Genetics of Triglycerides and the Risk of Atherosclerosis.

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Term Occurence Count Dictionary
abetalipoproteinemia 1 endocrinologydiseases
familial hypercholesterolemia 1 endocrinologydiseases
hypertriglyceridemia 36 endocrinologydiseases
hypobetalipoproteinemia 1 endocrinologydiseases
obesity 2 endocrinologydiseases

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abetalipoproteinemia 22057 that are associated with a range of other lipoprotein, biochemical and clinical abnormalities, such as abetalipoproteinemia and homozygous hypobetalipoproteinemia, which result, respectively, from bi-allelic mutations in MTTP
familial hypercholesterolemia 6153 Severe hypertriglyceridemia >10 mmol/L has a population frequency somewhat lower than heterozygous familial hypercholesterolemia [[]].Hypertriglyceridemia and AtherosclerosisUsing these definitions, the assimilated understanding
hypertriglyceridemia 3774 HypertriglyceridemiaHypertriglyceridemia is a commonly ascertained clinical phenotype. A proposed simplified definition of hypertriglyceridemia is based on somewhat arbitrary but clinically useful consensus thresholds [[]]. A normal TG level is
hypertriglyceridemia 5342 HypertriglyceridemiaThe distribution of fasting TG levels in North America permits approximation of patient numbers with hypertriglyceridemia according to the clinical cut-points proposed above. From the Canadian Heart Health Surveys, the mean
hypertriglyceridemia 5828 Assuming similar distributions of this trait in contemporary westernized societies, mild-to-moderate hypertriglyceridemia could be as prevalent as one in four people at the low-end of the definition. The traditional cut-point
hypertriglyceridemia 6060 top 5th percentile that was used to define “hyperlipoproteinemia type 4” is 3.3 mmol/L. Severe hypertriglyceridemia >10 mmol/L has a population frequency somewhat lower than heterozygous familial hypercholesterolemia
hypertriglyceridemia 6345 definitions, the assimilated understanding of biochemistry is that for individuals with mild-to-moderate hypertriglyceridemia , the predominant lipoprotein disturbance is VLDL, their remnants, and IDL [[]]. Chylomicrons can also
hypertriglyceridemia 7237 additively to further increase risk.From the population distribution of TG levels, most patients with “ hypertriglyceridemia ” fall within the mild-to-moderate range, and thus any potential atherosclerosis risk is tied to primarily
hypertriglyceridemia 7931 spectrum, may contribute to atherogenesis [[]].Thus, among the diverse range of patients with severe hypertriglyceridemia , those with monogenic impairment of lipolysis (discussed below) would have primarily chylomicronemia,
hypertriglyceridemia 8728 HypertriglyceridemiaMonogenic and polygenic factors contribute to both mild-to-moderate and severe hypertriglyceridemia ; the relative burden of these factors together with secondary non-genetic factors can determine the
hypertriglyceridemia 9188 qualitatively and quantitatively abnormal TG-rich lipoproteins distinguishes mild-to-moderate from severe hypertriglyceridemia [[], []].As mentioned, elevated VLDL is the predominant lipoprotein disturbance in individuals with
hypertriglyceridemia 9565 secretion, and catabolism of VLDL would be relatively more important in susceptibility to mild-to-moderate hypertriglyceridemia . In contrast, factors related to biosynthesis, secretion, and catabolism of chylomicrons are relatively
hypertriglyceridemia 9733 secretion, and catabolism of chylomicrons are relatively more important in susceptibility to severe hypertriglyceridemia , although there is considerable overlap with factors that modulate VLDL levels, particularly on the
hypertriglyceridemia 9943 particularly on the catabolic side [[]]. A corollary of this model is that individuals with polygenic severe hypertriglyceridemia have a greater burden of genetic susceptibility components than individuals with polygenic mild-to-moderate
hypertriglyceridemia 10072 greater burden of genetic susceptibility components than individuals with polygenic mild-to-moderate hypertriglyceridemia . Furthermore, secondary factors may be quantitatively and qualitatively more extreme in patients with
hypertriglyceridemia 10231 quantitatively and qualitatively more extreme in patients with severe compared to mild-to-moderate hypertriglyceridemia . Finally, control of secondary factors and medications might be relatively more efficacious in normalizing
hypertriglyceridemia 10416 relatively more efficacious in normalizing TG levels in individuals with polygenic mild-to-moderate hypertriglyceridemia than in those with severe hypertriglyceridemia. Both mild-to-moderate and severe hypertriglyceridemia
hypertriglyceridemia 10463 levels in individuals with polygenic mild-to-moderate hypertriglyceridemia than in those with severe hypertriglyceridemia . Both mild-to-moderate and severe hypertriglyceridemia are primarily polygenic traits, with the exception
hypertriglyceridemia 10518 hypertriglyceridemia than in those with severe hypertriglyceridemia. Both mild-to-moderate and severe hypertriglyceridemia are primarily polygenic traits, with the exception of the small subgroup with monogenic chylomicronemia
hypertriglyceridemia 10780 lipase (LPL) and related factors [[]].Genetics of Severe HypertriglyceridemiaAs discussed above, severe hypertriglyceridemia is basically synonymous with “chylomicronemia” [[], []]. Given their surface area-to-volume ratios,
hypertriglyceridemia 10997 ratios, chylomicrons are essentially the only particle physiologically able to produce such extreme hypertriglyceridemia [[], []]. If there is sufficient lipolytic capacity to generate chylomicron remnant particles, VLDL
hypertriglyceridemia 11957 occur between infancy and early adulthood [[], []]. With excess accumulation of chylomicrons, severe hypertriglyceridemia may be detected soon after birth. Chylomicronemia, but not elevated VLDL, produces plasma with a turbid,
hypertriglyceridemia 14270 proteins, through the mechanisms previously described, reduced chylomicron catabolism results in severe hypertriglyceridemia . Apo C-II and apo A-V are present on chylomicrons and are necessary for the interaction between these
hypertriglyceridemia 15432 much more likely to observe rare heterozygous variants in these genes in adult patients with severe hypertriglyceridemia . Rare heterozygous loss-of-function variants are an important genetic contributor to polygenic chylomicronemia.
hypertriglyceridemia 15636 to polygenic chylomicronemia. Most healthcare providers seem to recall the monogenic basis of severe hypertriglyceridemia but often retain the perception that every patient encountered with severe hypertriglyceridemia and
hypertriglyceridemia 15732 severe hypertriglyceridemia but often retain the perception that every patient encountered with severe hypertriglyceridemia and pancreatitis must have one of these ultra-rare deficiencies. This perception was perpetuated because
hypertriglyceridemia 17601 studies (GWAS) [[]]. Therefore, the list of rare heterozygous large-effect variants underlying severe hypertriglyceridemia is extensive.Common Small-Effect Variants in Polygenic ChylomicronemiaIn addition to the accumulation
hypertriglyceridemia 19965 scattered throughout the genome, all work in concert to produce polygenic chylomicronemia, including severe hypertriglyceridemia due to perturbations of chylomicrons, as well as other TG-rich lipoproteins.Genetics of Mild-to-Moderate
hypertriglyceridemia 20209 HypertriglyceridemiaThe same general architecture of genetic susceptibility is seen in patients with mild-to-moderate hypertriglyceridemia as in patients with severe hypertriglyceridemia [[]]. Specifically, the pool of patients with the milder
hypertriglyceridemia 20257 susceptibility is seen in patients with mild-to-moderate hypertriglyceridemia as in patients with severe hypertriglyceridemia [[]]. Specifically, the pool of patients with the milder hypertriglyceridemia phenotype formerly known
hypertriglyceridemia 20335 patients with severe hypertriglyceridemia [[]]. Specifically, the pool of patients with the milder hypertriglyceridemia phenotype formerly known as Fredrickson type 4 (here considered equivalent to “mild-to-moderate hypertriglyceridemia”)
hypertriglyceridemia 20454 hypertriglyceridemia phenotype formerly known as Fredrickson type 4 (here considered equivalent to “mild-to-moderate hypertriglyceridemia ”) also shows enrichment of rare heterozygous large-effect variants and common small-effect SNP loci
hypertriglyceridemia 20701 risk score, although not as extreme as Fredrickson type 5 (here considered equivalent to “severe hypertriglyceridemia ”) [[]]. These findings need to be replicated but suggest that hypertriglyceridemia along its spectrum
hypertriglyceridemia 20786 equivalent to “severe hypertriglyceridemia”) [[]]. These findings need to be replicated but suggest that hypertriglyceridemia along its spectrum of severity is a polygenic trait with similar genetic susceptibility components,
hypertriglyceridemia 21839 factors. The interested reader is referred to a more thorough review of this topic [[]]. As with familial hypertriglyceridemia , genetic determinants of hypotriglyceridemia include ultra-rare monogenic syndromic disorders that are
hypertriglyceridemia 34272 The integrated overview is that atherosclerosis risk is elevated in individuals with mild-to-moderate hypertriglyceridemia , a largely polygenic trait. In mild-to-moderate hypertriglyceridemia, cholesterol for arterial plaque
hypertriglyceridemia 34341 individuals with mild-to-moderate hypertriglyceridemia, a largely polygenic trait. In mild-to-moderate hypertriglyceridemia , cholesterol for arterial plaque formation is contributed from VLDL, their remnants, and IDL. Among
hypertriglyceridemia 34492 plaque formation is contributed from VLDL, their remnants, and IDL. Among rarer individuals with severe hypertriglyceridemia , atherosclerosis risk would be increased among individuals with a diffuse spectrum of large TG-rich
hypobetalipoproteinemia 22093 other lipoprotein, biochemical and clinical abnormalities, such as abetalipoproteinemia and homozygous hypobetalipoproteinemia , which result, respectively, from bi-allelic mutations in MTTP and APOB genes encoding, respectively,
obesity 2676 High TG is further correlated with such potentially causative non-lipoprotein parameters as abdominal obesity , insulin resistance, hypertension, hepatosteatosis, low-grade inflammation, a pro-coagulant state, and
obesity 21377 polygenic chylomicronemia. Importantly, secondary non-genetic factors, including diet, alcohol intake, obesity , diabetes control, liver, and renal disease, are at least as important as genetic susceptibility in

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