Monoclonal antibodies can precipitate low-density lipoprotein. II. Radioimmunoassays with single and combined monoclonal antibodies for determining apolipoprotein B in serum of patients with coronary artery disease.

1985 ◽  
Vol 31 (10) ◽  
pp. 1659-1663 ◽  
Author(s):  
S Marcovina ◽  
B A Kottke ◽  
S J Mao

Abstract We have established four lines of monoclonal antibodies against human low-density lipoproteins (LDL) that, mixed in equal proportions, can precipitate LDL in gel and so can be used for apolipoprotein (apo) B determination in plasma. One monoclonal antibody (clone A), with a relatively low binding affinity to LDL (ka = 0.6 X 10(9) L/mol) and recognizing only two species of apo B, significantly underestimated the concentration of apo B in 74 patients with and 27 without coronary artery disease (CAD). High-affinity monoclonal antibody C (Ka = 3.8 X 10(9) L/mol), which recognized all four apo B species, gave the same value for apo B as determined with the mixture of monoclonal antibodies. The latter results (by radioimmunoassay, y) correlated well with those by radial immunodiffusion (chi): y = 0.994 chi + 0.003 (r = 0.987). The CAD patients showed an increased concentration of apo B as compared to the angiographically documented CAD-negative patients. Except for the values determined by clone B (p = 0.07), the increase was statistically significant (p = 0.002-0.018) for values determined by use of the other clones or their mixture.

1983 ◽  
Vol 29 (11) ◽  
pp. 1898-1903 ◽  
Author(s):  
J G Patton ◽  
J J Badimon ◽  
S J Mao

Abstract We describe the importance of the low-density lipoproteins (LDL) used in preparing radioimmunoassay standard curves and the clinical application of monoclonal antibodies to LDL. LDL isolated from five normal men produced five parallel displacement curves with conventional mouse antiserum but there was a significant difference of immunoreactivity among the LDL. None of our four monoclonal antibodies could eliminate the heterogeneous immunoreactivity of different LDL. Thus, the determination of plasma apolipoprotein (apo) B will vary depending on the selection of LDL standards, and the comparison of absolute apo B values between laboratories will be of questionable value unless they use the same LDL standard. Nonetheless, in a radioimmunoassay our monoclonal antibody, LP-22, detected a more significant (p less than 0.0001) increase of plasma apo B in patients with angiographically documented coronary artery disease than did conventional antiserum (p less than 0.001). In addition, the overlap of apo B concentrations for patients with and without disease was less when monoclonal antibody LP-22 was used. We conclude that patients with coronary artery disease have a significant increase in the form of plasma apo B that is specifically recognized by LP-22 monoclonal antibody. Perhaps monoclonal antibodies will be able to sort out the various components of apo B, delineate their possible atherogenic roles, and offer us a predictive value for diagnosing such patients.


2004 ◽  
Vol 174 (2) ◽  
pp. 343-347 ◽  
Author(s):  
Kazunori Shimada ◽  
Hiroshi Mokuno ◽  
Eriko Matsunaga ◽  
Tetsuro Miyazaki ◽  
Katsuhiko Sumiyoshi ◽  
...  

2022 ◽  
Vol 8 ◽  
Author(s):  
Younan Yao ◽  
Jin Liu ◽  
Bo Wang ◽  
Ziyou Zhou ◽  
Xiaozhao Lu ◽  
...  

Background: The prognostic value of elevated lipoprotein(a) [Lp(a)] in coronary artery disease (CAD) patients is inconsistent in previous studies, and whether such value changes at different low-density-lipoprotein cholesterol (LDL-C) levels is unclear.Methods and Findings: CAD patients treated with statin therapy from January 2007 to December 2018 in the Guangdong Provincial People's Hospital (NCT04407936) were consecutively enrolled. Individuals were categorized according to the baseline LDL-C at cut-off of 70 and 100 mg/dL. The primary outcome was 5-year all-cause death. Multivariate Cox proportional models and penalized spline analyses were used to evaluate the association between Lp(a) and all-cause mortality. Among 30,908 patients, the mean age was 63.1 ± 10.7 years, and 76.7% were men. A total of 2,383 (7.7%) patients died at 5-year follow-up. Compared with Lp(a) <50 mg/dL, Lp(a) ≥ 50 mg/dL predicted higher all-cause mortality (multivariable adjusted HR = 1.19, 95% CI 1.07–1.31) in the total cohort. However, when analyzed within each LDL-C category, there was no significant association between Lp(a) ≥ 50 mg/dL and higher all-cause mortality unless the baseline LDL-C was ≥ 100 mg/dL (HR = 1.19, 95% CI 1.04–1.36). The results from penalized spline analyses were robust.Conclusions: In statin-treated CAD patients, elevated Lp(a) was associated with increased risks of all-cause death, and such an association was modified by the baseline LDL-C levels. Patients with Lp(a) ≥ 50 mg/dL had higher long-term risks of all-cause death compared with those with Lp(a) <50 mg/dL only when their baseline LDL-C was ≥ 100 mg/dL.


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