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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic insulinopenic diabetes was induced by i.v. streptozotocin in the non-human primate Macaca fuscata. Five diabetic monkeys were kept for 8-19 months and nine for 24-48 months without any insulin treatment. Hyperglycemia (241 +/- 22 mg/dl, M +/- SE less than or equal to 1 year) progressed to 376 +/- 34 mg/dl (greater than 2 years) and ketosis to 3.5 mM (greater than 2 years) during the course of diabetes; this was roughly inversely proportional to hypoinsulinemia (3.4 microU/ml, 2 years). Serum cholesterol increased from 184 +/- 11 (less than or equal to 1 year) to 328 +/- 66 mg/dl (greater than 2 years) with the major increase in LDL-cholesterol (2.7-fold over control, greater than 2 years). HDL-cholesterol did not change at all throughout the experimental period. TG increased from 144 +/- 25 (less than or equal to 1 year) to 676 +/- 116 (greater than 2 years) with a major increase in the VLDL fraction (15-fold over control, greater than 2 years). Serum levels of apo B increased to 141 +/- 16 (less than or equal to 2 years) and 223 +/- 8 mg/dl (greater than 2 years) in contrast to control, 73 +/- 2. Morphologically, lipid deposition in the intima and fatty streaks have been observed in the abdominal aorta of all the diabetic monkeys with duration of more than 2 years. In six of the diabetic monkeys atheromatous changes such as intimal and medial thickening with smooth muscle cell proliferation were observed with foam cell formation. Similar atherosclerotic lesions were observed in renal and coronary arteries in at least six of these monkeys. In diabetic monkeys with duration of less than 2 years, mild atherosclerotic lesions were observed in two out of five. The results indicate that long standing insulinopenia leads to metabolic derangements characterized by hyperglycemia, ketonemia and hyperlipidemia. Elevation of LDL-cholesterol and VLDL TG with an increase of apo B is a characteristic of lipoprotein disorder. Morphologically, early to moderately advanced lesions of atherosclerosis were observed in aorta, renal and coronary arteries as a result of metabolic derangement due to insulin deficiency.
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PMID:Hyperlipidemia and atherosclerosis in experimental insulinopenic diabetic monkeys. 142 36

Many patients with lipoprotein disorders are at increased risk for the development of premature atherosclerosis and, less commonly, other disorders that cause systemic morbidity. In some of these patients, xanthomas also develop and provide cutaneous markers for the lipoprotein disorder. As advances in molecular biology refine our understanding of lipoprotein metabolism, it has become increasingly clear that several types of xanthomas are associated with specific disease states. This article presents a differential diagnosis of xanthomas that incorporates contemporary thinking about lipoprotein disorders and focuses on the relationship between abnormalities in lipoprotein metabolism, content, or structure and the development of specific xanthomas.
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PMID:Dermal, subcutaneous, and tendon xanthomas: diagnostic markers for specific lipoprotein disorders. 304 20

Two types of end-point measurement are presently available in clinical trials of the effect of treatment of hyperlipidaemia on cardiovascular disease; these are the incidence of clinical events and the arteriographic assessment of progression or regression of atherosclerosis. These approaches are briefly reviewed. In the present trial, 25 hyperlipidaemic men with symptomatic femoral atherosclerosis underwent biplanar femoral arteriography at baseline. They were then randomised into treatment and usual-care groups; treatment was individualized, comprising a lipid-lowering diet with cholestyramine, nicotinic acid or clofibrate as appropriate for the lipoprotein disorder. Mean cholesterol and triglyceride levels were 19% and 37% lower in the treatment group. Arteriography was repeated after a mean period of 19 months. With attention to blinding of observers, changes in arteriograms were quantitated using computerised image analysis and visual methods, and expressed both by patient and by arterial segment. All end-points were in conformity and showed a lower rate of progression of arterial disease in the treatment group, and a higher frequency of segmental regression in treated patients. In this small trial of patients with functionally-significant atherosclerosis, effective treatment of hyperlipidaemia favourably affected the course of the arterial disease.
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PMID:Randomised controlled trial of the treatment of hyperlipidaemia on progression of atherosclerosis. 390 95

Twenty men with nodulocystic acne were treated with oral isotretinoin (13-cis-retinoic acid) for four months. Plasma lipids and lipoprotein determinations were obtained before and during treatment to quantitate the effects of oral isotretinoin on lipid metabolism. Maximum isotretinoin-induced elevations in plasma triglyceride and cholesterol levels were 67% and 16%, respectively. Additional maximal changes included very-low-density lipoprotein cholesterol increases of 56%, low-density lipoprotein cholesterol increases of 22%, and high-density lipoprotein decreases of 10% from pretreatment values. Chronic increases in plasma cholesterol levels, increases in low-density lipoprotein cholesterol levels, and decreases in high-density lipoprotein cholesterol levels may predispose subjects to premature atherosclerosis. Because of the potential for unmasking an occult lipid or lipoprotein disorder, the plasma lipid and lipoprotein profiles of subjects receiving isotretinoin should be carefully monitored.
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PMID:Changes in plasma cholesterol and triglyceride levels after treatment with oral isotretinoin. A prospective study. 622 96

The familial lipoprotein disorder type III hyperlipoproteinemia (HPL) carries a marked increase in the risk of accelerated and premature atherosclerosis, but there is considerable variation among affected individuals in susceptibility to cardiovascular disease (CVD). We studied the influence of independent risk factors for atherosclerosis in 67 patients with clinically overt type III HPL and homozygosity for apolipoprotein (apo) E2. Among the different risk factors (lipid and lipoprotein levels, age, sex, body mass index, smoking status, hypertension, and diabetes mellitus) there was only a statistically significant difference in age between 25 patients with atherosclerosis and 42 patients without atherosclerosis. Serum lipoprotein (a), [Lp, (a)], levels were 30.6% higher in the atherosclerosis group, but this was not statistically significant. We conclude that (in contrast to familial hypercholesterolemia) elevated Lp (a) concentrations may not be regarded as a component of the clinical syndrome of type III HPL.
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PMID:Relation of cardiovascular risk factors to atherosclerosis in type III hyperlipoproteinemia. 837 May 76

The clinical and biochemical characteristics of type III hyperlipoproteinemia are described in 64 patients (35 males and 29 females). Homozygosity for apolipoprotein E2, the presence of an abnormally cholesterol-rich very low density lipoprotein fraction (beta-VLDL) and an elevated ratio of very low density lipoprotein cholesterol to plasma triglycerides (> 0.3; normal ratio about 0.2) were the basis for the diagnosis. Mean serum cholesterol and triglyceride concentrations at the first visit in the clinic were 426 +/- 221 and 719 +/- 996 mg/dl, respectively. The mean age at diagnosis of the disorder was 49 years in males and 53 years in females. There was a high prevalence of obesity (72%), xanthomas (42%), and atherosclerosis (39%), especially peripheral vascular disease (31%). Early and correct diagnosis of this familial lipoprotein disorder seems necessary because of the prompt and beneficial response to therapeutic interventions.
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PMID:Clinical features of type III hyperlipoproteinemia: analysis of 64 patients. 850 5

The familial lipoprotein disorder type III hyperlipoproteinemia (HLP) is usually inherited as a recessive trait. Indeed, more than 90% of affected individuals are homozygous for a receptor binding-defective isoform of apolipoprotein (apo) E, apo E2. However, some rare apo E variants have been described that dominantly (thus in a single dose) predispose to the disease. Amino acid substitutions, which are accompanied with the loss of positive charges within the proposed apo E binding-region to lipoprotein receptors, seem to be responsible in most of these cases for the dominance with respect to the expression of type III HLP. So far available data in the literature on the naturally occurring human apo E2 (Arg136-->Cys) variant are not conclusive about its recessive or dominant character. We recently identified a subject heterozygous for this mutation, presenting the typical clinical and biochemical characteristics of type III HLP. In the present study we performed further analysis of the mutation on apo E structure and function based on computer modeling. Our combined data point to a dominant influence of the apo E2 (Arg136-->Cys) variant with respect to the transmission of the disease.
Atherosclerosis 1996 Oct 25
PMID:Three-dimensional structure of the LDL receptor-binding domain of the human apolipoprotein E2 (Arg136-->Cys) variant. 890 43

We have examined the prevalence of clinically significant atherosclerosis in 78 patients with type III hyperlipoproteinemia (HLP) and homozygosity for apolipoprotein (apo) E2. Forty-six of these individuals (59%) had no atherosclerosis, 32 patients (41%) had atherosclerosis, i.e., atherosclerosis of the extracranial carotid arteries (CAA), coronary arteries (CAD) or/and peripheral arteries of the legs (PVD), either singly or in combination. No association could be shown with respect to the co-prevalence of atherosclerotic lesions at these different arterial sites, except for the high predictive value (pv = 0.88, P = 0.006) of CAA for the presence of PVD. Hence, documentation of atherosclerosis under clinical aspects at one of these exposed arterial territories does not allow a reliable prediction of generalised atherosclerosis or local atherosclerosis at other sites of the arterial tree in individuals with this familial lipoprotein disorder. Therefore, assessment of the extent of clinically significant atherosclerosis in type III HLP patients should include careful and thorough examination of the extracranial carotid arteries, the coronary arteries, and the peripheral arteries of the legs.
Atherosclerosis 1996 Jan 05
PMID:Prevalence and association of atherosclerosis at three different arterial sites in patients with type III hyperlipoproteinemia. 892 60

We compared plasma lipid and lipoprotein parameters between 210 chronic renal failure patients treated by hemodialysis and 223 age- and sex-matched healthy control subjects to examine whether atherogenic lipoprotein changes were present in hemodialysis patients in the absence of hyperlipidemia. The hemodialysis group showed higher levels of plasma triglycerides, very low density lipoprotein (VLDL) cholesterol, and intermediate density lipoprotein (IDL) cholesterol and a lower level of high density lipoprotein (HDL) cholesterol. Low density lipoprotein (LDL) cholesterol of the hemodialysis group was not elevated but their LDL was significantly more triglyceride-enriched than that of controls. Subjects were then divided into five categories according to their plasma triglyceride levels at an interval of 50 mg/dl, and comparison was made between the two groups in the same range of plasma triglycerides. Hemodialysis patients again showed higher levels of VLDL- and IDL-cholesterol, and lower levels of HDL-cholesterol than the control group even in the plasma triglycerides-matched comparisons. Similarly, higher VLDL- and IDL-cholesterol levels in hemodialysis patients were significant in plasma total cholesterol-matched subgroup comparisons. Multiple regression analysis indicated that the relationship between plasma lipid concentrations and individual lipoprotein levels were substantially altered in uremic state. The 95th percentile level of IDL-cholesterol in the nonuremic controls was 15 mg/dl, and 45% of hemodialysis patients exceeded this level. Decreased HDL-cholesterol levels < or = 35 mg/dl were seen in 6% of the control and 38% of the hemodialysis group. Elevated IDL-cholesterol and decreased HDL-cholesterol were persistently found in hemodialysis patients with normal lipid levels. It is concluded that hemodialysis patients exhibited more atherogenic lipoprotein profile than nonuremic subjects with comparable levels of plasma triglycerides and total cholesterol. Especially, increased IDL- and decreased HDL-cholesterol levels in hemodialysis patients persisted even at very low levels of plasma lipids. Since elevated IDL and decreased HDL-cholesterol are implicated in the progression of atherosclerosis, these findings are of clinical importance in the diagnosis of lipoprotein disorder in chronic renal failure.
Atherosclerosis 1997 Jun
PMID:Atherogenic lipoprotein changes in the absence of hyperlipidemia in patients with chronic renal failure treated by hemodialysis. 919 76

Dyslipidemia is said to be present when lipid or lipoprotein levels lie within a range which is known from epidemiological studies to be associated with secondary complications, in particular atherosclerosis of the coronary arteries, or when a lipid or lipoprotein grossly deviates from the norm as in abetalipoproteinemia, hypobetalipoproteinemia or the HDL deficiency syndromes. In most cases, dyslipidemia is due not to a single genetic or environmental factor, but to a combination of the effects of several genes of small effect (polygenes) and environment. In other cases, however, dyslipidemia is caused by a mutation in a single gene of large effect. In such cases, the extent and nature of the phenotype depends primarily on the identity of the gene involved, but is also modulated to an important degree by the nature of the mutation and the genetic and environmental background against which this mutation occurs. In addition, many cases of hyperlipidemia are secondary to other disorders such as hypothyroidism or renal dysfunction. Such disorders may also unmask or exacerbate a genetic lipoprotein disorder. Examples of the latter are the unmasking of type III hyperlipidemia by diabetes mellitus or the exacerbation of familial hypercholesterolemia by hypothyroidism.
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PMID:Lipoproteins and cardiovascular risk-from genetics to CHD prevention. 963 14


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