Hypertriglyceridemias, treatment

The primary care provider prescribes fenofibrate (Tricor) for the treatment of hypertriglyceridemia. The patient is now taking 200 mg/d PO. Is this an appropriate dosage If not, what action would you take If the dose is appropriate, how many capsules would you administer if the drugis available in 54-mg capsules ... 

The principal use of niacin is for mixed hyperlipidemia or as a second-line agent in combination therapy for hypercholesterolemia. It is a first-line agent or alternative for the treatment of hypertriglyceridemia and diabetic dyslipidemia. 

Fish oil supplementation may be most useful in patients with hypertriglyceridemia, but its role in treatment is not well defined. 

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. 

Hozumi Y, Kawano M, Miyata M (1997) Severe hypertriglyceridemia caused by tamoxifen-treatment after breast cancer surgery. Endocr J 44 745-749... 

Hypertriglyceridemia A6 unct /e therapy to diet for treatment of adult patients with hypertriglyceridemia (Fredrickson types IV and V hyperlipidemia). 

The fibrates are mainly used to treat two hyperlipi-demias, familial hypertriglyceridemia (type IV) and dysbetalipoproteinemia (type III). They are also useful in the treatment of hypertriglyceridemia associated with type II diabetes (secondary hyperlipidemia). The fibrates are the drugs of choice in treating hypertriglyceridemias, particularly those associated with low levels of HDL cholesterol. The fibrates additionally appear to... 

Is an indigenous drug obtained from gum guggul used for treatment of hyperlipidemia, hypercholesterolemia and hypertriglyceridemia. 

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. 

For treatment of heterozygous familial hypercholesterolemia, most patients require 2-6 g of niacin daily more than this should not be given. For other types of hypercholesterolemia and for hypertriglyceridemia, 1.5-3.5 g daily is often sufficient. Crystalline niacin should be given in divided doses with meals, starting with 100 mg two or three times daily and increasing gradually. 

Colestipol, cholestyramine, and colesevelam are useful only for isolated increases in LDL. In patients who also have hypertriglyceridemia, VLDL levels may be further increased during treatment with resins. 

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. 

Life-threatening hypertriglyceridemia has been described during treatment with leflunomide (592). 

Increased levels of apolipoproteins and rate-limiting enzymes of lipogenesis and their mRNAs have been demonstrated in the liver of nephrotic rats (V5), although increased liver cholesterol synthesis has not been confirmed in nephrotic patients (D9). Cholesterol synthesis in the liver probably does not change during antipro-teinuric treatment (D9). The rate of synthesis of LDL apoprotein B is variable and depends on the presence or absence of hypertriglyceridemia (V6). 

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