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PubMedDate not supplied

[The role of hyperlipidemia in the pathogenesis of acute thrombophlebitis of the surface veins of the lower extremities].

Biochemical investigations carried out in patients with acute thrombophlebitis of the lower limb superficial veins showed that 70% of such patients develop marked changes in blood plasma lipid spectrum, hyperlipidemia. Blood serum lipid spectrum was examined in 19 patients with various forms of acute thrombophlebitis of the lower limb superficial veins and in 17 with varicose disease. Histologic material for morphologic examination (a fragment of the great subcutaneous vein near saphenofemoral anastomosis and of the wall near the thrombus) was collected during surgery. Venous wall fragments were examined under a light microscope for lipid content. The findings did not confirm the expected changes in venous wall in hyperlipidemia analogous with arterial wall changes in atherosclerosis. That is why we may propose that hyperlipidemia, though not directly changing venous wall structure, contributes to thrombogenesis process via other mechanisms.

Acute Disease↗
PubMed1977

Dietary intake and hyperlipidemia in controlled diabetic outpatients.

Statistical analyses were performed in order to determine the effects of the control of the diabetes as well as the food intake on serum lipid levels of 73 diabetic outpatients. They had had elevated fasting blood glucose levels, mostly complicated by various grades of hyperlipidemia, before the initiation of treatment. Hyperlipidemia was found to be ameliorated in nearly half of those patients after the start of diabetic treatment. However, the elevation of serum triglyceride persisted in 30 per cent of controlled diabetics, and no differences were found in occurrence of hypertriglyceridemia between diet-treatment group, sulfonylurea group, biguanide group, combined group and insulin group. Estimation of diet intake revealed that the controlled hypertriglyceridemic patients consumed slightly (but significantly) greater amounts of sucrose, alcohol, and total calories than the controlled normotriglyceridemic patients. In addition to such inadequate diet consumptions, the tendency to be overweight and the subtle increment of fasting blood glucose levels were also shown to have contributed to hypertriglyceridemia. It is thus concluded that the lipid disorder in controlled diabetic outpatients is the result of multifactorial influences and that well-conducted diet therapy and stricter regulation of blood glucose are essential in the management of posttreatment hyperlipidemia.

Adult↗
PubMed1993

Pharmacist management of a hyperlipidemia clinic.

A hyperlipidemia clinic in which a pharmacist provides primary care is described. The clinic was established at a Veterans Affairs medical center in January 1990. A pharmacist performs limited physical assessments, refers patients to other clinics as necessary, orders laboratory and diagnostic tests, and selects and monitors the use of lipid-lowering medications. Interventions are performed according to the pharmacist's clinical judgment; there is no set protocol. Recommendations for patient management are approved by an attending physician, who prescribes the antilipemic drugs. The pharmacist teaches patients about hyperlipidemia, the impact of diet and life-style, and the mechanism of action, administration, and adverse effects of the antilipemics prescribed. The pharmacist also monitors compliance, laboratory test values, and the response to treatment. Treatment is modeled after the recommendations of the National Cholesterol Education Program. If a patient has not achieved the targeted cholesterol concentration after receiving dietary therapy for three months, further education about diet and lifestyle is provided. If, after three more months, the cholesterol level remains high, drug therapy is begun. Four antilipemic drugs--colestipol, gemfibrozil, lovastatin, and niacin--are used in the clinic. Since it began operating, the clinic has enrolled 284 patients. Compliance with the lipid-lowering agents has ranged from 43% to 100%. Adverse effects have accounted for the majority of cases of noncompliance. A pharmacist provides primary care for patients with hyperlipidemia in an ambulatory-care clinic.

Chicago↗
PubMed1996

Prevalence of hyperlipidemia in a cohort of CAPD patients. Italian Cooperative Peritoneal Dialysis Study Group (ICPDSG).

An association between hyperlipidemia and cardiovascular disease is well described in the literature. We conducted an observational study in order to evaluate the lipid profile, the prevalence of hyperlipidemia and its relationship with age, sex, duration of CAPD, peritoneal glucose load (PGL), serum albumin (ALB), serum glucose (GLU), and BMI in a large cohort of uremics undergoing long-term treatment with CAPD. 457 nondiabetic patients (245 males, 212 females; mean age 63.8 +/- 11.9 years; mean duration of CAPD: 41.8 +/- 26.9 months) treated during 1992 in 25 centers participating in the Italian Cooperative Peritoneal Dialysis Study Group (ICPDSG) were studied. The serum lipid parameters evaluated were triglycerides (TG), total cholesterol (CHO), HDL-cholesterol (HDL). Indications given in the New England Journal of Medicine, SI Unit Conversion Guide, 1992, were adopted for normal ranges. In the whole population the evaluation of lipid parameters showed: TG 227.4 +/- 123.3 mg/dl, CHO 232.8 +/- 56.0 mg/dl, HDL 40.7 +/- 12.0 mg/dl. No differences were found between the two sexes with regard to age, BMI, duration of CAPD, distribution of renal diseases, TG, ALB, and GLU; whereas CHO and HDL were significantly lower in males than in females (CHO: 222.2 +/- 53.5 vs. 245.0 +/- 56.5 mg/dl, p < 0.001; HDL: 39.3 +/- 11.4 vs. 42.6 +/- 12.6 mg/dl, p < 0.05). The prevalence of hypercholesterolemia was significantly lower in males than in females (19.7 vs. 35.4%; p < 0.001). The multiple regression analysis indicated that TG were directly correlated to PGL (p < 0.05), and HDL was inversely correlated with TG (p < 0.001). The coexistence of the two variables (TG and HDL) may increase the risk of cardiovascular events. Further strategies should therefore be developed to select and manage CAPD patients to reduce the incidence of hyperlipidemia.

Blood Glucose↗
PubMed1996

[Hyperlipidemia in pregnancy].

Hyperlipidemia is one of the most striking modification of biological parameters occurring during normal pregnancy. Hypertriglyceridemia is the most prominent feature, with a less dramatic increase of total cholesterol levels. Besides these quantitative changes, most lipoproteins undergo qualitative modification throughout pregnancy such as triglyceride enrichment of the particles. Kinetics and magnitude of plasma lipids changes have been well recognized, but the mechanisms, metabolic fate and impact on the pathogenesis of cardiovascular disease are not totally unravelled. The primary modulators are estrogens, insulin and lipoprotein lipase. Hyperlipidemia is a result of the metabolic adaptation of the maternal organism to pregnancy allowing to save glucose and energy for the fetus, reversible within a few weeks in postpartum. However some have suggested a trend toward an increased risk for coronary disease after multiple pregnancies. In case of preexisting hyperlipidemia, whether familial or not-primary or secondary, pregnancy presents an additional challenge. Except from exceptional complications, dietary counselling will be the only treatment, under a close follow-up.

Female↗
PubMed1998

[Hyperlipidemia in children and adolescents: diagnosis and therapy].

Severe hyperlipidemias should be diagnosed and treated even in childhood and adolescence, because vascular lipid deposition in the form of fatty streaks and progressive atherosclerotic lesions start to develop early in life. The heterozygous form of familial hypercholesterolemia found in about 1 of 500 newborn infants, and polygenic forms of hypercholesterolemia, are the most frequent forms of primary genetic hypercholesterolemia found in children. Secondary hyperlipidemias, e.g. in diabetes mellitus, hypothyroidism and renal disease, are relatively frequent in children and adolescents and need to be searched for in the diagnostic evaluation, because they can be influenced by treatment of the underlying disorder. Children and adolescents with severe forms of hyperlipidemias should be diagnosed and treated early in life. Dietary modification is the basis of treatment of affected children and can lower LDL cholesterol by about 15-20%. In patients with severe hypercholesterolemia, dietary cholesterol intake should not exceed 150 mg/day in children or 250-300 mg/day in adolescents. Even more important is a reduction of the intake of saturated fats and trans fatty acids and their replacement by polyunsaturated and particularly monounsaturated fats. Some additional lowering of LDL cholesterol may be achieved by the preferential use of vegetable over animal proteins and of complex carbohydrates over sugars. Repeated motivation, counseling and intensive practical training of the patient and family, supported by appropriate teaching materials, are essential for effective dietary treatment. Additional drug treatment is considered in children from the age of 8-9 years of age onwards if, in spite of adequate dietary modification, LDL cholesterol remains above 190 mg/dl (4.9 mmol/l), or above 160 mg/dl (3.9 mmol/l) in the presence of additional risk factors. The drugs of first choice are anion exchange resins (colestyramine or colestipol) because of their well documented efficacy and safety. More convenient to take but often somewhat less effective is beta-sitosterol. If efficacy or compliance with resins or sitosterin is unsatisfactory, fibrates (e.g. bezafibrate, fenofibrate) may be considered as a drug of second choice. Cholesterol synthesis inhibitors are not recommended for general use in children at this time.

Adolescent↗
PubMed1998

Hyperlipidemia of diuretic therapy.

Hyperlipidemia is a widely acknowledged side effect of thiazide diuretic therapy, but it is often dismissed as a short-term effect of high-dose therapy. Large clinical trials usually show no lipid change during late follow-up. These large trials use intention-to-treat analysis which masks the lipid effect. On-treatment analysis regularly reveals the persistence of hyperlipidemia during 4-5 years of treatment. Studies of low-dose thiazide therapy give conflicting results. Meta-analysis of these studies reveals hyperlipidemia of a milder degree than with high-dose thiazide treatment. However, a trade-off of effects is apparent because systolic blood pressure is lowered less well with low doses. Thus, thiazide effects on blood pressure and lipids are dose-dependent. Similar meta-analysis of indapamide 2.5 mg daily shows no adverse lipid effect and a lowering of blood pressure equivalent to 50 mg of hydrochlorothiazide. Regarding clinical events, low-dose thiazide treatment exerts primary prevention of coronary heart disease but provides less benefit against stroke and congestive heart failure than does high-dose therapy. Thus, an evidence-based therapeutic strategy for further reducing cardiovascular risk is as follows: initiate antihypertensive therapy with low-dose diuretics. Add beta-blockers and dihydropyridine-type calcium channel blockers for further antihypertensive effect, if needed. Hypertension resistant to a 3-drug regimen should be treated with high-dose thiazides. Lipids should be monitored at each step and treated with diet and statin drugs to maintain lipid goals. Risk factor control is an old concept that has yet to be effectively implemented.

Adrenergic beta-Antagonists↗
PubMed1998

[Causes and risks of hyperlipidemia during dialysis and after renal transplantation].

The most widely studied hyperlipidemies in patients affected by renal insufficiency or subsequent to kidney transplant present phenotype IIa, IIb or IV. The lipidic alteration most frequently observed in chronic renal insufficiency and/or dialytic treatment is represented by hypertrigliceridemia as a result of: 1) altered VLDL metabolism; 2) reduced activity of lecithin cholesterol acyltransferase (LCAT); 3) decrease in Apo-A1 and HDL3. Furthermore, marked anomalies in lipoprotein Lp (a) have been reported in hemodialysis. In patients undergoing peritoneal dialysis, hyperlipidemia arises from both an anomalous retrograde absorption of glucose and protein dispersion. Following kidney transplant the most frequent hyperlipidemia is hypercholesterolemia, consequent to immunosuppressive treatment (mainly steroids and cyclosporin). The documented significant increase of cardiovascular risk in the presence of hyperlipidemia points to the need for a clearer etiopathogenic definition of this anomaly, as well as the necessity to find an efficacious pharmacological treatment.

Humans↗
PubMed2002

Hyperlipidemia induced by high cholesterol diet inhibits heat shock response in rat hearts.

We examined whether heat shock response is affected by experimental hyperlipidemia in rat hearts. Therefore, isolated hearts of male Wistar rats fed a 2% cholesterol-enriched diet or standard diet for 12 weeks were subjected to either 20 min heat stress at 42 degrees C or global normothermic ischemia followed by 120 min normothermic, normoxic perfusion. Both heat stress and ischemia resulted in a significant increase in cardiac mRNA and protein levels of the inducible member of the 70-kDa heat shock protein family (HSP70) when compared to time-matched controls as assessed by reverse transcriptase polymerase chain reaction and Western blotting in hearts of normal rats. However, in hyperlipidemic groups, increase in cardiac hsp70 mRNA and HSP70 protein in response to heat stress and ischemia was markedly attenuated. We further observed that the basal level of hsp70 mRNA was significantly higher in the hyperlipidemic group when compared to normal controls; however, the HSP70 protein level was not different. This is the first demonstration that hyperlipidemia inhibits cardiac heat shock response. We further conclude that basal HSP70 expression might be downregulated at a posttranscriptional level in hyperlipidemia.

Animals↗
PubMed1986

Treatment of the hyperlipidemia of the nephrotic syndrome: a controlled trial.

The hyperlipidemia of the nephrotic syndrome is often associated with elevated total and low-density lipoprotein (LDL) cholesterol levels and low or normal high-density lipoprotein (HDL) cholesterol levels. This pattern of hyperlipidemia has been associated with an increased risk of accelerated atherosclerosis in other populations. Despite extensive studies of diet and drug therapy in other populations, few such therapeutic studies exist in patients with the nephrotic syndrome. To investigate the effect of diet and lipid-lowering drugs on the lipoprotein-lipid profile of patients with unremitting nephrotic syndrome and marked hyperlipidemia, we conducted a controlled trial using two such drugs: colestipol and probucol. Colestipol lowered the mean total fasting plasma cholesterol of seven patients from 397 +/- 27 to 317 +/- 37 mg/dL, a 20.2% decrease, and lowered the LDL cholesterol from 398 +/- 28 to 203 +/- 18 mg/dL, a 31.9% decrease. It did not affect the HDL cholesterol level, and thus lowered the LDL-to-HDL cholesterol ratio. Probucol lowered the mean total cholesterol from 439 +/- 72 to 339 +/- 60 mg/dL, a 22.6% decrease, and the LDL cholesterol from 282 +/- 43 to 215 +/- 26 mg/dL, a 23.8% decrease. Although the HDL cholesterol was lowered from 49 +/- 9 to 43 +/- 7 mg/dL by probucol, a 12.2% decrease, the LDL-to-HDL cholesterol ratio still declined. Both drugs were well tolerated and proved safe in this short-term trial. Antihyperlipidemic therapy may well be indicated in certain patients with unremitting nephrotic syndrome.

Adult↗
PubMedDate not supplied

Simvastatin reduces plasma concentration of high-sensitivity C-reactive protein in type 2 diabetic patients with hyperlipidemia.

High-sensitivity C-reactive protein (hs-CRP) is positively associated with the prevalence of coronary artery disease by epidemiologic data. Prospective studies indicate that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors reduced the plasma hs-CRP concentration and the risk of recurrent coronary events after myocardial infarction. Type 2 diabetes is associated with high mortality risk of coronary heart disease and this high risk may be involved in the inflammatory factors. We have therefore conducted a prospective study to assess whether simvastatin can rapidly reduce the plasma hs-CRP concentration in type 2 diabetic patients with hyperlipidemia. Seventeen type 2 diabetic patients with hyperlipidemia were enrolled in the study after 6 weeks on a lipid-lowering diet. Fourteen patients completed the study, taking simvastatin 20 mg daily for 8 weeks. Fasting blood samples were collected from each patient before and after 8-week administration of simvastatin. In response to 8-week administration of simvastatin, hs-CRP levels significantly decreased from 0.312+/-0.057 to 0.193+/-0.045 mg/dl (P<.01). Plasma LDL cholesterol also decreased significantly from 130+/-9 to 74+/-3 mg/dl (P=.001). This study shows that plasma hs-CRP concentration can be reduced by 8-week administration of simvastatin in type 2 diabetic patients with hyperlipidemia.

Blood Glucose↗
PubMed2001

Management of hyperlipidemia in children.

Atherosclerosis is a major cause of death and disability in adults. Recent investigations suggest that although cardiac end-points such as myocardial infarction and strokes mainly occur in middle-age and older subjects, the pathological basis for atherosclerosis begins in childhood. Hypercholesterolemia is one of the most important risk factors for atherosclerosis in adults and elevated cholesterol in children is associated with sub-clinical deposition of lipids in the aorta and coronary arteries. This report summarizes an approach to the diagnosis and treatment of hyperlipidemia in children. Based on guidelines from the National Cholesterol Education Program, children over 2 years of age should be screened for hypercholesterolemia if there is a family history of premature heart disease or hyperlipidemia. Therapy must be individualized. The majority of children with hyperlipidemia should be managed with a low-saturated fat and low-cholesterol diet. Children over 10 years of age with severe elevations of LDL-cholesterol and who come from high-risk families may be considered for more aggressive dietary therapy or medication in some cases. This is especially true for children with inherited disorders of lipid metabolism such as LDL-receptor deficiency. By identifying high-risk children and instituting therapy during childhood it is hoped that premature onset of adult coronary heart disease can be delayed or avoided altogether.

Journal Article↗
PubMedDate not supplied

An ounce of prevention. Drugs used to treat hyperlipidemia (Part 2).

For more than a century, coronary heart disease (CHD) has been the number one cause of death in the United States. Today, we know that although treatment of CHD may reduce some of those deaths, it is the prevention that is the real answer to eliminating this national scourge. The key to prevention lies in identifying those persons who are at risk for developing CHD and reducing the primary risk factor--hyperlipidemia. Preventing or controlling hyperlipidemia involves therapeutic lifestyle changes (TLC) and antilipidemic medications. In part 1, two useful medications--niacin and fibric acid derivatives--were discussed; in this second section, three other classes of drugs used as antilipidemics--bile-acid binding resins, the newer intestinal sterol absorption inhibitors and HMG-CoA reductase inhibitors (the statins)--are reviewed. Knowledgeable nurses will be able to help educate patients about these drugs and their importance in preventing or controlling hyperlipidemia.

Anticholesteremic Agents↗
PubMed1992

The effects of pravastatin on hyperlipidemia in renal transplant recipients.

Hyperlipidemia may be one of the risk factors in the development of atherosclerotic disease in renal transplant recipients. In the present study, 24 kidney recipients with hyperlipidemia were treated with an HMG-CoA reductase inhibitor, pravastatin (10 mg/day). All recipients had been treated with cyclosporine (CsA), azathioprine (Az), and prednisolone (Pred). The mean total cholesterol (T-chol) level decreased from 323 +/- 7.4 to 261 +/- 7.9 mg/dl at one month after starting treatment (P less than 0.01) and this level did not change during treatment for further 6 months. The mean LDL cholesterol level was also decreased from 205.9 +/- 11.2 to 118.7 +/- 8.1 mg/dl at 3 months after starting treatment (P less than 0.01). On the other hand, pravastatin did not affect the levels of HDL-cholesterol and triglycerides. Pravastatin did not show any effects on the white blood cell, monocyte, and lymphocyte counts, or the hemoglobin concentration (NS). One patient displayed a slight elevation of aspartate aminotransferase and alanine aminotransferase levels, but this was not sufficient to cease treatment. Pravastatin did not adversely affect the renal function or creatinine phosphokinase (CPK) levels. Two recipients developed nausea and vomiting and their treatment was stopped. Pravastatin appears to be a safe and efficacious method of treating hyperlipidemia in renal transplant recipients.

Cholesterol↗
PubMed1999

Hyperlipidemia of ApoE2(Arg(158)-Cys) and ApoE3-Leiden transgenic mice is modulated predominantly by LDL receptor expression.

To investigate the relative roles of the LDL receptor- and non-LDL receptor-mediated pathways in the clearance of apolipoprotein E (apoE) variants in vivo, we have generated apoE2(Arg(158)-Cys) (apoE2) and apoE3-Leiden transgenic mice deficient for the endogenous mouse Apoe and Ldl receptor genes (Apoe-/-.Ldlr-/- mice). Unexpectedly, on the Apoe-/-.Ldlr-/- background, expression of neither apoE2 nor apoE3-Leiden results in a decrease of the hyperlipidemia. In contrast, serum cholesterol levels are increased by the introduction of apoE2 and apoE3-Leiden in Apoe-/-.Ldlr-/- mice (to 39.1+/-7.1 and 37.6+/-7.6 mmol/L, respectively, from 25. 9+/-6.5 mmol/L). In addition, in these transgenic mice, the serum triglyceride levels are substantially increased (to 9.6+/-7.0 and 5. 8+/-2.8 mmol/L, respectively, from 0.7+/-0.5 mmol/L), which is associated with a decreased efficiency of in vitro LPL-mediated lipolysis of circulating VLDL. The VLDL-triglyceride secretion rate is not affected by the expression of apoE2 or apoE3-Leiden on the Apoe-/-.Ldlr-/- background. These results indicate that in the absence of the LDL receptor, clearance of triglyceride-rich apoE2 and apoE3-Leiden-containing lipoproteins via alternative hepatic receptors, such as the LDL receptor-related protein (LRP) is inefficient. Although apoE2 and apoE3-Leiden are disturbed in binding to the LDL receptor in vitro, expression of 1 or 2 mouse Ldlr alleles in an apoE2.Apoe-/- or apoE3-Leiden.Apoe-/- background results in a gene dose-dependent decrease of the hyperlipidemia. Furthermore, overexpression of the LDL receptor via adenovirus-mediated gene transfer rescues the hyperlipidemia associated with apoE2 and apoE3-Leiden expression. These data indicate that in apoE2 and apoE3-Leiden transgenic mice, the LDL receptor constitutes the predominant route for clearance of VLDL remnants, carrying even poorly binding apoE variants, and that this pathway is functional despite an apoE-mediated disturbance in VLDL triglyceride lipolysis.

Animals↗
PubMedDate not supplied

Management of hyperlipidemia in women with diabetes.

OBJECTIVE: To review gender-related factors in coronary artery disease, possible mechanisms for increased atherogenesis in women with diabetes, and potential therapeutic strategies for hyperlipidemia. METHODS: Pertinent published studies and personal experiences are discussed, and lipoprotein profiles are outlined. RESULTS: In the normal population, the increase in atherosclerotic vascular disease with aging in women lags behind that in men by 10 to 15 years. With the presence of diabetes, however, the atherosclerotic changes are similar in men and women. Several studies have substantiated that triglyceride levels are a stronger risk factor than cholesterol in men and women with diabetes who have coronary artery disease. In general, hypertriglyceridemia is a stronger risk factor for cardiovascular disease in women than in men. Gender differences in lipid levels can be explained physiologically by the presence of estrogen in female patients, which accelerates the rate of metabolism of lipoproteins and, in a setting of insulin deficiency, induces hypertriglyceridemia. Dietary measures and various classes of drugs, including reductase inhibitors, are used alone or in combination for management of the combined hyperlipidemia typically found in subjects with insulin resistance, diabetes, or both. CONCLUSION: Gender-related differences in lipoprotein-associated cardiovascular risk should be considered in choosing treatment options for patients with diabetes and hyperlipidemia.

Journal Article↗
PubMed1994

Apolipoprotein E in hyperlipidemia.

PURPOSE: To review DNA analysis of apolipoprotein E used to assess patients with hyperlipidemia. DATA SOURCES AND STUDY SELECTION: 44 basic science studies of molecular analysis; 42 basic science studies of the biochemical, cellular biological, and molecular biological features of apolipoprotein E; and 29 clinical investigational studies, meta-analyses, and case series of patients with mutations in apolipoprotein E. DATA EXTRACTION: Methods of DNA analysis were reviewed, using specific examples in human disease, and the role of apolipoprotein E in normal and disordered lipoprotein metabolism was reviewed. Genetic analysis of apolipoprotein E in populations and particularly in persons with type III hyperlipoproteinemia is reviewed. DATA SYNTHESIS: In the general population, common DNA variants of apolipoprotein E are consistently associated with modest differences in plasma lipids and lipoproteins. Homozygosity for the E2 isoform of apolipoprotein E predisposes some patients to the development of type III hyperlipoproteinemia, a condition that involves an additional genetic or environmental factor for full clinical expression. Rare mutations of apolipoprotein E also cause hyperlipidemia. CONCLUSIONS: DNA variation of apolipoprotein E is one of several genetic and environmental factors that interact in a complex manner to affect plasma lipoproteins. DNA analysis of apolipoprotein E can be used in persons with hyperlipidemia to identify those with type III hyperlipoproteinemia and in relatives of affected persons to identify those who are predisposed.

Apolipoproteins E↗
PubMed1999

[Aggressive therapy and combination therapy in severe hyperlipidemia].

In cases of severe hyperlipidemia, we have very effective therapeutic tools nowadays. LDL-apheresis is still the most effective therapy for familial hypercholesterolemia, especially in its homocygous form. In combination with statins, LDL-cholesterol can be lowered by 80%. Most other genetic and secondary hyperlipidemias can effectively be treated by lipid lowering drugs. This aggressive treatment gains more and more on importance in view of the tough recommendations of specific scientific societies. Atorvastatin and simvastatin can lower LDL-cholesterol by 60%. In this report different therapies and combination therapies for hyperlipidemia are discussed.

Anticholesteremic Agents↗