Hyperlipidemia combination products

Familial combined hyperlipidemia lib LDL, VLDL Chol,TG Increased VLDL production, increased conversion of VLDL to LDL. CHD, stroke... 

In the pathogenesis of nephrotic hyperlipidemia, both increased production and impaired catabolism of lipoproteins were demonstrated to play a role. Pathogenic mechanisms may be different in nephrotic patients with isolated hypercholesterolemia and in patients with combined hypercholesterolemia and hypertriglyceridemia (V6). 

PUFAs are potent inhibitors of the HMG-CoA reductase enzyme and similar to statins are useful in the treatment of hyperlipidemias (99-102). Statins enhance plasma AA levels and decrease the ratio of EPA to AA significantly (100). This finding suggests that PUFAs mediate many actions of statins (103) and that this could be one mechanism by which they lower cholesterol levels. Statins and PUFAs have many overlap actions such as the inhibition of IL-6 and TNF-a production and NF-kB activation plus the ability to enhance eNO production thus, both possess anti-inflammatory actions and both are useful in atherosclerosis, coronary heart disease, osteoporosis, stroke, Alzheimer s disease, and inflammatory conditions such as lupus and cancer (3, 4, 94, 104-121). These similar and overlap actions strongly indicate that the molecular mechanisms of actions of statins and PUFAs are similar, if not identical. Furthermore, when a combination of statins and PUFAs are given together, a synergistic beneficial effect was seen in patients with combined hyperlipemia (122). 

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