Hyperlipidemia Hypercholesterolemia Hypertriglyceridemia

This modern diet - excessive in calories in relation to energy expenditure, high in total fat, saturated fat, cholesterol, sugar, and salt - leads to high prevalence rates of hyperlipidemia (hypercholesterolemia, hypertriglyceridemia, hyperlipoproteinemia) in the adult population. And sustained hypercholesterolemic hyperlipidemia markedly increases risk of premature severe atherosclerotic disease and its clinical sequelae. 

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

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. 

Excess lipid in the blood can result from primary genetic deficiencies, most of which are rare, or as a secondary consequence of another disease. Two primary hyperlipidemias, type I hypertriglyceridemia and type IIA hypercholesterolemia, are summarized in Table 1-15-2. 

It is indicated as an adjunct to diet to reduce elevated total cholesterol, LDL-cholesterol and TG levels in patients with primary hypercholesterolemia, diabetic dyslipidaemia or mixed hyperlipidemia, hypertriglyceridemia, dysbetalipo-proteinemia and familial hypercholesterolemia. 

Monogenic dyslipoproteinemias can generally be grouped into five categories (1) hypertriglyceridemia with an increase in chylomicrons and the clinical sign of pancreatitis, (2) mixed hyperlipidemia with an increase in chylomicron and VLDL remnants and an increased risk of premature atherosclerosis, (3) hypercholesterolemia with an increase in LDL and an increased risk for premature atherosclerosis, (4) hypoalphalipoproteinemia with low HLD and an increased risk for premature atherosclerosis, and (5) hypolipoproteinemia with a decrease in VLDL and LDL, which may lead to neurological disease. 

Hyperlipidemia associated with antipsychotic drugs has been reviewed (SEDA-29, 64). Haloperidol and the atypical antipsychotic drugs ziprasidone, risperidone, and aripiprazole would be associated with lower risks of hyperlipidemia, whereas chlorpromazine, thioridazine, and the atypical drugs quetiapine, olanzapine, and clozapine would be associated with higher risks. However, severe clozapine-induced hypercholesterolemia and hypertriglyceridemia has been reported in a patient taking clozapine (55). 

Hypertriglyceridemia due to sirolimus often does not respond to dosage reduction or hypolipidemic drugs. After liver transplantation (n — 6), significant hyperlipidemia improved after withdrawal of sirolimus (1070). The incidence of sirolimus-associated hyperlipidemia is up to 44%. After liver transplantation, there was hypercholesterolemia in 15% and hypertriglyceridemia in 10% of recipients. Sirolimus in combination with tacrolimus... 

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). 

Familial Combined Hyperlipidemia About 10% to 15% of patients with premature CHD actually have familial combined hyperlipidemia (FCHL). This disorder is recognized as a distinct phenotype by studying family members of survivors of myocardial infarction. Patients with FCHL can have increased plasma concentrations of total and LDL cholesterol (type Ila), or triglyceride (type IV), or both (type lib). In all cases, apo B-lOO concentrations are increased. The presentation of lipoprotein patterns can vary in an individual with time. Furthermore, patients with hypertriglyceridemia with normal partners tend to have offspring with hypercholesterolemia, and vice versa. 

All HMGRIs are approved for the treatment of primary hypercholesterolemia and familial combined hyperlipidemia (Fredrickson s type Ha and lib) (Table 30.2) In patients who have not responded to diet, exercise, and other non pharmacological methods (Table 30.6) (15,21). They may be used either alone or In combination with bile acid sequestrants, ezetimibe, or niacin. As previously mentioned, they should be administered at least 1 hour before or 4 to 6 hours after bile acid sequestrants when this combination Is desired. Fluvastatin, lovastatin, pravastatin, and simvastatin have been specifically Indicated to reduce the mortality of CHD and stroke. By reducing plasma LDL levels, these compounds slow the progression of atherosclerosis and reduce the risk of myocardial Infarction and other ramifications of vascular occlusion. Atorvastatin, rosuvastatin, and simvastatin have been shown to be effective In homozygous familial hyperlipidemia and are Indicated for this use. Additionally, atorvastatin, pravastatin, and simvastatin are Indicated for primary dysbetallpoprotelnemla (Fredrickson s type III) (Table 30.2). Finally, atorvastatin, pravastatin, rosuvastatin, and simvastatin are Indicated for the treatment of hypertriglyceridemia. 

In a large population study Goldstein et al. discussed three frequent lipid disorders, familial hypercholesterolemia, familial hypertriglyceridemia, and familial combined hyperlipidemia. Ascorbate deficiency unmasks these underlying genetic defects and leads to an increased plasma concentration of lipids (e.g. cholesterol, triglycerides) and Hpoproteins (e.g. LDL, VLDL) as well as to their deposition in the impaired vascular wall. As with Lp(a), this deposition is a defense measure counteracting the increased permeability. It should, however, be noted that the deposition of lipoproteins other than Lp(a) is a less S[>ecific defense mechanism and fre-... 

Dietary and non-dietary (chemotherapeutic) methods are presently used to control hyperlipidemia. The ideal method as defined by Oliver [34] should lead to a sustained reduction of hypertriglyceridemia, as well as of hypercholesterolemia and to a reduction in the accumulation of hpid in tissues accompanied by enhanced cataboHsm of Hpids and sterols. There should be no accumulation of cholesterol precursors or metabolites, no toxic effects and only minimal side effects. The treatment should be easily administered and should not affect the normal way of living. 

A negative correlation between deficient biotin status and blood lipid concentrations was found in rats (Marshall et al. 1976) as well as in humans (Marshall et al. 1980). A decrease in plasma lipids was observed in human healthy volunteers within 30 min of absorption of 100 mg of biotin infusion. It was shown that oral biotin supplementation affected plasma lipid concentrations. The administration of 5 mg/day of biotin decreased hypercholesterolemia in atherosclerosis and hyperlipidemia patients (Dukusova and Krivoruchenko 1972). A 15 mg/day treatment by biotin for 28 days decreased hypertriglyceridemia of subjects whose triacylglycerol concentrations were more than 25% above the normal of 1.8mmol/L (Baez-Saldana 2004). 

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

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