Titlebook: Dyslipidemias; Pathophysiology, Eva Abhimanyu Garg Book 2015 Humana Press 2015 Abetalipoproteinemia.Chronic kidney disease.Drug-induced dys

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Monogenic Hypercholesterolemias,lesterol and a high risk of premature cardiovascular disease (CVD). There are autosomal dominant and recessive MHs, although the latter are very rare. The most common and best studied MH is familial hypercholesterolemia (FH), an autosomal codominant disease caused by mutations in the LDL receptor ge

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Primary Hypertriglyceridemia,terns of inheritance. The exception is “familial chylomicronemia,” in which severe HTG results from autosomal recessive inheritance rare loss-of-function mutations in genes such as lipoprotein lipase (.), apolipoprotein C-II (.), apolipoprotein A-V (.), lipase maturation factor 1 (.), and glycosyl-p

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Genetic Abetalipoproteinaemia and Hypobetalipoproteinaemia, of the condition, together with the severity of the mutation or mutations present. These disorders may or may not be associated with clinical manifestations such as fat malabsorption, growth failure, fat-soluble vitamin deficiency, fatty liver disease, and neuro-ophthalmological dysfunction. We hav

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Lipodystrophies and Dyslipidemias,o developing insulin resistance and its complications such as premature diabetes mellitus, hypertriglyceridemia, low levels of high-density lipoprotein (HDL) cholesterol, and nonalcoholic hepatic steatosis. The severity of metabolic complications in general parallels the extent of body fat loss, and

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Perspectives on Cholesterol Guidelines,of Health. These guidelines were produced by the National Cholesterol Education Program. From this program, an Adult Treatment Panel (ATP) has organized the major sets of guidelines. Three reports were issued by ATP. The third and last was updated by a smaller panel in 2004. More recently, the Natio

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Nutrition and Coronary Heart Disease Prevention,sodium to