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Hyperlipidemia secondary

Hyperlipidemia, secondary causes Prior to initiating therapy, exclude secondary causes of hyperlipidemia (eg, poorly controlled diabetes mellitus, hypothyroidism, nephrotic syndrome, dysproteinemias, obstructive liver disease, other drug therapy, alcoholism) and measure total-C, HDL-C, and triglycerides. [Pg.619]

Toto RD, Grundy SM, Vega GL. Pravastatin treatment of very-low-density, intermediate-density and low-density lipoproteins in hypercholesterolemia and combined hyperlipidemia secondary to the nephrotic syndrome. Am J Nephrol 2000 20 12-17. [Pg.452]

Hyperlipidemia is frequently divided into primary hyperlipidemia (genetic) and secondary hyperlipidemia. Secondary hyperlipidemia is a sequelae of metabolic disturbances such as diabetes... [Pg.80]

TABLE 9-3. Secondary Conditions and Drugs That May Cause Hyperlipidemias... [Pg.181]

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... [Pg.379]

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... [Pg.111]

A complete history and physical examination should assess (1) presence or absence of cardiovascular risk factors or definite cardiovascular disease in the individual (2) family history of premature cardiovascular disease or lipid disorders (3) presence or absence of secondary causes of hyperlipidemia, including concurrent medications and (4) presence or absence of xanthomas, abdominal pain, or history of pancreatitis, renal or liver disease, peripheral vascular disease, abdominal aortic aneurysm, or cerebral vascular disease (carotid bruits, stroke, or transient ischemic attack). [Pg.113]

In patients treated for secondary intervention, symptoms of atherosclerotic cardiovascular disease, such as angina or intermittent claudication, may improve over months to years. Xanthomas or other external manifestations of hyperlipidemia should regress with therapy. [Pg.123]

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. [Pg.218]

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... [Pg.274]

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. [Pg.1016]

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). [Pg.779]

Yeshurun D, Hamood H, Morad N, Naschitz J. [Acipimox (Olbetam) as a secondary hypolipemic agent in combined hypertriglyceridemia and hyperlipidemia.JHarefuah 2000 138(8) 650-3710. [Pg.529]

Cardiovascular diseases are the leading cause of death in the Western world. Basically, atherosclerosis manifests itself in three major organs and thereby leads to severe secondary diseases. Coronary disease results from atherosclerosis of the coronary arteries and culminates in myocardial infarction when vessels are occluded by a thrombus. In the brain, atherosclerosis gives rise to arterial thrombi or ruptures that result in a stroke. Atherosclerosis in the kidney leads to renal failure. Since these diseases significantly lower life expectancy, early recognition and elimination of risk factors (hypertension, diabetes mellitus, hyperlipidemia, and smoking) that promote atherosclerosis are essential. [Pg.314]

Type TV hyperlipoproteinemia is common and occurs in adulthood primarily in patients who are obese, diabetic, and hyperuricemic and do not have xanthomas. It may be secondary to alcohol ingestion and can be aggravated by stress, progestins, oral contraceptives, thiazides, or 8-blockers. Two genetic patterns occur in type IV hyperlipoproteinemia familial hypertriglyceridemia, which does not carry a great risk for premature CAD, and familial combined hyperlipidemia, which is associated with increased risk of cardiovascular disease. [Pg.434]

Mortality secondary to cardiovascular disease is 10 to 30 times greater in dialysis patients than in the general population. In addition to traditional cardiac risk factors such as diabetes, hypertension, hyperlipidemia, tobacco use, and physical inactivity, patients with kidney disease have other unique risk factors. Among these are hyper-homocysteinemia, elevated levels of C-reactive protein, increased oxidant stress, and hemodynamic overload. Complications previously discussed such as anemia and metabolic disorders of CKD are also contributory. In particular, arterial vascular disease (i.e., atherosclerosis) and cardiomyopathy are the primary types of cardiovascular disorders present in the CKD population. These disorders lead to development of ischemic heart disease and its manifestations including myocardial infarction. As a predominant comorbidity, cardiovascular disorders and their sequela are the leading cause of death in the ESKD population. ... [Pg.842]

Hyperlipidemia is defined as elevated lipoprotein levels in the plasma, which may be primary or secondary. Several different types of hereditary hyperlipidemias have been defined. [Pg.277]

Treatment strategies focus first on diet and correction of underl)dng metabolic diseases. Diets that are low in cholesterol and saturated animal fats reduce lipoprotein levels in nearly all patients. In addition, overweight patients should reduce their total caloric intake. Exercise increases serum concentrations of HDL, which is associated with reduced risk of coronary artery disease. Secondary hyperlipidemia frequently subsides spontaneously upon treatment of the underlying metabolic disease or cessation of aggravating factors. [Pg.80]

Knoll RW, Ciafone R, Galen M. Rhabdomyolysis and renal failure secondary to combination therapy of hyperlipidemia with lovastatin and gemfibrozil. Corm Med (1993) 593-4. [Pg.1102]


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See also in sourсe #XX -- [ Pg.207 ]




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