Hyperlipidemias primary

Hyperlipidemia, primary and secondary prevention of cardiovascular events in patient with elevated cholesterol levels PO Initially, 40 mg/day. Titrate to desired response. Range 10-80 mg/day. 

A patient in the medical clinic is taking cholestyramine (Questran) for hyperlipidemia. The primary health care provider has prescribed TLC for the patient. The patient is on a low-fat diet and walks daily for exercise. His major complaint at this visit is constipation, which is very bothersome to him. Discuss how you would approach this situation with the patient. What information would you give the patient concerning his constipation ... 

Hyperlipidemia plays a role in the development of cardiovascular disease (CVD) in patients with CKD. The primary goal of treatment of dyslipidemras is to decrease the risk of atherosclerotic cardiovascular disease. A secondary goal in patients with CKD is to reduce proteinuria and decline in kidney function. Treatment of hyperlipidemia in patients with CKD has been demonstrated to slow the decline in GFRby 1.9 mL/minute per year of treatment with antihyper Epidemic agents.21... 

Metabolic disease (e.g., Wilson s disease, primary oxalosis, and hyperlipidemia)... 

Hyperlipidemia is seen in up to 60% of heart, lung, and renal transplant patients and greater than 30% of liver transplant patients.64 66 As a result of elevated cholesterol levels, transplant recipients are not only at an increased risk of atherosclerotic events, but emerging evidence also shows an association between hyperlipidemia and allograft vasculopathy.66 Hyperlipidemia, along with other types of cardiovascular disease, is now one of the primary causes of morbidity and mortality in long-term transplant survivors.67... 

Primary or genetic lipoprotein disorders are classified into six categories for the phenotypic description of dyslipidemia. The types and corresponding lipoprotein elevations include the following I (chylomicrons), Ha (LDL), lib (LDL + very low density lipoprotein, or VLDL), III (intermediate-density lipoprotein), IV (VLDL), and V (VLDL + chylomicrons). Secondary forms of hyperlipidemia also exist, and several drug classes may elevate lipid levels... 

BARs are useful in treating primary hypercholesterolemia (familial hypercholesterolemia, familial combined hyperlipidemia, type Ila hyperlipoproteinemia). 

Many patients treated for primary hyperlipidemia have no symptoms or clinical manifestations of a genetic lipid disorder (e.g., xanthomas), so monitoring is solely laboratory based. 

Observations in different types of primary hyperlipidemia revealed in general an inverse correlation between Lp(a) concentrations and plasma triglyceride and triglyceride-rich lipoprotein concentrations in hypertriglyceridemic subjects (A 10, B22, H30, W11). As far as this observation is not troubled by technical problems in the analysis (E8), the possibility exists that Lp(a) catabolism is partly related to the catabolism of triglyceride-rich and/or cholesterol-rich particles (P10, R16). 

F4, Famier, M., Bonnefous, F., Debbas, N., and Irvine, A., Comparative efficacy and safety of micronized fenofibrate and simvastatin in patients with primary type Ila or lib hyperlipidemia. Arch. Intern. Med. 154, 441-449 (1994). 

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. 

The cornerstone of treatment in primary hyperlipidemia is diet restriction and weight reduction. Limit or eliminate alcohol intake. Use drug therapy in conjunction with diet, and after maximal efforts to control serum lipids by diet alone prove unsatisfactory, when tolerance to or compliance with diet is poor or when hyperlipidemia is severe and risk of complications is high. Treat contributory diseases such as hypothyroidism or diabetes mellitus. 

Primary hypercholesterolemia or mixed hyperlipidemia Initial dose 130 mg/day Initial dose 200 mg/day Initial dose 145 mg/day Initial dose 160 mg/day... 

The answer is a. (Hardman, pp 875-898.) In type I hyperlipoproteinemia, drugs that reduce levels of lipoproteins are not useful, but reduction of dietary sources of fat may help. Cholesterol levels are usually normal, but triglycerides are elevated. Maintenance of ideal body weight is recommended in all types of hyperlipidemia. Clofibrate effectively reduces the levels of VLDLs that are characteristic of types 111, IV, and V hyperlipoproteinemia administration of cholestyramine resin and lovastatin in conjunction with a low-cholesterol diet is regarded as effective therapy for type 11a, or primary, hyperbetalipoproteinemia, except in the homozygous familial form. 

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. 

Lipoprotein disorders are detected by measuring lipids in serum after a 10-hour fast. Risk of heart disease increases with concentrations of the atherogenic lipoproteins, is inversely related to levels of HDL, and is modified by other risk factors (Table 35-1). Evidence from clinical trials suggests that LDL cholesterol levels of 60 mg/dL may be optimal for patients with coronary disease. Ideally, triglycerides should be below 120 mg/dL. Differentiation of the disorders requires identification of the lipoproteins involved (Table 35-2). Diagnosis of a primary disorder usually requires further clinical and genetic data as well as ruling out secondary hyperlipidemias (Table 35-3). 

In 80 patients with primary mixed hyperlipidemia, gemfibrozil used together with lovastatin resulted in 3% discontinuation because of myositis, but none attributable to rhabdomyolysis or myoglobinuria (72). 

Hyperlipidemia, an abnormally high concentration of lipids in the bloodstream, is one of the primary causes of cardiovascular disease in industrialized nations. This condition typically causes deposition of fatty plaquelike lesions on the walls of large and mediumsized arteries atherosclerosis), which can lead to throm-... 

Wl. Wallentin, L., Lecithin cholesterol acyl transfer rate in plasma and its relation to lipid and lipoprotein concentrations in primary hyperlipidemia. Atherosclerosis 26, 233-248 (1977). 

The promising second oral therapy is Temsirolimus (Wyeth Pharm). Temsirolimus is believed to block the proliferation of immune T cells activated by interleukin, IL-2. The phase It clinical trial of Temsirolimus was also an international double blind placebo controlled trial. The trial involved 296 patients with either RR MS or SP MS with relapses. Participants received one of three doses of oral temsirolimus or placebo daily for 9 months. The primary outcome measure was the number of enhancing lesions after 9 months in study. By 32 w eeks into the study, those in the highest treatment dose had 47.8% fewer new enhancing lesions compared to those on placebo. The high dose group also had 51 % fev er relapses than the placebo group. Side effects included mouth ulceration or inflammation, menstrual dysfunction, hyperlipidemia and rashes. 

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