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PubMed1979

[Hypopituitarism and hyperlipidemia. Protective effect of growth hormone deficiency against atherosclerosis (author's transl)].

Twelve cases of hypopituitarism (Sheehan's syndrome, pituitary adenoma, idiopathic) associated with hyperlipidemia (type IIb in general) are reported. It is suggested that: 1 - Growth hormone deficiency seems to have a protective effect against atherosclerosis in hyperlipidemia because there are no cardiovascular signs in 10 cases with a history of growth hormone deficiency lasting from 5 to 57 years and a patent hyperlipidemia (lasting a mean of 23 years), and there is stabilisation or improvement of ischemic signs in 2 other cases. 2 - Lipid abnormalities are frequently seen in hypopituitarism even after thyroid replacement therapy. 3 - The hyperlipidemia can be familial or can result from growth hormone deficiency alone.

Adult↗
PubMed1995

Dietary treatment of hyperlipidemia in patients with systemic lupus erythematosus.

OBJECTIVE: To evaluate dietary therapy in the treatment of hyperlipidemia in patients with systemic lupus erythematosus (SLE). METHODS: Using the National Cholesterol Education Program (NCEP) guidelines, we screened 89 patients with SLE for hyperlipidemia. Step 1 dietary therapy was instituted in 28 patients as recommended by the NCEP. Twenty-six patients failed Step 1 intervention and received Step 2 dietary therapy for an additional 3 months. Twenty-nine control patients with SLE were tested for hyperlipidemia. RESULTS: The 89 patients with SLE (94% women, 77% black) had a mean age of 37.2 years. Fasting values were total cholesterol (TC) 6.22 +/- 0.16 mmol/l (240.9 +/- 6.0 mg/dl), low density lipoprotein cholesterol (LDL-C) 4.08 +/- 0.14 mmol/l, (157.6 +/- 5.3 mg/dl), high density lipoprotein (HDL-C) 1.37 +/- 0.08 mmol/l (53.0 +/- 3.1 mg/dl), and triglyceride (TG) 1.71 +/- 0.12 mmol/l, (151.9 +/- 10.6 mg/dl). The mean dose of prednisone was 14.2 +/- 1.6 mg/day. Prednisone dose correlated with levels of TC (p < 0.01) by linear regression. The 28 patients receiving Step 1 dietary intervention had TC 6.11 +/- 0.19 mmol/l (236.4 +/- 7.3 mg/dl), LDL-C 4.05 +/- 0.19 mmol/l (156.6 +/- 7.5 mg/dl), HDL-C 1.31 +/- 0.08 mmol/l (50.7 +/- 3.0 mg/dl), and TG 1.64 +/- 0.12 mmol/l (145.4 +/- 10.3 mg/dl). The 26 patients receiving Step 2 dietary intervention had TC 5.84 +/- 0.17 mmol/l (226.0 +/- 6.6 mg/dl), LDL-C 3.83 +/- 0.19 mmol/l (148.0 +/- 7.2 mg/dl), HDL-C 1.25 +/- 0.08 mmol/l (48.5 +/- 3.2 mg/dl), and TG 1.66 +/- 0.15 mmol/l (147.1 +/- 13.4 mg/dl). The mean prednisone dose was 14.8 +/- 3.0 mg/day for both study groups. There was no significance between prednisone doses in all groups studied (p = 0.08). After 6 months of dietary therapy, there was a significant decrease in only the TC (p = 0.158). CONCLUSION: TC correlated directly with the prednisone dose. Six months of dietary intervention was required to significantly decrease the TC. Further management of hyperlipidemia will probably require drug intervention.

Adult↗
PubMed1994

[Frameworks of recognition and classification of primary hyperlipidemia].

A both useful and simple classification of primary hyperlipidemias must be at the disposal of all medical doctors, namely general practitioners and cardiologists. The practical classification we have proposed and published since 1971, fulfills this aim. Three main frames of hyperlipidemias are individualized: 1) pure or essential hypercholesterolemia 2) mixed or combined hyperlipidemias 3) major hyperglyceridemia: either exogenous or endogenous. In each of these frames, some clinical specific features, as well as some very simple biologic characteristics allow sometimes an immediate orientation towards some definite varieties of primary hyperlipidemias, now perfectly identified at the level of molecular genetic (tendinosum xanthoma with or without planar xanthomas, palm creases syndrome, tuberous or tubero eruptive xanthomas, etc...). Similarly, occurrence of cardiovascular complications, chiefly coronary, in a rather early age, and with a striking repetition in other members of family, as well of attacks of acute or subacute pancreatitis in other forms, helps considerably for orientation of the diagnosis. For all these reasons, systematic reconstitution of genetic tree on, at least, three generations in absolutely necessary. Prevalence, in various populations, of the genetic origin of these various primary disorders of lipid metabolism is round one out of 500 at the heterozygote state. Even if all the genes candidates are not yet finished to be identified, much of them are now perfectly known, in their localisation on DNA and in their multiple mutations. Possibility of combination of different gene defects can be also met; and more and more are described. This extraordinary and explosive knowledge in this field is now to be described.

Genes, Dominant↗
PubMedDate not supplied

Hypertension, hyperlipidemia, and abdominal obesity and the development of microalbuminuria in patients with non-insulin-dependent diabetes mellitus.

BACKGROUND: The hyperlipidemia syndrome (also called syndrome X or the deadly quartet) is a recognized constellation known to increase cardiovascular mortality, but its effect on renal decline is not well-described. This study examined the differential effects of hypertension, hyperlipidemia, and abdominal obesity on overnight urinary albumin excretion ratios (UAERs) among patients with non-insulin-dependent diabetes mellitus (NIDDM), who by definition possess the remaining component of the syndrome, insulin resistance. METHODS: We conducted a survey of 317 primary care NIDDM patients measuring waist-to-hip ratios, fasting lipid levels and glycemic values, and overnight UAERs. The study was carried out between January 1989 and June 1991. RESULTS: Using logistic regression controlling for age, race, sex, duration of NIDDM, and smoking status, elevated glycosylated hemoglobin (odds ratio [OR] = 1.95, 95 percent confidence interval [CI] = 1.16-3.27) or the addition of one component of the deadly quartet to pure diabetes doubled or tripled the odds of an elevated UAER (NIDDM plus obesity OR = 2.00, 95 percent CI = 1.02-3.93; NIDDM plus hypertension OR = 3.45, 95 percent CI = 1.38-8.63; NIDDM plus hyperlipidemia OR = 1.60, 95 percent CI = 0.53-4.81). In a dose-response manner, two additional factors exerted additive effects; all three additional factors combined with pure NIDDM multiplied the effect, with an odds ratio of 9.34 (95 percent CI = 2.24-38.9). CONCLUSIONS: These data quantify the incremental effects of abdominal obesity, hypertension, and hyperlipidemia on abnormal UAERs among NIDDM patients and strongly suggest the need for aggressive and simultaneous correction of multiple risk factors to prevent end organ damage in this population.

Aged↗
PubMed1996

Effects of hyperlipidemia on aortic endothelial cell turnover and transendothelial macromolecular transport in cholesterol-fed rats.

BACKGROUND: Hyperlipidemia, hypertension, cigarette smoking and diabetes are some major risk factors for atherosclerosis and cardiovascular disease. Repeated endothelial injury and enhanced focal intimal influx of plasma lipoproteins are the pivotal mechanisms involved in atherogenesis. We previously demonstrated that the endothelial cell turnover and associated endothelial permeability were significantly increased in the aorta of spontaneously hypertensive rats, chronic oral nicotine-treated rats, and streptozotocin-diabetic rats. In the present investigation, we examined the effects of hyperlipidemia on arterial endothelial cell turnover and transendothelial macromolecular transport in cholesterol-fed rats. METHODS: Sixteen male Sprague-Dawley rats were fed a diet containing 5% cholesterol for 6 weeks. A group of 14 agematched rats fed a regular diet and maintained over the same time period, were served as the controls. In en face preparations of the thoracic aorta, mitotic endothelial cells were identified by hematoxylin staining, IgG-containing dead endothelial cells were identified by an indirect immunoperoxidase method, and endothelial leakage to Evans blue-albumin complexes was quantified by fluorescence microscopy. RESULTS: The results showed that plasma cholesterol and triglyceride levels were higher in cholesterol-fed rats. The hyperlipidemic rats, compared to control rats, had higher values for the frequency of endothelial cell death (1.08 +/- 0.28% vs 0.75 +/- 0.16%), the frequency of endothelial cell mitosis (0.015 +/- 0.005% vs 0.013 +/- 0.003%) and the number density of Evans blue-albumin leaky foci (6.19 +/- 0.64/mm2 vs 5.23 +/- 0.76/mm2) in the aorta. CONCLUSIONS: Similar to the situations in hypertension, nicotine consumption and diabetes, the observed trend of increases in the frequency of endothelial cell turnover and endothelial permeability to large molecules in the aorta of cholesterol-fed rats suggested that these changes may contribute to accelerated atherogenesis in hyperlipidemia. However, since rat is not a favored animal model for studies of dietinduced hyperlipidemia and atherosclerosis, further investigations using other animal models such as rabbit, are needed to verify these observations.

Animals↗
PubMed1997

Hyperlipidemia in four related male cheetahs (Acinonyx jubatus).

Hyperlipidemia was identified in an 11-yr-old male cheetah (Acinonyx jubatus) and three related 3-yr-old male cheetah littermates. Hyperlipidemia in these four cheetahs was characterized by hypertriglyceridemia and hypercholesterolemia. The mean percentages of chylomicron and beta-lipoproteins were greater (P < 0.05) and the mean percent of alpha-lipoproteins was lower (P < 0.05) than the respective means for a group of 20 nonhyperlipidemic and clinically normal cheetahs. The etiology of the hyperlipidemia in these four cheetahs was not determined. However, the older cheetah also had chronic renal insufficiency and a parathyroid adenoma, conditions that have been associated with hyperlipidemia.

Acinonyx↗
PubMed1998

[Is combined statin and fibrate therapy indicated in the management of mixed hyperlipidemia?].

INSUFFICIENT PROGRESS: The treatment of hyperlipidemia leads to a reduced risk of coronary disease. This has been displayed notably since clinical trials have used statins. However, despite these treatments, a risk of coronary ischemia remains, which is not insignificant. There are several causes of this persistent risk which need to be analyzed. THE QUALITATIVE ASPECT OF LOW DENSITY LIPOPROTEINS: LDL are heterogeneous. This is displayed by a distribution of sizes varying from one subject to another. The predominance of small LDL is frequently found in coronary subjects detected during prospective or retrospective studies. The atherogenicity of small LDL can be explained by their physico-chemical characteristics. A remarkable fact is the predominance of small LDL in subjects with a mixed hyperlipidemia presenting a high risk of atherosclerosis. THE EFFECTS OF HYPOLIPIDEMIANTS: Statins greatly decrease LDL-cholesterol without changing LDL distribution according to size. Conversely, fibrates noticeably modify LDL distribution, reducing the percentage of small LDL. A PROPOSAL FOR THE TREATMENT OF SUBJECTS SUFFERING FROM MIXED HYPERLIPIDEMIA: If the concentration of LDL (reflected by LDL-cholesterol) and LDL distribution are two risk factors of atherosclerosis, hypolipidemic treatment should aim to act upon these two parameters, but no commercialized hypolipidemiant is effective enough as fas as they are both concerned. Therefore the combination of two hypolipidemiants, a statin and a fibrate, each having a predominant effect on one of the two factors, could be particularly effective in reducing coronary risk. This therapeutic association is effective on classic lipid parameters, does not entail more side effects than a monotherapy, and is not precluded by the RMO when there is a high vascular risk, which is often the case in mixed hyperlipidemia.

Anticholesteremic Agents↗
PubMedDate not supplied

[Prevalence of hyperlipidemia in children adn adolescents in the Province of Cáceres].

BACKGROUND: The lipid factor is currently considered to be the main agent responsible for cardiovascular risk in young individuals. This is already present during infancy in proportions that give rise to concern, and is growing, as has would seem to have been shown by several national studies. This study analyses the prevalence of hyperlipidemia in children within the province of Caceres according to several different criteria, and describes changes according to age groups and sex, comparing the overall results with those of other national studies. METHODS: A cross-sectional descriptive study of a representative and proportional sample of 2,150 children aged 2 to 6 years old in the province of Caceres (N = 91,083). The following were determined: total cholesterol, fractions, apolipoproteins and risk coefficients (enzymatic technique). RESULTS: 27.9% of children presented total cholesterol values of > 200 mg/dl; 7.5% of females and 4.7% of males had figures of more than 230 mg/dl. Levels of C-LDL > 130 mg/dl appear in 26.4%, Apo-B > 75 mg/dl in 65.5% and C-NO-HDL > 165 in 8.4%. C-HDL- < 35 mg/dl was found in 3.3% of individuals, while Apo-A < 100 mg/dl was only found in 0.3%. The ratios between CT/HDL > 3.5 and LDL/HDL > 2.2 were found to be 36.1% and 39.8%, respectively. The prevalence of hyperlipidemia is higher in females and pre-puberty stages. CONCLUSIONS: Overall, and independently of the criteria used, the proportion of cases of hyperlipidemia is high, and is above the levels cited in other Spanish studies. The prevalence of hyperlipidemia is highest in females before puberty, who display the most discriminatory risk coefficients, and best identify the change in the lipid profile at puberty.

Adolescent↗
PubMed2005

Evaluation of rat and rabbit sera lipoproteins in experimentally induced hyperlipidemia by analytical ultracentrifugation.

Animals of various species are widely used as models with which to study atherosclerosis and the lipoprotein metabolism. The objective of this study was to investigate the lipoprotein profiles in Wistar rats and New Zealand white rabbits with experimentally induced hyperlipidemia by means of ultracentrifugation. The Schlieren curves were utilized to compare suckling and adult rat sera to determine whether aging causes alterations in lipoprotein profiles. A striking feature of the data is the high concentration of low-density lipoproteins (LDL), (>5.2 mmol/l cholesterol) in the 2-week old rat serum pool which was greatly decreased in the 3-weeks rat serum pool (<1.3 mmol/l cholesterol). Additional experiments were performed to permit a direct comparison of the amounts of lipoprotein present in rat sera in experimental hyperlipidemia post-Triton WR 1339 administration. Rapid changes in concentrations in very low-density lipoproteins (VLDL), LDL and high-density lipoproteins (HDL) were observed after Triton injection. The administration of Triton WR 1339 to fasted rats resulted in an elevation of serum cholesterol levels. Triton physically alters VLDL, rendering them refractive to the action of lipolytic enzymes in the blood and tissues, preventing or delaying their removal from the blood. Whereas the VLDL concentration was increased markedly, those of LDL and HDL were decreased at 20 h after Triton treatment. Rabbits were fed a diet containing 2% cholesterol for 60 days to develop hyperlipidemia and atheromatous aortic plaques. A combination of preparative and analytical ultracentrifugation was used to investigate of LDL aliquots, to prepare radioactive-labeled lipoproteins and to study induced hyperlipidemia in rabbits. Analytical ultracentrifugation was applied to investigate the LDL flotation peaks before and after cholesterol feeding of rabbits. Modified forms of LDL were detected in the plasma of rabbits with experimentally induced atherosclerosis. ApoB-containing particles, migrating as LDL, intermediate density lipoproteins and VLDL were the most abundant lipoproteins. Gamma camera in vivo scintigraphy on rabbits with radiolabeled lipoproteins revealed visible signals corresponding to atherosclerotic plaques of the aorta and carotid arteries.

Age Factors↗
PubMed2003

Hyperlipidemia in pediatric kidney transplant recipients treated with cyclosporine.

Hyperlipidemia is a risk factor for cardiovascular disease in adult kidney transplant (Tx) recipients. We sought to determine the prevalence of, and the risk factors associated with, hyperlipidemia in pediatric kidney Tx recipients on cyclosporine (CsA). We identified 59 patients (mean age 8.2+/-5.7 years) transplanted between 1 January 1991 and 31 December 1993. Pre Tx, 34% had elevated total cholesterol [TC >200 mg/dl (5.17 mmol/l)]; 54% had elevated triglycerides [TG >200 mg/dl (2.26 mmol/L)]. Mean TG was higher pre Tx in dialysis (versus nondialysis) patients: 306 mg/dl (3.46 mmol/l) versus 228 mg/dl (2.58 mmol/l) ( P=0.04). Mean TC was higher in peritoneal dialysis than hemodialysis patients: 222 mg/dl (5.74 mmol/l) versus 169 mg/dl (4.37 mmol/l) ( P=0.03). Pre Tx and 3-year values correlated (TC, r=0.49, P=0.0008; TG, r=0.41, P=0.001); 3- and 5-year TC values correlated ( r=0.57, P=0.003). At 5 years post Tx, 41% of the recipients had elevated TC; 14% had elevated TG. Recipients with elevated TC had higher mean CsA concentrations at 1 year post Tx ( P=0.03). Recipients with elevated TG tended to receive more prednisone ( P=0.06). At 5 years post Tx, recipients had a high prevalence of hyperlipidemia. The identification and treatment of hyperlipidemia should be included in pediatric kidney Tx protocols.

Adolescent↗
PubMed1984

Distribution of apolipoprotein E isoforms between very low and high density lipoproteins of normal subjects and hyperlipidemic patients with special reference to type III hyperlipidemia.

Serum very low (VLDL) and high density lipoproteins (HDL) from 17 hyperlipidemic patients and 10 normal subjects have been isolated by preparative ultracentrifugation, and the electrophoretic patterns of apolipoprotein E (apo E) isoforms in the lipoproteins have been examined by isoelectric focusing. Type III hyperlipidemia (dyslipoproteinemia) has been suggested to be a disease caused by an abnormal mutant of the apo E-3 isoform. In accordance with this, all patients with type III hyperlipidemia in the present study showed lack of apo E-3 in VLDL. However, all these patients demonstrated a protein zone corresponding to apo E-3 in their HDL fraction. Patients with other types of hyperlipidemia or normal subjects who showed an apo E-4 variant in VLDL had an HDL that lacked apo E-4. The results support the hypothesis that type III hyperlipidemia is due to an abnormal composition of the VLDL particles rather than a result of an abnormal mutant of apo E-3.

Apolipoproteins↗
PubMed2005

Safety and efficacy of colesevelam hydrochloride in combination with fenofibrate for the treatment of mixed hyperlipidemia.

OBJECTIVE: The aim of this study was to evaluate the amount of low-density lipoprotein cholesterol (LDL-C) reduction achieved by adding the specifically engineered bile acid sequestrant (SE-BAS) colesevelam HCl to a stable dose of fenofibrate in patients with mixed hyperlipidemia. RESEARCH DESIGN AND METHODS: Patients with mixed hyperlipidemia (n = 129) were enrolled in a randomized, double-blind, placebo-controlled, parallel-group study investigating the efficacy of fenofibrate plus colesevelam HCl versus fenofibrate monotherapy. After a 4- to 8-week washout period, subjects received fenofibrate 160 mg/day for 8 weeks and were then randomized to receive colesevelam HCl 3.75 g/day or placebo, in addition to fenofibrate 160 mg/day, for 6 weeks. MAIN OUTCOMES MEASURES: The primary efficacy endpoint was mean percent change in LDL-C during randomized treatment. Secondary endpoints included absolute and percent changes in mean levels of LDL-C, triglycerides (TGs), high-density lipoprotein cholesterol (HDL-C), non-HDL-C, total cholesterol (TC), and apolipoproteins (apo) A-I and B during randomized treatment and from washout to end of randomized treatment. RESULTS: Of the 129 patients randomized to treatment, 119 completed the study. After 6 weeks of treatment, fenofibrate plus colesevelam HCl produced a mean percent change in LDL-C of -10.4% versus +2.3% with fenofibrate monotherapy (p < 0.0001). Fenofibrate plus colesevelam HCl was significantly more effective than fenofibrate alone at reducing levels of non-HDL-C, TC, and apo B (p < or = 0.0002). Colesevelam HCl did not significantly affect the TG-lowering effects of fenofibrate. Both treatment regimens were safe and well tolerated. CONCLUSIONS: Compared with fenofibrate monotherapy in patients with mixed hyperlipidemia, fenofibrate/colesevelam HCl combination therapy significantly reduced mean LDL-C, non-HDL-C, TC, and apo B levels without significantly affecting the TG-lowering or HDL-C-raising effects of fenofibrate. Fenofibrate/colesevelam HCl combination therapy is a safe, useful alternative for the treatment of mixed hyperlipidemia.

Allylamine↗
PubMed2002

[Effect of protein and anthraquinone glucosides from cassia seed on serum lipid of hyperlipidemia rats].

OBJECTIVE: To study the effect of protein and anthraquinone glucosides from cassia seed on serum lipid of hyperlipidemia rats. METHOD: The rat hyperlipidemia model was set up by ig lipid emulsion. The effects of the protein 0.25 and 1 mg.kg-1. d-1, the anthraquinone glucosides 5 and 20 mg.kg-1.d-1, and the protein 0.25 mg.kg-1.d-1 plus the anthracene glucosides 5 mg.kg-1.d-1 on total cholesterol (TC), triglyceride (TG), low density lipoprotein (LDL-C) and high density lipoprotein (HDL-C) in serum of the rats were determined. RESULT: The protein 1 mg.kg-1.d-1, the anthraquinone glucosides 20 mg.kg-1.d-1 reduced the raised TC, TG, LDL-C of hyperlipidemia rats (P < 0.05). The above indexes could also be reduced by the protein 0.25 mg.kg-1.d-1 plus the anthraquinone glucosides 5 mg.kg-1.d-1(P < 0.05, P < 0.01). CONCLUSION: Protein and anthraquinone glucosides from cassia seed can lower TC, TG, LDL-C of hyperlipidemia rats.

Animals↗
PubMed1993

[Genealogy and the clinical manifestations of familial hyperlipidemias types IIa and IIb].

To analyze genealogical and clinical characteristics of family hyperlipidemia type IIa and IIb, the author examined 40 probands and 179 close relatives. Blood lipid composition was investigated in 85 of them. Hyperlipidemia was found in 42 examinees which is in accordance with previous findings on this trait inheritance. Sons inherit hyperlipidemia from their fathers more frequently than daughters (60.0% against 40.0%, respectively). Coronary heart disease and other related clinical conditions arose more frequently in probands than in their relatives with hyperlipidemia though 10-year mortality in them was actually the same: 20.0 and 18.6%, respectively.

Adolescent↗
PubMed1987

DNA polymorphisms in and around the Apo-A1-CIII genes and genetic hyperlipidemias.

We have studied the frequency of DNA polymorphisms in and around the apolipoprotein A-1 (Apo-A1) and apolipoprotein CIII (Apo-CIII) gene loci in 53 persons of Caucasian descent with genetic hyperlipidemias. Three restriction-fragment-length polymorphisms (RFLPs) have previously been located 5' and 3' to the Apo-A1 gene and in the Apo-CIII gene and were detected after digestion with XmnI, PstI, and SstI, respectively, and hybridization with a 2.2-kb fragment of the Apo-A1 gene. These RFLPs are in linkage equilibrium. The rare variant sites for XmnI (X2) and SstI (S2) were more frequent in familial combined hyperlipidemia (FCH) than in controls and persons with other genetic hyperlipidemias. When considered as a haplotype, this difference was significant (P less than .03). The findings in this study suggest that the previously reported association between S2 and hypertriglyceridemia may be accounted for, in part, by inclusion of numerous patients with FCH. Our data provide further evidence that these RFLPs around and within the Apo-A1/Apo-CIII genes do not participate in unmasking clinical expression in persons with familial dysbetalipoproteinemia.

Adult↗
PubMed1982

[Diagnosis, clinical features and treatment of hyperlipidemias in children].

Hyperlipidemias represent one of the most important risk factors for the development of premature atherosclerotic disease. If prevention of ischaemic cardiovascular disease, which is responsible for about 50% of the deaths in Western Europe, should be successful, diagnosis and treatment of hyperlipidemic states should start as early as possible. A short overview concerning the composition and the metabolism of the lipoproteins is given and theoretical and practical aspects for the classification of the different forms of hyperlipoproteinemia during childhood are pointed out. Laboratory determinations are described and therapeutic approaches of the main pediatric hyperlipidemias are given: polygenetic and combined familial hyperlipidemias should be treated by diet alone, whereas familial hypercholesterolemias request drug treatment: cholestyramine, given in doses between 4 and 8 g seems to be the drug of choice. Possible future aspects of drug treatment are discussed, even those who are shown to increase the number of LDL-receptors, which are blocked in that disease. Finally, efforts are emphasized to screen all children of families, in which premature heart disease or hypercholesterolemia occur.

Adolescent↗
PubMed1981

The clinical laboratory and hyperlipidemia: a clinician's view.

Many patients with hyperlipidemia are without symptoms, thus laboratory data are often the sole index of therapeutic success or failure. Aggressive laboratory investigation of patient and family may identify inherited hyperlipidemia long before the clinical manifestations of atherosclerosis. The classification system of Fredrickson et al and Goldstein et al are reviewed from an historical and a clinician's point of view. Specific phenotypes and phenocopies, their causes, clinical manifestations, and management are presented. The basic laboratory assessment of hyperlipidemia is described, specialized testing is reviewed, and promising new methodologies are discussed.

Cholesterol↗
PubMed2001

Overrestriction of dietary fat intake before formal nutritional counseling in children with hyperlipidemia.

OBJECTIVE: To assess the nutritional adequacy of the diets of children with hyperlipidemia following medically unsupervised low-fat diets compared with children receiving unrestricted diets. DESIGN: Case comparison study. PATIENTS AND OTHER PARTICIPANTS: Forty-six children were referred to the Children's Cardiovascular Health Center, Columbia-Presbyterian Medical Center, New York, NY, for treatment of hyperlipidemia who had achieved the Step I diet recommendations for total fat before formal nutritional counseling (mean age +/- SE, 9.7 +/- 0.3 years; sex distribution, 24 boys [53%]; ethnicity, 26 Latinos [57%] and 20 whites [43 %]; body mass index +/- SE, 22.4 +/- 0.7 kg/m(2)), and 34 healthy children participating in well-child visits at a local pediatric practice (mean age +/- SE, 10.2 +/- 0.4 years; sex distribution, 18 boys [54%]; ethnicity, 19 Latinos [57%] and 15 whites [43%]; body mass index +/- SE, 22.5 +/- 1.1 kg/m(2)). MAIN OUTCOME MEASURES: Three-day food records were analyzed by a registered dietitian using the Minnesota Nutrient Data System. Outcome measures were intakes of calories, total and saturated fats, carbohydrate, protein, essential fatty acids, fat-soluble vitamins, folate, vitamin C, calcium, iron, and zinc. RESULTS: The percentage of calories from fat and saturated fat was significantly lower in the hyperlipidemic population (mean +/- SE, hyperlipidemic vs control subjects: total fat, 22.7% +/- 0.7% vs 34.5% +/- 0.6%, P<.001; saturated fat, 7.9% +/- 0.3% vs 12.9% +/- 0.4%, P<.001). The caloric intake in controls was 17% higher than in patients with hyperlipidemia. Ninety percent of the decrease in calories in the hyperlipidemic group could be accounted for by the decrease in total fat intake. After adjusting for calories, no significant difference was noted between the groups for any of the vitamins and minerals mentioned earlier. CONCLUSION: Our findings suggest that before formal nutritional counseling, overzealous dietary fat restriction can occur in children with hypercholesterolemia.

Child↗