 36 women). The subjects were participating in a weight-reduction program of diet, exercise, and behavior modification plus combination anorectic drug therapy (fenfluramine and phentermine). This placebo-controlled, double-blind study lasted 104 weeks. We also determined concentrations of fasting insulin, triglycerides, total cholesterol, high-density lipoprotein cholesterol, apolipoprotein (apo) A-I, low-density lipoprotein cholesterol, and apo B. Results showed the following: a highly skewed, nongaussian distribution of serum Lp(a) values in the obese population, virtually identical to that reported for healthy adults; no clinically significant change in Lp(a) concentrations with weight loss; and further evidence of normalization of insulin, lipid, and lipoprotein concentrations with weight loss.

scholarly journals Elevated lipoprotein (a) levels are associated with the acute myocardial infarction in patients with normal low-density lipoprotein cholesterol levels

2019 ◽  
Vol 39 (4) ◽  
Author(s):  
Gaojun Cai ◽  
Zhiying Huang ◽  
Bifeng Zhang ◽  
Lei Yu ◽  
Li Li
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Large Scale ◽  
Late Onset ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Lipoprotein A

Abstract Elevated lipoprotein (a) [Lp(a)] and coronary artery disease (CAD) risk has been renewed interested in recent years. However, the association between Lp(a) and acute myocardial infarction (AMI) risk in patients with normal low-density lipoprotein cholesterol (LDL-C) levels has yet to been established. A hospital-based observational study including 558 AMI patients and 1959 controls was conducted. Lp(a) level was significantly higher in AMI patients with normal LDL-C levels than that in non-CAD group (median: 134.5 mg/l vs 108 mg/l, P<0.001). According to Lp(a) quartiles (Q1, <51 mg/l; Q2, 51–108 mg/l; Q3, 108–215 mg/l; Q4, ≥215 mg/l), the incidence of AMI increased with the elevated Lp(a) quartiles (P<0.001 and P for trend<0.001). Logistic regression analysis suggested that patients with Q3 and Q4 of Lp(a) values had 1.666 (95%CI = 1.230–2.257, P<0.001) and 1.769 (95%CI = 1.305–2.398, P< 0.001) folds of AMI risk compared with patients with Q1, after adjusting for traditional confounders. Subgroup analyses stratified by gender and age showed that the association only existed in male and late-onset subgroups. In addition, we analyzed the association of Lp(a) with AMI risk in different cut-off values (cut-off 1 = 170 mg/l, cut-off 2 = 300 mg/l). A total of 873 (34.68%) and 432 (17.16%) participants were measured to have higher Lp(a) levels according to cut-off 1 and cut-off 2, respectively. Participants with high Lp(a) levels had 1.418- (cut-off1, 95%CI = 1.150–1.748, P<0.001) and 1.521- (cut-off 2, 95%CI = 1.179–1.963, P< 0.001) folds of AMI risk compared with patients with low Lp(a) levels. The present large-scale study revealed that elevated Lp(a) levels were associated with increased AMI risk in Chinese population with normal LDL-C levels.

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