scholarly journals Estimation of Plasma Small Dense LDL Cholesterol From Classic Lipid Measures

2011 ◽  
Vol 136 (1) ◽  
pp. 20-29 ◽  
Author(s):  
Pornpen Srisawasdi ◽  
Sirirat Chaloeysup ◽  
Yaovalak Teerajetgul ◽  
Anothai Pocathikorn ◽  
Chonlaphat Sukasem ◽  
...  
2011 ◽  
Vol 412 (15-16) ◽  
pp. 1423-1427 ◽  
Author(s):  
Yoshifumi Fukushima ◽  
Satoshi Hirayama ◽  
Tsuyoshi Ueno ◽  
Tomotaka Dohi ◽  
Tetsuro Miyazaki ◽  
...  

2011 ◽  
Vol 5 (3) ◽  
pp. 215
Author(s):  
Torrance Laury ◽  
Parag Joshi ◽  
Abhinav Sharma ◽  
Gustavo Vazquez ◽  
Zhen Qian ◽  
...  

2011 ◽  
Vol 18 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Ikumi Sugino ◽  
Koji Kuboki ◽  
Tomoko Matsumoto ◽  
Eiichi Murakami ◽  
Chiaki Nishimura ◽  
...  

2017 ◽  
Vol 08 (09) ◽  
Author(s):  
Wahid Ali ◽  
Mukesh Kumar ◽  
Kauser Usman ◽  
Mohd Tasleem ◽  
Mohd Wamique

2008 ◽  
Vol 9 (1) ◽  
pp. 152-153
Author(s):  
Y. Ito ◽  
T. Hirano ◽  
M. Kinoshita ◽  
M. Shiba ◽  
T. Shoji ◽  
...  

2016 ◽  
Vol 157 (19) ◽  
pp. 746-752 ◽  
Author(s):  
László Márk ◽  
Győző Dani

The incidence and the public health importance of diabetes mellitus are growing continuously. Despite the improvement observed in the latest years, the leading cause of morbidity and mortality of diabetics are cardiovascular diseases. The diagnosis of diabetes mellitus constitutes such a high risk as the known presence of vascular disease. Diabetic dyslipidaemia is characterised by high fasting and postprandial triglyceride levels, low HDL level, and slightly elevated LDL-cholesterol with domination of atherogenic small dense LDL. These are not independent components of the atherogenic dyslipidaemia, but are closely linked to each other. Beside the known harmful effects of low HDL and small dense LDL, recent findings confirmed the atherogenicity of the triglyceride-rich lipoproteins and their remnants. It has been shown that the key of this process is the overproduction and delayed clearance of triglyceride-rich lipoproteins in the liver. In this metabolism the lipoprotein lipase has a determining role; its function is accelerated by ApoA5 and attenuated by ApoC3. The null mutations of the ApoC3 results in a reduced risk of myocardial infarction, the loss-of-function mutation of ApoA5 was associated with a 60% elevation of triglyceride level and 2.2-times increased risk of myocardial infarction. In case of diabetes mellitus, insulin resistance, obesity, metabolic syndrome and chronic kidney disease the non-HDL-cholesterol is a better marker of the risk than the LDL-cholesterol. Its value can be calculated by subtraction of HDL-cholesterol from total cholesterol. Target values of non-HDL-cholesterol can be obtained by adding 0.8 mmol/L to the LDL-cholesterol targets (this means 3.3 mmol/L in high, and 2.6 mmol/L in very high risk patients). The drugs of first choice in the treatment of diabetic dyslipidaemia are statins. Nevertheless, it is known that even if statin therapy is optimal (treated to target), a considerable residual (lipid) risk remains. For its reduction treatment of low HDL-cholesterol and high triglyceride levels is obvious by the administration of fibrates. In addition to statin therapy, fenofibrate can be recommended. Orv. Hetil., 2016, 157(19), 746–752.


Author(s):  
Andreas Krebs ◽  
Thomas Kratzin ◽  
Jürgen Doerfer ◽  
Karl Winkler ◽  
Michael Wurm ◽  
...  

AbstractGrowth hormone deficiency (GHD) and small for gestational age (SGA) status are associated with cardiovascular risks. We therefore, investigated antiatherogenic effects of growth hormone (GH).Subfractions of low-density lipoprotein (LDL) and high-density lipoprotein (HDL), lipoprotein-associated phospholipase AThe overall group showed post-treatment reductions of LDL cholesterol (LDL-C) (p=0.016), small-dense LDL cholesterol (sdLDL-C, p<0.001), Lp-PLA2 (p<0.001), and hsCRP (p=0.005), but increase of HDL2a cholesterol (HDL2a-C, p=0.025). SGA children revealed significant correlations between Lp-PLA2 and LDL-C and sdLDL-C both before and after GH, significant reductions of sdLDL-C, Lp-PLA2, hsCRP, and an increase of HDL2a-C. GHD children showed the same lipid responses, though not significantly.Children with GHD or born SGA may benefit from GH by growth acceleration and reduction of cardiovascular long-term risks.


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