Elevated triglycerides

Hypertriglyceridemia Hypertriglyceridemia in adult patients (Types IV and V hyperlipidemia) who present a risk of pancreatitis and who do not respond to diet. Consider therapy for those with triglyceride elevations between 1000 and 2000 mg/dL, and who have a history of pancreatitis or of recurrent abdominal pain typical of pancreatitis. 

Pancreatitis Pancreatitis has been observed in patients receiving lopinavir/ritonavir therapy, including those who developed marked triglyceride elevations. Fatalities have been observed. Although a causal relationship to lopinavir/ritonavir has not been established, marked triglyceride elevation is a risk factor for development of pancreatitis. 

Lab test abnormalities Liver function test abnormalities, CPK or creatinine elevations, lymphopenia, triglyceride elevations occurred in at least 3% of patients. 

Any relationship between obesity and stroke is likely to be confounded by the positive association of obesity with hypertension, diabetes, hypercholesterolemia and lack of exercise, and the negative association with smoking and concurrent illness. Nevertheless, stroke is more common in the obese, and abdominal obesity appears to be an independent predictor of stroke (Suk et al. 2003). The constellation of metabolic abnormalities including central obesity, decreased high density lipoprotein, elevated triglycerides, elevated blood pressure and impaired glucose tolerance is known as the metabolic syndrome and is associated with a three-fold increase risk of type 2 diabetes and a two-fold increase in cardiovascular risk (Eckel et al. 2005 Grundy et al. 2005). 

Following reports of triglyceride elevation in normal subjects on high carbo-hjrdrate diets, Ahrens et al. (1961) proposed that essential hyperlipemia may... 

Colestipol was well tolerated and reduced plasma cholesterol levels during a 2 year study in types II, III and IV hyperlipoproteinemic subjects.In another study, colestipol, at a daily dose of 15 g, decreased plasma cholesterol levels in type II and IV subjects. The addition of clofibrate further reduced cholesterol values. Serum triglyceride levels were elevated by colestipol but the effect could be reversed by clofibrate.61 Similar triglyceride elevations have been observed with cholestyramlne62 which, during the past year received FDA approval for a lipid-lowering indication. 

Leptin is a cytokine produced and secreted by adipose tissue in proportion to the body fat content [3]. Mice and humans lacking leptin or its receptor develop a severe hyperphagia and a dramatic degree of obesity which is considerably more pronounced than that of the NDRKO mouse. Thus, leptin is the key adiposity signal in rodents and humans. Leptin secretion appears to reflect the metabolic status of the adipocyte rather than the sheer size of triglyceride deposits, and leptin levels may transiently be dissociated from total body fat. Nonetheless, over the course of a day with unrestricted food supply, plasma leptin levels reliably reflect the amount of total body fat. Local administration of leptin into the brain results in reduced food intake. The vast majority of patients with obesity have elevated serum levels of leptin. Thus, it is believed that the polygenic obesity is due to leptin resistance rather than to inadequate leptin secretion, or to a reduced blood/brain transport of the cytokine. 

Lipoprotein formed by hydrolysis of triglycerides in VLDL elevated in type III hyperlipoproteinemia. 

Disorders of lipoprotein metabolism involve perturbations which cause elevation of triglycerides and/or cholesterol, reduction of HDL-C, or alteration of properties of lipoproteins, such as their size or composition. These perturbations can be genetic (primary) or occur as a result of other diseases, conditions, or drugs (secondary). Some of the most important secondary disorders include hypothyroidism, diabetes mellitus, renal disease, and alcohol use. Hypothyroidism causes elevated LDL-C levels due primarily to downregulation of the LDL receptor. Insulin-resistance and type 2 diabetes mellitus result in impaired capacity to catabolize chylomicrons and VLDL, as well as excess hepatic triglyceride and VLDL production. Chronic kidney disease, including but not limited to end-stage... 

In many individuals, hyperlipidemia has no symptoms and the disorder is not discovered until laboratory tests reveal elevated cholesterol and triglyceride levels, elevated LDL levels, and decreased HDL levels. Often, these drags are initially prescribed on an outpatient basis, but initial administration may occur in the hospitalized patient. Seram cholesterol levels (ie, a lipid profile) and liver functions tests are obtained before the drugs are administered. 

Patients with extremely elevated serum triglycerides (greater than 1,000 mg/dL [11.3 mmol/L]) can develop pancreatitis and tuberoeruptive xanthomas. 

Triglycerides greater than or equal to 150 mg/dL (1.70 mmol/L) or on drug treatment for elevated triglycerides... 

Patients with metabolic syndrome are twice as likely to develop type 2 diabetes and four times more likely to develop CHD.3,11 These individuals are usually insulin resistant, obese, have hypertension, are in a prothrombotic state, and have atherogenic dyslipidemia characterized by low HDL cholesterol and elevated triglycerides, and an increased proportion of their LDL particles are small and dense.3... 

Resins are moderately effective in lowering LDL cholesterol but do not lower triglycerides (Table 9-8). Moreover, in patients with elevated triglycerides, the use of a resin may worsen the condition. This may be due to a compensatory increase in HMG-CoA reductase activity and results in an increase in assembly and secretion of VLDL. The increase in HMG-CoA reductase activity can be blocked with a statin, resulting in enhanced reductions in serum lipids (see section on combination therapy). Resins reduce LDL cholesterol from 15% to 30%, with a modest increase in HDL cholesterol (3% to 5%) (Table 9-8). Resins are most often used as adjuncts to statins in patients who require additional lowering of LDL cholesterol. Since these drugs are not absorbed, adverse effects are limited to the gastrointestinal tract (Table 9-9). About 20%... 

Niacin (vitamin B3) has broad applications in the treatment of lipid disorders when used at higher doses than those used as a nutritional supplement. Niacin inhibits fatty acid release from adipose tissue and inhibits fatty acid and triglyceride production in liver cells. This results in an increased intracellular degradation of apolipoprotein B, and in turn, a reduction in the number of VLDL particles secreted (Fig. 9-4). The lower VLDL levels and the lower triglyceride content in these particles leads to an overall reduction in LDL cholesterol as well as a decrease in the number of small, dense LDL particles. Niacin also reduces the uptake of HDL-apolipoprotein A1 particles and increases uptake of cholesterol esters by the liver, thus improving the efficiency of reverse cholesterol transport between HDL particles and vascular tissue (Fig. 9-4). Niacin is indicated for patients with elevated triglycerides, low HDL cholesterol, and elevated LDL cholesterol.3... 

Fibrates are the most effective triglyceride-lowering drugs and are used primarily in patients with elevated triglycerides and low HDL cholesterol. 

Niacin can be combined with a fibrate in patients with high elevations in serum triglycerides. The combination may increase the risk of myopathy compared to either agent alone. 

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