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Lipoprotein lipase deficiency/type I hyperlipoproteinemia
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
A distinct molecular abnormality in the lipoprotein lipase enzyme complex has been defined as a deficiency in the apolipoprotein C-II (apoC-II) activator of the complex [59–65]. These patients tend to present clinically later than those with classic lipoprotein lipase deficiency, in post-adolescence or adult life. The nature of the defect was suggested in the first patient who had displayed hyperlipemia and no activity of lipoprotein lipase, when the concentration of triglycerides fell sharply following a transfusion of blood for anemia. It was demonstrated that his plasma completely lacked apoC-II.
Fever In Inherited and Metabolic Disorders
Published in Benedict Isaac, Serge Kernbaum, Michael Burke, Unexplained Fever, 2019
The increase in triglycerides in either or both of these particles (>1000 mg/dl), lead to lipemia retinalis, eruptive type of skin xanthomata, and attacks of acute pancreatitis, making this nosological entity easily recognized. The presence of “milky” appearing plasma, and an overlying creamy layer in refrigerated plasma obtained from a fasting patient, establish the correct diagnosis. Confirmation may be achieved through analysis of plasma triglycerides (>1000 mg/dl), cholesterol (within normal limits), plasma lipoproteins (elevated VLDL), and quantification of lipoprotein lipase and apolipoprotein C-II.19,20
Beneficial Effects of Omega-3 Fatty Acids on Cardiovascular Disease
Published in Catherina Caballero-George, Natural Products and Cardiovascular Health, 2018
Estela Guerrero De León, Mahabir Prashad Gupta, Juan Antonio Morán-Pinzón
Even though risk management of coronary heart disease (CHD) has historically focused primarily on low-density lipoproteins (LDL) targets, greater emphasis recently has been placed on non-high-density lipoproteins (HDL) and apolipoprotein B (apo B) as more robust predictors of CHD death. Also, high plasma triglyceride (TG) levels represent a risk factor for atherosclerosis and related cardiovascular disease (Labreuche et al., 2009), and treatment with ω–3 PUFAs is an established intervention to reduce TGs (Harris, 2013; Mori, 2014). The role of TGs in the development of CHD is a function of several pathophysiological factors such as: (1) In normal conditions, TGs are transported mainly by TG-rich lipoproteins, such as very low-density lipoproteins (VLDL) derived from the liver and chylomicrons (CMs) derived from the intestine. After lipoprotein lipase (LPL) mediated triglyceride hydrolysis to free fatty acids (FFAs), the remaining lipoproteins, including LDL, are formed. Thus, it is considered that hypertriglyceridemia can generate an excessive amount of highly atherogenic LDL (Goldberg et al., 2011; Schwartz and Reaven, 2012) (2). In hypertriglyceridemic conditions, the metabolism of VLDL shifts from a system dominated by apolipoprotein E (apo E), and characterized by its rapid elimination from vascular circulation, to a system dominated by apolipoprotein C III (apo C III), which is characterized by a preferential conversion of TG-rich lipoproteins into small amounts of highly dense atherogenic LDL.
Serum miRNA-146a and vitamin D values in chronic renal ailment with and without comorbid cardiovascular disease
Published in Egyptian Journal of Basic and Applied Sciences, 2023
Fatma K. A. Hamid, Alshaymaa M. Alhabibi, Mona A. Mohamed, Hanaa Hussein El-Sayed, Nehad Rafaat Ibrahim, Ghadir Mohamed Hassan Elsawy, Entsar M. Ahmad
Dyslipidemia is one of the most common complications of chronic renal failure (CRF) and usually parallels the deterioration in renal function. It progresses with the stage of CKD [21]. The most prevalent lipid anomaly in CKD patients is hypertriglyceridemia, which is predominantly brought on by increased lipoprotein triglyceride levels and delayed triglyceride breakdown [22]. Increased serum levels of apolipoprotein C (Apo C) make it less likely for triglyceride-rich lipoproteins to be broken down, which causes higher triglyceride levels in CKD patients [23]. In a recent one-year prospective analysis of 150 patients with CKD stages 1 to 5, triglyceride levels were found to rise with CKD development, peaking in CKD stage 4 [24]. Elevated triglycerides and low HDL-C in CKD patients have been associated with a high frequency of cardiovascular events [25]. Similar to this, those with advanced stages of CKD are more likely to have lipid profiles with high amounts of triglyceride-rich lipoproteins [26].
Clinical trials of eicosapentaenoic acid (EPA) prescription products for the treatment of hypertriglyceridemia
Published in Expert Opinion on Pharmacotherapy, 2019
In MARINE, the effect of icosapent ethyl on lipoproteins was also investigated, as these are also indicators of cardiovascular disease. Thus, apolipoprotein B-100 (ApoB, which is the major protein constituent of the particles of LDL), intermediate-density lipoprotein (IDL) and very low-density lipoprotein (VLDL), may be a better predictor of coronary artery risk than LDL cholesterol itself [16]. Apolipoprotein C-III (ApoC-III) is an important regulator of triglyceride-rich lipoprotein metabolism and triglyceride homeostasis, and elevated levels may lead to atherosclerosis [17]. Remnant lipoproteins are a sub-fraction of triglyceride-rich lipoproteins composed primarily of IDL and VLDL, and these remnants are predictive for cardiovascular events in subjects with coronary artery disease, after they have achieved their LDL cholesterol goals with statins [18].
Applications of multiple reaction monitoring targeted proteomics assays in human plasma
Published in Expert Review of Molecular Diagnostics, 2019
Georgia Kontostathi, Manousos Makridakis, Jerome Zoidakis, Antonia Vlahou
Bipolar disorder, also known as manic-depressive illness, accounted for 44,015 incidents in 2016 [100]. Knochel et al. [101] applied MRM (Tier 2 study) to investigate protein abundance differences in plasma from patients with schizophrenia (SZ), bipolar disorder (BD) and individuals with no evidence of these diseases (n = 147) (Table S1). Out of 42 tested proteins, 19 were detected at different (p < 0.05) abundance levels in cases (SZ/BD) versus controls, whereas 5 proteins were differentially expressed (p < 0.05) between BD and SZ. Apolipoprotein C was highlighted, as it has been linked to brain morphological changes in both BD and SZ. In this study, a correlation of the proteomics data with clinical characteristics pertinent to the above neurological diseases (e.g. psychomotor speed) was performed, however, adjustments for the received medication were not made [101].