Lipoprotein(a) level is higher inpatients with familial hypercholesterolaemia than in normal healthy subjects, contribution of variants in the LPA gene

2017 ◽  
Vol 263 ◽  
pp. e207
Author(s):  
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Mahtab Sharifi ◽  
Devaki Nair ◽  
Anijly Jain ◽  
Jahm Persuad ◽  
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Adriana Saltijeral Cerezo ◽  
Rodrigo Alonso ◽  
Pedro Mata

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...  

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Morio ITO ◽  
Hideki OZAWA ◽  
Tomonori WAKI ◽  
Yasuhiro MAGARI ◽  
...  

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1988 ◽  
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pp. 1262-1263 ◽  
Author(s):  
K. Widhalm ◽  
Dieter Genser ◽  
Tissa Vitarana ◽  
Gaya Colombage ◽  
Vasanthi Bandaranayake ◽  
...  

1992 ◽  
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M. Libura ◽  
T. Sacha ◽  
...  

2012 ◽  
Vol 1 (3) ◽  
pp. 1-9 ◽  
Author(s):  
Mary Seed ◽  
D John Betteridge ◽  
Jackie Cooper ◽  
Muriel Caslake ◽  
Paul N Durrington ◽  
...  

Objective To assess the relationship of levels of inflammatory risk markers to presence of clinical coronary artery disease (CAD) in patients with treated heterozygous familial hypercholesterolaemia. Design A cross-sectional study of patients on the Simon Broome Familial Hyperlipidaemia Register. Setting Six hospital outpatient clinics in the UK. Participants A total of 211 men and 199 women with heterozygous familial hypercholesterolaemia. Main outcome measures Analysis of conventional risk factors and concentrations of high-sensitivity C-reactive protein (hsCRP), lipoprotein (a), serum intercellular adhesion molecule (sICAM), interIeukin-6 (IL-6) and lipoprotein-associated phospholipase A2 (LpPLA2) mass. Results CAD was present in 104 men and in 55 women; the mean ages of onset were 43.1 and 46.5 years, respectively. On univariate analysis there was a positive relationship of CAD with age, male sex, smoking, IL-6 and sICAM, and an inverse relationship with low-density lipoprotein (LDL) and LpPLA2. On multivariate analysis, age, smoking, low LDL and low LpPLA2 were associated with CAD. When LpPLA2 values were adjusted for apoB and aspirin usage, there was no significant difference between those with and without CAD. Only age and smoking were independently associated with CAD in men, and IL-6 and lipoprotein(a) in women. Conclusions Although on univariate analysis inflammatory marker levels were associated with CAD in these patients, the majority of the associations, including that for hsCRP, disappeared when corrected for smoking and apoB. This may be because atherosclerotic plaques in these statin-treated patients were quiescent or an effect of aspirin usage. In this observational study newer risk markers were not usefully associated with the presence or absence of symptomatic CAD.


1991 ◽  
Vol 37 (4) ◽  
pp. 576-578 ◽  
Author(s):  
C M Huang ◽  
H G Kraft ◽  
R E Gregg

Abstract We describe a modified immunoblotting method for phenotyping lipoprotein(a) [Lp(a)]. This immunoblotting procedure uses commercially available reagents that have a long shelf life. The method is sensitive and takes only 18 microL of sera. Lp(a) phenotyping can be performed on sera stored at 4 degrees C for as much as a week or at -80 degrees C for as long as a year. In a study of 145 unrelated healthy subjects, we found Lp(a) allelic frequencies of LpF = 1.8%, LpB = 2.6%, LpS1 = 5.1%, LpS2 = 14.8%, LpS3 = 35.9%, LpS4 = 11.6%, and LpO = 28.0%.


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