Triglycerides hypertriglyceridemia

Hyperlipidemia increase in lipids either increase in cholesterol (Hypercholesterolemia), in glycerides (Hyperglyceridemia) or in triglycerides (Hypertriglyceridemia). 

BARs are not used as first-line therapy if triglycerides are elevated at baseline because hypertriglyceridemia may worsen with a BAR alone. 

Treatment of type I hyperlipoproteinemia is directed toward reduction of chylomicrons derived from dietary fat with the subsequent reduction in plasma triglycerides. Total daily fat intake should be no more than 10 to 25 g/day, or approximately 15% of total calories. Secondary causes of hypertriglyceridemia should be excluded, and, if present, the underlying disorder should be treated appropriately. 

Because of the similarity, it is difficult to conclude whether the lipid changes induced by SERMs offer any advantage over the profile determined by HT. Triglyceride levels have been proposed as an independent risk factor for CVD in postmenopausal women (Miller 1998). Further, there are some indications that increases in triglycerides may favor the reduction in the size of LDL particles. Smaller LDL particles are more susceptible to oxidation and have been associated with a higher risk potential (Austin et al. 1988), but whether this observation confers any clinical prejudice to hypertriglyceridemia has not been proven at present. 

Mosca L, Harper K, Sarkar S, O Gorman J, Anderson PW, Cox DA, Barrett-Connor E (2001b) Effect of raloxifene on serum triglycerides in postmenopausal women influence of predisposing factors for hypertriglyceridemia. Clin Ther 23 1552-1565... 

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 ritonavir therapy, including those who developed hypertriglyceridemia. Patients with advanced HIV disease may be at increased risk of elevated triglycerides and pancreatitis. 

LT044 Scribner, K. A., T. M. Gadbois, M. Gowri, S. Azhar, and G. M. Reaven. Masoprocol decreases serum triglyceride concentrations in rats with fructose-induced hypertriglyceridemia. Metabolism 2000 49(9) 1106-1110. 

Hypertriglyceridemia is associated with increased risk of coronary disease. VLDL and IDL have been found in atherosclerotic plaques. These patients tend to have cholesterol-rich VLDL of small-particle diameter and small, dense LDL. Hypertriglyceridemic patients with coronary disease or risk equivalents should be treated aggressively. Patients with triglycerides above 700 mg/dL should be treated to prevent acute pancreatitis because the LPL clearance mechanism is saturated at about this level. 

In the presence of hypertriglyceridemia, HDL cholesterol is low because of exchange of cholesteryl esters from HDL into triglyceride-rich lipoproteins. Treatment of the hypertriglyceridemia may increase or normalize the HDL level. 

The effect of dietary fats on hypertriglyceridemia is dependent on the disposition of double bonds in the fatty acids. Omega-3 fatty acids found in fish oils, but not those from plant sources, activate peroxisome proliferator-activated receptor-alpha (PPAR- ) and can induce profound reduction of triglycerides in some patients. They also have antiinflammatory and antiarrhythmic activities. In contrast, the omega-6 fatty acids present in vegetable oils may cause triglycerides to increase. 

Hypertriglyceridemia suggests the presence of chylomicronemia, which may be caused by deficiency of LPL or its co-factors apoCII and apoAV. Blood triglyceride... 

Low LPL activity can also be found secondary to metabolic dysregulation, notably in insulin resistance and type 2 diabetes mellitus. In fact, diabetic hypertriglyceridemia is caused in part by decreased LPL secretion in response to reduced insulin action. Another preanalytical pitfall results from the high affinity of LPL for triglyceride-rich lipoproteins. When extremely hypertriglyceridemic plasma is prepared by cen-... 

Patients with HL deficiency present with hypercholesterolemia and hypertriglyceridemia, and accumulate VLDL remnants, triglyceride-rich LDL, and HDL [84]. These remnants mainly derive from a reduced catabolism of apoB-containing lipoproteins [82]. The disorder appears to be inherited in an autosomal recessive trait and is associated with an increased risk for coronary artery disease [8]. 

CETP exchanges cholesteryl esters of HDL with triglycerides of VLDL, IDL, and LDL. The HDL-derived cholesteryl esters are subsequently removed from the circulation via the LDL receptor pathway [28, 91]. Absence of functional CETP results in pronounced elevations of plasma concentrations of HDL cholesterol (2.5-8 mmol/1) and apoA-I. In parallel, plasma concentrations of LDL cholesterol and apoB are relatively low. Heterozygous CETP deficiency is associated with a milder elevation of HDL cholesterol. Most patients with CETP deficiency do not present with specific clinical symptoms. Some were reported to exhibit corneal opacities. CETP deficiency has been claimed to reduce the risk of atherosclerotic vascular disease and to prolong life expectancy. However, in some situations (e.g., in hypertriglyceridemia or in the absence of high HDL cholesterol), CETP deficiency may also increase cardiovascular risk [15, 28,91]. 

The ion exchange resins tend to increase serum triglyceride concentrations, especially in patients with hypertriglyceridemia (1). 

In a prospective, non-randomized analysis of 212 patients treated with a regimen containing a protease inhibitor, the overall incidences of hypertriglyceridemia and hypercholesterolemia at 12 months of treatment were 38% and 25% respectively (155). Increased concentrations of triglycerides and LDL cholesterol were more pronounced in patients taking ritonavir or lopinavir/rito-navir compared with other protease inhibitors. 

Three patients also developed chylomicronemia and two of those had severe hypertriglyceridemia. All three patients had triglycerides over 2 pg/ml before treatment, suggesting that patients with abnormal serum triglyceride concentrations at baseline are more likely to develop marked hypertriglyceridemia. 

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