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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe a case of severe intracranial atherosclerosis in a young man who had received therapeutic radiation for a presumed brain neoplasm. Since there was no evidence of vascular disease outside the radiation ports, we speculate that accelerated atherosclerosis was induced by radiation and that hyperlipidemia may have predisposed him to this effect.
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PMID:Intracranial atherosclerosis following radiotherapy. 338 38

The possible role of Mg in the pathogenesis of vascular disease has recently received increasing attention. Accumulating evidence indicates that Mg strongly influences vascular tone and responsiveness to pressor agents and that Mg deficiency may be associated with an increased risk of hypertension. Moreover, experimental Mg deficiency produces vascular lesions with calcifications while increasing the dietary intake of Mg has been shown to prevent atheroma and thrombotic complications. The modifications of lipid metabolism during experimental Mg deficiency have been recently characterized. Severe Mg deficiency in weanling rats produces a marked hypertriglyceridemia and a decrease in the percentage of cholesterol transported by high-density lipoprotein. The decreased clearance of circulating triglycerides appears to be the major mechanism contributing to hyperlipemia. The same animals were found to have a reduced insulin response after intravenous glucose challenge and a slight reduction in heparin release lipoprotein lipase. A marked reduction in plasma activity of LCAT and a significant decrease in esterified/total plasma cholesterol ratio have also been reported. Severe Mg deficiency in weanling rats produces marked changes in the fatty acid pattern of total plasma lipids, as shown by decreased levels of stearic acid, increased of oleic acid and linoleic acid, and decreased levels of arachidonic acid. Platelets from Mg-deficient rats become more sensitive to thrombin. Such an increased sensitivity of platelets may in turn play an important role in initiating the vascular lesion as well as in thrombotic complications. In view of these experimental data in animal models, more work seems necessary in man to assess the effect of Mg on lipid metabolism and vascular disease.
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PMID:Magnesium, lipids and vascular diseases. Experimental evidence in animal models. 352 56

Gypsies are a cohesive cultural group who may have difficult relations with the American medical community. There are several hundred thousand Gypsies in this country; they maintain a private society with an internal moral code and legal system. There is a strong cultural basis for obesity, tobacco use, fatty diet, and inbreeding among Gypsies. These traits predispose them to hypertension, diabetes, hyperlipidemia, and occlusive vascular disease. When ill they present a striking dichotomy of primitive fears of disease process with surprising sophistication for medical terms and the workings of the hospital hierarchy. Specific recommendations are made for more effective and compassionate relations with Gypsy patients.
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PMID:Gypsies and American medical care. 388 25

Type II diabetic subjects, 26 with symptoms and/or signs of large vessel disease (LVD group) and 26 free from clinical vascular disease (FVD group), matched for sex, age, body weight, and duration of diabetes after diagnosis, together with 28 healthy controls participated in a preliminary study on new potential risk factors of large vessel disease. The activity of erythrocyte aldehyde dehydrogenase (ALDH) was significantly higher (P less than 0.005) in the LVD than in the FVD group and in the controls, as indicated by a shorter half-life of acetaldehyde in homogenates of erythrocytes and plasma (100 +/- 11, 203 +/- 28, and 180 +/- 21 min, respectively). The results were unaffected by antidiabetes therapy, blood glucose control, alcohol consumption, or by recognized risk factors of angiopathy, such as blood pressure, hyperlipidemia, or smoking. Whether ALDH activity is a primary factor in large vessel disease or is merely a secondary phenomenon is unknown. However, ALDH activity is a critical factor determining chlorpropamide alcohol flush (CPAF), which has been suggested to be an inherited trait in some type II diabetic subjects. In conclusion, high ALDH activity was shown to be associated with an increased risk of large vessel disease in diabetes.
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PMID:Aldehyde dehydrogenase activity and large vessel disease in diabetes mellitus. A preliminary study. 394 78

In order to evaluate the prevalence of common and/or internal carotid stenoses together with metabolic abnormalities in dementia nineteen patients were investigated. Dementia and differential diagnosis between Alzheimer type (DAT) and multi-infarctual (MID) dementia were performed on the basis of Computerized Tomography scan, behavioural anamnesis, neurological and neuropsychological examinations. Eight patients were diagnosed as MID and 11 as DAT. Noninvasive study of neck arteries was performed in supine position by a Duplex Scanner, able of detecting a wide range of stenosis, even when very mild. Arterial hypertension, hyperlipidemia, diabetes and high hematocrit level were present in both groups, although to a higher extent in MID (p 0.05). Results from Duplex Scanner demonstrate 12 vascular stenoses 16-49% and one between 50-99% (13/76), being vascular abnormalities equally distributed among DAT and MID patients. These data suggest that patients with metabolic abnormalities and arteriosclerosis can develop dementia not necessarily of vascular type. On the other hand, MID patients do not present higher number of stenosis as compared to DAT, indicating that vascular disease of carotid arteries is not prominent in the clinical context of dementia.
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PMID:Non invasive study of carotid arteries by echo-doppler and metabolic abnormalities in patients with dementia. 402 28

A total of 594 patients admitted for cerebrovascular disease (CVD) and for peripheral vascular disease (PVD), were examined in a study aimed at clarifying by a simple, inexpensive out-patient method, a) the relationship existing between the different locations of the vascular disease: brain, lower limbs, coronaries; b) the prevalence in the patients studied of risk factors such as hypertension, hyperlipidaemia and diabetes, and of migraine. The results were as follows: a) of the patients admitted for CVD, 44% also presented arteriosclerosis in other locations; this figure was 32% for PVD cases; b) hypertension was found in 38.5% of CVD and 27% of PVD cases; diabetes in 11.5% of CVD and in 18% of PVD cases; hyperlipidaemia in 31% of CVD and 24% of PVD cases; migraine in 11% of CVD and 1% of PVD cases.
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PMID:Validity of out-patient screening in arteriosclerosis to identify multiple lesions. 406 67

Primary hyperbetalipoproteinemia (type II hyperlipoproteinemia) is a common disorder associated with premature vascular disease. It is frequently due to genetic abnormalities, some of which are expressed in childhood. We have examined the manner in which that form of hyperbetalipoproteinemia known as familial hypercholesterolemia may be expressed in 236 children aged 1-19 born of 90 matings in which one parent had hyperbetalipoproteinemia of this variety and one parent did not.Two Gaussian populations were fitted to the distribution of both low density lipoprotein cholesterol (C(LDL)) and plasma cholesterol (C) in these children and a likelihood ratio test strongly favored a two over a one population model for both C(LDL) (X(2) = 18.41, P < 0.0005) and C (X(2) = 7.81, P < 0.025). 45% of the children were in the population identified as affected; their mean C(LDL) was 229. The remaining 55% were in the normal population with a mean C(LDL) of 110 which was indistinguishable from that of an unrelated control population, aged 1-19. On the basis of an assumed frequency of hyperbetalipoproteinemia in the general population of 5%, the Edwards' test indicated that a polygenic model of inheritance was highly unlikely (expected, 22%; observed, 45%). The segregation ratio obtained from the derived intersection between the two population curves (C(LDL), 164 mg/100 ml; C, 235 mg/100 ml) was 45/55 (abnormal/normal). The percentage of abnormal children in the first decade (52%) significantly exceeded that in the second (39%) (P < 0.01). The ratios (II/N) were 50/47 and 55/84 in the offspring of affected female and male parents, respectively (X(2) = 3.819, 0.05 < P < 0.10). Only 10% of hyperbetalipoproteinemic children were considered to have hyperglyceridemia. These children, frequently, but not invariably, had a parent with hyperglyceridemia in addition to hyperbetalipoproteinemia (P < 0.05). None of the affected children who were examined had ischemic heart disease (IHD) and 7% had tendon xanthomas. Half of the parents (mean age, 37.4 yr) who were examined had IHD and three-quarters had xanthomas. The data agree well with the hypothesis that hyperbetalipoproteinemia is inherited as a monogenic trait with early expression in these children. More than one genetic defect within the group is not excluded, but retrospective analyses of the 345 first-degree adult relatives of the affected parents indicated that most of the abnormal parents probably represented familial hypercholesterolemia, rather than combined hyperlipidemia, the other most generally recognized form of familial hyperbetalipoproteinemia.
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PMID:Familial hypercholesterolemia (one form of familial type II hyperlipoproteinemia). A study of its biochemical, genetic and clinical presentation in childhood. 436 6

In 101 subjectively healthy persons, who at a routine health examination were found to be markedly hyperlipidaemic, the erythrocyte sedimentation rate (E.S.R.) was significantly raised. The E.S.R. was raised above 25 mm/hr in 44, 64, and 23% respectively of subjects with type II A, II B, and IV hyperlipoproteinaemia in comparison to only 6% in sex- and age-matched normolipidaemic controls.Several explanations for this E.S.R. elevation have been studied. The levels of plasma lipoproteins do not appear themselves to influence the E.S.R., as among other things there was no difference in plasma concentrations of cholesterol and triglycerides in hyperlipidaemic persons with high and low E.S.R. The concentration of lysolecithin, which may decrease the E.S.R. was the same in the hyperlipidaemic persons with high E.S.R. as in those with low. However, the incidence of ischaemic exercise E.C.G. changes was 38% in the hyperlipidaemic subjects with E.S.R. below 24 mm/hr and 72% in those with E.S.R. above 25 mm/hr. For the time being one possible reason for the raised E.S.R. thus seems to be that the hyperlipidaemia causes silent vascular disease that in its turn produces the E.S.R. elevations.
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PMID:Raised erythrocyte sedimentation rate in asymptomatic hyperlipidaemia. 473 47

Many studies of atherosclerosis have indicated hyperlipidaemia as a predisposing factor to vascular disease. The relationship holds even for mild degrees of hyperlipidaemia, a fact that underlines the importance of this category of disorders. Both primary and secondary hyperlipidaemias represent such a variety of abnormalities that an internationally acceptable provisional classification is highly desirable in order to facilitate communication between scientists with different backgrounds.The present memorandum presents such a classification; it briefly describes the criteria for diagnosis of the main types of hyperlipidaemia as well as the methods of their determination. Because lipoproteins offer more information than analysis of plasma lipids (most of the plasma lipids being bound to various proteins), the classification is based on lipoprotein analyses by electrophoresis and ultracentrifugation. Simpler methods, however, such as the observation of plasma and measurements of cholesterol and triglycerides, are used to the fullest possible extent in determining the lipoprotein patterns.
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PMID:Classification of hyperlipidaemias and hyperlipoproteinaemias. 493 42

The plasma concentration of beta-thromboglobulin (BTG), a platelet-specific protein released during platelet aggregation, is considered a sensitive marker of in vivo platelet activity. The mean plasma level in 133 asymptomatic individuals was 32.3 +/- 1.1 ng/ml, and there was no difference between those with no risk factors (32.2 +/- 1.2 ng/ml, n = 56), those who smoked (31.8 +/- 1.8 ng/ml, n = 45), those with hyperlipidemia (32.8 +/- 1.7 ng/ml, n = 15), and those exposed to both of these risk factors (34.1 +/- 2.7 ng/ml, n = 17). The mean plasma BTG level in 104 patients with symptomatic ischemic heart disease was significantly elevated (40.9 +/- 1.4 ng/ml, p less than 0.01), but there was considerable overlap with normal levels. Although no difference was found between patients with no risk factors (38.1 +/- 4.0 ng/ml, n = 13) and those with only 1 risk factor (37.0 +/- 1.8 ng/ml, n = 44), patients with 2 or more risk factors ahd a significantly elevated plasma BTG level (45.2 +/- 2.2 ng/nl, n = 47, p less than 0.01). It is concluded that risk factors themselves do not increase platelet activity, but that patients with vascular disease have activated platelets that may contribute to the progression of the disease. Plasma BTG was also measured serially for 10 days in 29 patients after hospitalization with acute ischemic cardiac pain. Although the median plasma level was elevated above normal there were no acute changes in plasma BTG after either acute infarction (n = 22) or acute ischemia (n = 7), except in 2 patients in whom pericardial friction rubs developed. Thus, measurement of systemic plasma BTG did not detect platelet involvement in acute coronary occlusion or acute ischemia.
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PMID:Plasma beta-thromboglobulin as a measure of platelet activity. Effect of risk factors and findings in ischemic heart disease and after acute myocardial infarction. 618 69


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