Hypertriglyceridemia - Common Causes, Prevention and treatment Strategies

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Term Occurence Count Dictionary
hyperlipidemia 2 endocrinologydiseases
metformin 1 endocrinologydiseasesdrugs
raloxifene 1 endocrinologydiseasesdrugs
diabetes mellitus 6 endocrinologydiseases
ezetimibe 3 endocrinologydiseasesdrugs
niacin 5 endocrinologydiseasesdrugs
hypertriglyceridemia 35 endocrinologydiseases
metabolic syndrome 3 endocrinologydiseases
mixed hyperlipidemia 1 endocrinologydiseases
obesity 6 endocrinologydiseases
simvastatin 1 endocrinologydiseasesdrugs
hyperglycemia 1 endocrinologydiseases
hypothyroidism 3 endocrinologydiseases
atorvastatin 1 endocrinologydiseasesdrugs
type 2 diabetes mellitus 1 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
atorvastatin 20806 Outcomes: Vytorin Efficacy International Trial) trial [[46]]. Similarly, a combination of ezetimibe with atorvastatin , has revealed beneficial effects on the coronary plaque regression (compared to monotherapy with a statin),
ezetimibe 20344 population would be necessary to confirm these preliminary results.Recently, it has been reported that ezetimibe (a cholesterol-absorption-inhibitor), when added to statin therapy, resulted in incremental lowering
ezetimibe 20522 resulted in incremental lowering of LDL-C levels, and improved CV outcomes. Moreover, a simvastatin- ezetimibe combination therapy has shown some positive effects on lowering TG levels, and decreasing the risk of
ezetimibe 20791 Reduction of Outcomes: Vytorin Efficacy International Trial) trial [[46]]. Similarly, a combination of ezetimibe with atorvastatin, has revealed beneficial effects on the coronary plaque regression (compared to monotherapy
metformin 32081 with IR, who had a high risk of developing diabetes were randomized to either pharmacotherapy with metformin , or lifestyle change, including weight loss and physical activity interventions. The DPP results have
niacin 18464 Protection Study 2–Treatment of HDL to Reduce the Incidence of Vascular Events) using extended-release niacin (a vitamin B3) against a background of statin therapy (with optimal control of LDL-C levels) were unable
niacin 18617 therapy (with optimal control of LDL-C levels) were unable to demonstrate an incremental benefit of niacin beyond the treatment with statin [[41], [42]]. It should be pointed out that the results of both AIM-HIGH
niacin 18928 clinical trial, which was conducted in the “pre-statin era”, and demonstrated a good effectiveness of niacin on CVD morbidity and mortality, and modification of lipid levels (reduction of TG, and elevation of
niacin 19054 and mortality, and modification of lipid levels (reduction of TG, and elevation of HDL-C levels) when niacin was used in patients not treated with statins [[43]]. Unfortunately, niacin can worsen glucose metabolism
niacin 19130 elevation of HDL-C levels) when niacin was used in patients not treated with statins [[43]]. Unfortunately, niacin can worsen glucose metabolism (contributing to hyperglycemia or new onset diabetes mellitus), and can
raloxifene 35105 dyslipidemia (e.g.: nonselective beta-blockers, thiazide diuretics, corticosteroids, estrogens, tamoxifen, raloxifene , protease inhibitors, retinoic acid, phenothiazines, antipsychotics, and immunosuppressants) should
simvastatin 20510 statin therapy, resulted in incremental lowering of LDL-C levels, and improved CV outcomes. Moreover, a simvastatin -ezetimibe combination therapy has shown some positive effects on lowering TG levels, and decreasing
Select Disease Character Offset Disease Term Instance
diabetes mellitus 2758 coping strategies in response to chronic stress. These risk factors, as well as elevated blood pressure, diabetes mellitus , and dyslipidemias can be modified [[1], [2]].Traditionally, the SCORE (Systematic COronary Risk Evaluation)
diabetes mellitus 4145 moderate to intense statin therapy in four groups of patients: 1) with atherosclerotic CVD, 2) with diabetes mellitus (T2DM), 3) with primary elevations of LDL-C above 4.9 mmol/l (190 mg/dl)), and 4) without clinical CVD,
diabetes mellitus 7265 consequences, especially among patients with insulin resistance (IR), central (visceral) obesity, type 2 diabetes mellitus (T2DM), or inborn errors of metabolism. For instance, too much FFA in the bloodstream leads to impairment
diabetes mellitus 12198 and more common, acquired causes of hypertriglyceridemia, usually due to medical conditions, such as diabetes mellitus , metabolic syndrome, central obesity, hypothyroidism, and chronic kidney disease, as well as medication-induced
diabetes mellitus 19211 [[43]]. Unfortunately, niacin can worsen glucose metabolism (contributing to hyperglycemia or new onset diabetes mellitus ), and can cause possible side effects (e.g., skin flushing, or liver damage) [[44], [45]].In addition,
diabetes mellitus 35992 atherogenic dyslipidemia, and CVD risk factor (associated with central obesity, metabolic syndrome, diabetes mellitus , insulin resistance, and hypothyroidism) that should be carefully evaluated and managed, via lifestyle
hyperglycemia 19184 not treated with statins [[43]]. Unfortunately, niacin can worsen glucose metabolism (contributing to hyperglycemia or new onset diabetes mellitus), and can cause possible side effects (e.g., skin flushing, or liver
hyperlipidemia 22175 severity, due to various factors [[2], [40]]. In case of patients with hypertriglyceridemia or mixed hyperlipidemia , who cannot take statins or fibrates, a therapy with omega-3 fatty acids should be considered. One such
hyperlipidemia 38789 polygenic (high TG due to excess hepatic VLDL production, normal cholesterol levels)Familial combined hyperlipidemia (FCHL) (polymorphisms in molecules and enzymes participating in lipoprotein metabolism; (e.g.: apoC2,
hypertriglyceridemia 404 prophylaxis. Consequently, the effective management of different types of lipid disorders, including hypertriglyceridemia , should be a priority for the healthcare practi-tioners (e.g.: cardiology and endocrinology specialists,
hypertriglyceridemia 816 improve their outcomes. The aim of this review is to facilitate the translation of current trends in hypertriglyceridemia management into a daily practice. The article fo-cuses on the common causes and consequences of hypertriglyceridemia,
hypertriglyceridemia 933 hypertriglyceridemia management into a daily practice. The article fo-cuses on the common causes and consequences of hypertriglyceridemia , and discusses diagnostic evaluation and therapeutic options for patients with high Triglyceride (TG)
hypertriglyceridemia 3472 patient management has to be made by the medical practitioner and engaged patient. This review focuses on hypertriglyceridemia (as an important component of dyslipidemia) and discusses evidence-based strategies to reduce the risk
hypertriglyceridemia 7595 FFA, the capacity of systemic tissues to metabolize glucose is often compromised). In consequence, hypertriglyceridemia and elevated FFA levels perpetuate IR, contributing to a cascade of cardio-metabolic derangements [[2],
hypertriglyceridemia 7877 analyzing over sixty prospective studies, it has been indicated that the genetic predispositions to hypertriglyceridemia can lead to excess of TG in the bloodstream, or poor capacity to remove TG from the blood. In result,
hypertriglyceridemia 9051 [[9]].Contribution of Remnant Lipoprotein Particles (RLP) to atherogenicity and CVD risk4In patients with hypertriglyceridemia , elevated levels of TG in the circulation are correlated with the activation of two enzymes: Cholesteryl
hypertriglyceridemia 11447 facilitates atherosclerosis [[16], [17]].Diagnostic criteria and common primary and secondary causes of hypertriglyceridemia 5Criteria for hypertriglyceridemia (according to the Endocrine Society clinical practice guidelines,
hypertriglyceridemia 11481 [17]].Diagnostic criteria and common primary and secondary causes of hypertriglyceridemia5Criteria for hypertriglyceridemia (according to the Endocrine Society clinical practice guidelines, and the National Cholesterol Education
hypertriglyceridemia 11788 Table 1. They should help clinicians with risk assessment of premature CVD. In addition, a very severe hypertriglyceridemia (TG levels above 2000 mg/dl; 22.4 mmol/l) indicates the risk of acute pancreatitis that is a life-threatening
hypertriglyceridemia 12004 life-threatening condition, which requires immediate treatment.Common primary and secondary causes of hypertriglyceridemia are summarized in Table 2. They include some rare congenital disorders, and more common, acquired causes
hypertriglyceridemia 12133 summarized in Table 2. They include some rare congenital disorders, and more common, acquired causes of hypertriglyceridemia , usually due to medical conditions, such as diabetes mellitus, metabolic syndrome, central obesity,
hypertriglyceridemia 12414 medication-induced dyslipidemia (with high TG level). Physicians need to keep in mind that patients with hypertriglyceridemia should always be assessed for possible secondary causes of dyslipidemia, and in case of suspected primary
hypertriglyceridemia 12541 always be assessed for possible secondary causes of dyslipidemia, and in case of suspected primary hypertriglyceridemia , the patients should be evaluated for family history (genetic predispositions) of dyslipidemia and CVD
hypertriglyceridemia 12850 Treatment Panel III (NCEP ATP III) guidelines, the secondary treatment target in patients with high hypertriglyceridemia (TG levels 200 to 499 mg/dl; 2.3–5.6 mmol/l) is non-high-density lipoprotein cholesterol (non-HDL-C)
hypertriglyceridemia 17551 risk, resulting from lipid-modifying therapy, among patients specifically selected for the presence of hypertriglyceridemia . Findings from subgroup analyses of ACCORD Lipid study [[35]], and results of major fibrate trials,
hypertriglyceridemia 20094 the treatment with fibrates could reduce the CVD incidence among patients with T2DM and concurrent hypertriglyceridemia and low level of HDL-C. Also, it should be kept in mind that a dedicated study, focused on fibrate therapy,
hypertriglyceridemia 22145 adverse effects, of different severity, due to various factors [[2], [40]]. In case of patients with hypertriglyceridemia or mixed hyperlipidemia, who cannot take statins or fibrates, a therapy with omega-3 fatty acids should
hypertriglyceridemia 23263 are now in progress will provide some new evidence related to decreasing CVD risk among patients with hypertriglyceridemia [[49], [50]]. The STRENGTH trial addresses a common clinical scenario, concerning patients with elevated
hypertriglyceridemia 24693 best-available RCT evidence, into a daily management of numerous, often asymptomatic patients with hypertriglyceridemia and high CV risk, it is crucial to create a common path for physicians and pharmacists, who constantly
hypertriglyceridemia 31832 [55]-[58]]. Apparently, many of these strategies can also be, to some degree, adopted in patients with hypertriglyceridemia , to successfully manage their lipid disorders, and the relevant CVD risk. In the Diabetes Prevention
hypertriglyceridemia 33025 carbohydrates that contribute to the significantly increased caloric intake that in turn can perpetuate hypertriglyceridemia [[2]]. Instead, the best approach is to decrease the total caloric intake (especially from high glycemic
hypertriglyceridemia 34260 medical practitioners and patients, they are absolutely necessary as the first step to reduction of hypertriglyceridemia , and impending CVD risk [[2], [55]]. The next step in this direction consists of pharmacotherapy with
hypertriglyceridemia 34622 LDL) particles that are highly atherogenic, and predictive of high risk of CV events.Patients with hypertriglyceridemia should always be evaluated for common secondary causes of dyslipidemia (e.g.: hypothyroidism, chronic
hypertriglyceridemia 34832 hypothyroidism, chronic kidney disease, autoimmune disorders, and HIV infection). In case of suspected primary hypertriglyceridemia , the patients need to be evaluated for genetic predispositions to dyslipidemia and CVD.Review of medications,
hypertriglyceridemia 35622 metabolic syndrome, pre-diabetes, and T2DM, as conditions associated with elevated CVD risk.Treatment of hypertriglyceridemia , including statins, fibrates, and omega-3 fatty acids needs to be selected, based on the safety and
hypertriglyceridemia 37423 Hopefully, further outcome trials will provide more implications for medical practice, to stem the tide of hypertriglyceridemia and CVD.CONSENT FOR PUBLICATIONNot applicable.Fig. (1)Remnant cholesterol and atherosclerosis.Table
hypertriglyceridemia 37558 CVD.CONSENT FOR PUBLICATIONNot applicable.Fig. (1)Remnant cholesterol and atherosclerosis.Table 1Criteria for hypertriglyceridemia .NCEP ATP III [[6], [19]]The Endocrine Society 2010 [[18]]Borderline-high TG150–199 mg/dl1.7–2.3
hypertriglyceridemia 37690 III [[6], [19]]The Endocrine Society 2010 [[18]]Borderline-high TG150–199 mg/dl1.7–2.3 mmol/lMild hypertriglyceridemia 150–199 mg/dl1.7–2.3 mmol/lHigh TG200–499 mg/dl2.3–5.6 mmol/lModerate hypertriglyceridemia200–999
hypertriglyceridemia 37788 mmol/lMild hypertriglyceridemia150–199 mg/dl1.7–2.3 mmol/lHigh TG200–499 mg/dl2.3–5.6 mmol/lModerate hypertriglyceridemia 200–999 mg/dl2.3–11.2 mmol/lVery high TG≥500 mg/dl≥5.6 mmol/lSevere hypertriglyceridemia1000–1999
hypertriglyceridemia 37884 mmol/lModerate hypertriglyceridemia200–999 mg/dl2.3–11.2 mmol/lVery high TG≥500 mg/dl≥5.6 mmol/lSevere hypertriglyceridemia 1000–1999 mg/dl11.2–22.4 mmol/lVery severe hypertriglyceridemia≥2000 mg/dl≥22.4 mmol/lNCEP ATP
hypertriglyceridemia 37951 TG≥500 mg/dl≥5.6 mmol/lSevere hypertriglyceridemia1000–1999 mg/dl11.2–22.4 mmol/lVery severe hypertriglyceridemia ≥2000 mg/dl≥22.4 mmol/lNCEP ATP III, The National Cholesterol Education Program (NCEP).Adult Treatment
hypertriglyceridemia 38200 III).Abbreviations: mg/dl, milligram/deciliter; mmol/l, milimol/liter; TG, triglycerides.Table 2Causes of hypertriglyceridemia .Primary [[1], [2]]Genetic syndromes presenting as chylomicronemia (rare)Other genetic syndromes with
hypertriglyceridemia 38322 hypertriglyceridemia.Primary [[1], [2]]Genetic syndromes presenting as chylomicronemia (rare)Other genetic syndromes with hypertriglyceridemia (relatively common)Primary genetic susceptibilityLipoprotein lipase (LPL) deficiencyApolipoprotein C-II
hypertriglyceridemia 38652 high-density lipoprotein–binding protein 1 (GPIHBP1) deficiency (expressed in childhood)Familial hypertriglyceridemia (FHTG) likely polygenic (high TG due to excess hepatic VLDL production, normal cholesterol levels)Familial
hypothyroidism 12254 usually due to medical conditions, such as diabetes mellitus, metabolic syndrome, central obesity, hypothyroidism , and chronic kidney disease, as well as medication-induced dyslipidemia (with high TG level). Physicians
hypothyroidism 34721 hypertriglyceridemia should always be evaluated for common secondary causes of dyslipidemia (e.g.: hypothyroidism , chronic kidney disease, autoimmune disorders, and HIV infection). In case of suspected primary hypertriglyceridemia,
hypothyroidism 36035 factor (associated with central obesity, metabolic syndrome, diabetes mellitus, insulin resistance, and hypothyroidism ) that should be carefully evaluated and managed, via lifestyle modification and pharmacotherapy. Although,
metabolic syndrome 12217 acquired causes of hypertriglyceridemia, usually due to medical conditions, such as diabetes mellitus, metabolic syndrome , central obesity, hypothyroidism, and chronic kidney disease, as well as medication-induced dyslipidemia
metabolic syndrome 35517 of patients with atherogenic dyslipidemia, characteristic for central obesity, insulin resistance, metabolic syndrome , pre-diabetes, and T2DM, as conditions associated with elevated CVD risk.Treatment of hypertriglyceridemia,
metabolic syndrome 35972 important component of atherogenic dyslipidemia, and CVD risk factor (associated with central obesity, metabolic syndrome , diabetes mellitus, insulin resistance, and hypothyroidism) that should be carefully evaluated and managed,
mixed hyperlipidemia 22169 different severity, due to various factors [[2], [40]]. In case of patients with hypertriglyceridemia or mixed hyperlipidemia , who cannot take statins or fibrates, a therapy with omega-3 fatty acids should be considered. One such
obesity 7249 negative health consequences, especially among patients with insulin resistance (IR), central (visceral) obesity , type 2 diabetes mellitus (T2DM), or inborn errors of metabolism. For instance, too much FFA in the
obesity 12245 hypertriglyceridemia, usually due to medical conditions, such as diabetes mellitus, metabolic syndrome, central obesity , hypothyroidism, and chronic kidney disease, as well as medication-induced dyslipidemia (with high TG
obesity 16029 HDL-C is characteristic for the atherogenic dyslipidemia, typically occurring in central (visceral) obesity , MS, pre-diabetes, and T2DM. Metabolically, the TG/HDL-C ratio is linked to IR, and preponderance of
obesity 35488 particularly useful in the assessment of patients with atherogenic dyslipidemia, characteristic for central obesity , insulin resistance, metabolic syndrome, pre-diabetes, and T2DM, as conditions associated with elevated
obesity 35963 as an important component of atherogenic dyslipidemia, and CVD risk factor (associated with central obesity , metabolic syndrome, diabetes mellitus, insulin resistance, and hypothyroidism) that should be carefully
obesity 39052 [18]]DiseasesMedicationsDietHypothyroidismDiabetes mellitus(Poorly controlled, insulinopenic)Central obesity Renal diseasesNephrotic syndromeAutoimmune disorderse.g., systemic lupuserythematosus (SLE)HIV- associated
type 2 diabetes mellitus 7258 health consequences, especially among patients with insulin resistance (IR), central (visceral) obesity, type 2 diabetes mellitus (T2DM), or inborn errors of metabolism. For instance, too much FFA in the bloodstream leads to impairment

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