Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three of our regularly controlled patients suffering from Type IV hyperlipoproteinemia and treated with clofibrate complained of impotence within one year after commencement of treatment with this drug. Two of the patients had previously suffered from myocardial infarction. Two patients observed improvement of the symptom 3 and 4 weeks after interruption of clofibrate therapy; one patient again complained of impotence when clofibrate therapy was resumed. The third patient continued intake of the drug up to the present day, and still complains of impotence.
Atherosclerosis
PMID:Impotence in patients treated with clofibrate. 5 74

Cultures of human diploid fibroblasts were shown to accumulate elevated levels of intracellular triglyceride when grown in medium supplemented with sera from patients with endogenous hypertriglyceridemia (Type IV hyperlipoproteinemia). Time course studies indicated cell triglyceride levels reached maxium in 6 to 12 hours. Isotopic studies indicated that the source of the accumulated cell triglyceride was serum triglyceride, and that most of the triglyceride was taken up without hydrolysis. Triglyceride was not significantly removed by trypsinization or extensive washing. The accumulated triglyceride was also demonostrated to be metabolized, as indicated by conversion to phospholipids and free fatty acids. Increasing concentrations of hypertriglyceridemic serum in the medium resulted in increasing cell triglyceride levels. However, increasing amounts of normal serum did not result in comparable cell triglyceride accumulation. Intracellular triglyceride accumulation seemed to correlate with levels of hypertriglyceridemic serum triglyceride, whether this serum was present at equivalent concentrations or normalized to triglyceride levels equivalent to normal serum. It is concluded that elevated serum triglyceride levels can result in intracellular triglyceride accumulation even in the absence of lipolytic activity.
Atherosclerosis
PMID:Triglyceride accumulation in cultured human fibroblasts: the effects of hypertriglyceridemic serum. 17 27

Lipoprotein concentrations were compared in serum and in samples of arterial intima obtained during cardiovascular surgery. The interval between blood sampling and surgery did not exceed 48 hours. Apolipoproteins B and C, the major proteins of low density lipoprotein (LDL) and very low density lipoprotein (VLDL) respectivity, were detectable by immuno-assay in all arterial specimens. Highly significant positive correlations existed between the levels of lipoproteins in the intima and in serum. In patients with elevated serum VLDL levels (Type IV hyperlipoproteinaemia) arterial concentrations of apolipoproteins B and C were increased about two-fold; in those with raised LDL levels in serum (Type II), with or without concomitant elevation of VLDL levels, the concentration of apolipoprotein B was increased almost 5-fold in the arterial intima. The arterial wall therefore contains lipoproteins or their immunologically-similar metabolites at concentrations which are determined in part by serum lipoprotein levels.
Atherosclerosis
PMID:Lipoprotein concentrations in serum and in biopsy samples of arterial intima: a quantitive comparison. 17 26

The formation of deoxycholic acid (D) was studied in 8 patients with Type II hyperlipoproteinaemia and in 6 with Type IV hyperlipoproteinaemia, using orally administered [2.4--3H]cholic acid and [24--14C]deoxycholic acid. The diet was standardized and of natural type. The mean values for fractional turnover, pool size and D synthesis in the patients with Type II pattern were 0.23 days-1, 331 mg and 75 mg/day, respectively; in Type IV they were 0.39 days-1, 587 mg and 191 mg/day. Compared with a group of healthy subjects, the pool size and formation of D were normal in Type IV, but significantly reduced in Type II. The mean conversion of cholic acid into the circulating pool of D was calculated to be 37% in Type II, and 38% in Type IV patients. Both these values are within normal limits.
Atherosclerosis
PMID:The formation of deoxycholic acid in patients with type II and IV hyperlipoproteinaemia. 18 86

In Type V hyperlipoproteinaemia the concentration of LDL and HDL cholesterol is low. When the hypertriglyceridaemia is normalized, either by diet or micotinic acid, both LDL and HDL increase. In Type IV hyperlipoproteinaemia both LDL and HDL cholesterol decrease with increasing VLDL levels. During treatment of Type IV the change in LDL cholesterol is linearly related to the pretreatment LDL concentration so that higher LDL levels will fall and the lower will rise. HDL levels will also rise. The fall in VLDL during treatment is rapid and the rise in LDL also occurs rapidly indicating a relationship between these two reciprocal changes. HDL cholesterol, however, however, remains constant some time after VLDL has reached its lowest level and the rise occurs later indicating another mechanism than for LDL. These changes in the three major lipoprotein classes deserve clinical attention. While both the fall in VLDL and the rise in HDL may be benefical from the point of view of atherosclerosis the rise in LDL may be harmful. These is at present no way to evaluate the effect of these complex changes. However, these findings stress the imporance of considering changes in lipoprotein levels and not only in total serum triglycerides and cholesterol during treatment of hyperlipoproteinaemia.
Atherosclerosis 1977 Apr
PMID:On the rise in low density and high density lipoproteins in response to the treatment of hypertriglyceridaemias in type IV and type V hyperlipoproteinaemias. 19 26

We determined serum high-density lipoprotein cholesterol content and analyzed the approtein structure of the various lipoprotein fractions in 21 patients on chronic hemodialysis. High-density lipoprotein cholesterol was significantly reduced in all patients as compared with 11 normal persons (mean +/-1 standard deviation: 26 +/- 13 vs. 52 +/- 9 mg per 100 ml; P less than 0.001) whether or not triglyceride levels were raised. In seven of those with Type IV hyperlipoproteinemia, protein content of high-density lipoprotein and its subfractions 1, 2 and 3 were also reduced (P less than 0.001) in parallel with reductions in cholesterol in these fractions. Apoprotein electrophoresis showed an increase in "arginine-rich" peptide in very-low-density lipoprotein and high-density lipoprotein fraction 1, and a reduction in apoprotein Cll in very-low-density and high-density lipoprotein. In addition to their reduced high-density lipoprotein cholesterol levels, a major factor in the atherosclerosis of these patients may be their abnormal high-density lipoprotein composition. Their raised triglyceride levels could be due to defective lipoprotein lipase activation by the reduced very-low-density lipoprotein apoprotein.
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PMID:Defective high-density lipoprotein composition in patients on chronic hemodialysis. A possible mechanism for accelerated atherosclerosis. 21 15

Three different assays for selective measurement of plasma lipoprotein lipase (LPL) and hepatic triglyceride lipase (H-TGL) were compared. These were: an immunochemical method based on enzyme antibody precipitation (IM), a procedure in which both enzymes were separated by affinity chromatography on small heparin--Sepharose columns (HS), and an assay in which one enzyme was inhibited by protamine sulfate (PS). Good correlations were found between the immunochemical and the heparin--Sepharose method, but not between these and the protamine sulfate assay procedure. The IM was then used to evaluate the effect of clofibrate on the two lipolytic enzymes. It was found that both in normals and in patients with Type IV hyperlipoproteinemia, clofibrate treatment leads to a specific increase of plasma LPL while H-TGL activity remains almost unaffected. The magnitude of the LPL response was different in normals and in patients with endogenous hyperlipoproteinemia. Furthermore, in normals the maximal increase of LPL activity was already reached one week after drug treatment was begun, while in hypertriglyceridemic patients, this effect was not evident prior to four weeks of clofibrate treatment. The marked enzyme increase following clofibrate administration indicates that an increased peripheral removal rate for triglycerides is one major mechanism responsible for the lipid-lowering effect of this drug.
Atherosclerosis 1977 Apr
PMID:Comparison of assay methods for selective measurement of plasma lipase. The effect of clofibrate on hepatic and lipoprotein lipase in normals and patients with hypertriglyceridemia. 85 26

The nature of Type V hyperlipoproteinemia including mode of presentation, prominent clinical and biochemical features, and genetics, was examined in 29 adults presenting with the Type V lipoprotein phenotype. Initially 23 of the 29 patients had various metabolic stimuli (diabetes out of control, estrogenic agents, pancreatitis, ethanolism) superposed on their acute hypertriglyceridemia. After metabolic stabilization, 17 of the 29 subjects were shown to have familial hypertriglyceridemia. In the 17 kindreds with familial hypertriglyceridemia, the lack of a specific, distinctive genetic marker for the Type V genotype and for the Type IV genotype restricts the conclusion that the pattern of inheritance was consistent with an autosomal dominant trait.
Atherosclerosis
PMID:Familial and acquired type V hyperlipoproteinemia. 107 94

A new strain of rat characterized by genetic obesity, endogenous hyperlipidemia, and hypertension was obtained in this laboratory. The abnormal phenotype is inherited as a homozygous recessive trait. The animals exhibit marked hypertriglyceridemia, moderate hypercholesterolemia, and an electrophoretic pattern resembling that of human Type IV hyperlipoproteinemia. The average life-span is less than 1 year, due largely to the development of premature renal and vascular disease. The kidney lesion has both glomerulonephritic and nephrosclerotic components and is accompanied by marked proteinuria. About 12% of animals develop urinary tract calculi. The vascular disease consists of fibrous and fatty-fibrous intimal plaques, and polyarteritis. The obese animal offers a useful model for investigating abnormal lipid metabolism and the etiology and pathogenesis of atherosclerosis.
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PMID:Pathologic findings and laboratory data in a new strain of obese hypertensive rats. 117 27

The hyperlipoproteinemias are disturbances in the metabolism of lipoproteins. Elevated levels of total and low density lipoprotein-cholesterol, and low levels of high density lipoprotein-cholesterol are proven risk factors for atherosclerosis. The significance of hypertriglyceridemia as an independent risk factor for atherosclerosis is controversial, however, at high levels triglycerides are a major risk factor for pancreatitis. Lipoprotein abnormalities can be divided into dietary, primary (genetic), and secondary disorders. The major causes of moderate and severe hypercholesterolemia are familial hypercholesterolemia, familial combined hyperlipidemia, severe primary (polygenic) hypercholesterolemia, and familial dysbetalipoproteinemia. Causes of hypertriglyceridemia include familial hypertriglyceridemia, familial lipoprotein lipase deficiency, sporadic hypertriglyceridemia, and secondary causes.
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PMID:Hyperlipoproteinemias: Part I. Lipoprotein classification and abnormalities. 194 97


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