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)

Familial defective apolipoprotein B-100 (FDB) is a recently identified dominantly inherited genetic disorder, which leads to increased serum levels of low density lipoprotein (LDL) cholesterol with reduced affinity for the LDL receptor. This genetic disorder is characterized by defective binding of the apolipoprotein B-100 (apo B-100), which is virtually the sole protein constituent of LDL, to the LDL receptor. The defective binding results from a G to A mutation at amino acid 10,708 in exon 26 of the apolipoprotein B (apo B) gene creating a substitution of glutamine for arginine in the codon for amino acid 3500. It is postulated that FDB can exhibit the same clinical features as familial hypercholesterolemia (FH) caused by a defective LDL receptor. The purpose of this paper is to report on an individual with a defective LDL and a defective LDL receptor. The clinical features of this individual were the same as in the family members with either defective LDL or a defective LDL receptor: premature arcus lipoides, tendon xanthomata, and premature atherosclerosis. Although the clinical features were present to the same degree as in individuals with either defect the prognosis and treatment of such an individual could be different.
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PMID:Identification of a heterozygous compound individual with familial hypercholesterolemia and familial defective apolipoprotein B-100. 206 18

Hypertriglyceridemia is a common disorder of lipid transport occurring either as a primary or secondary manifestation of the underlying metabolic derangement. Although most prospective studies have provided no evidence for the independent contribution of plasma triglycerides to atherosclerosis, results of several clinical and metabolic studies have indicated that some modified triglyceride-rich lipoproteins may be as atherogenic as the typical cholesterol-rich low density lipoproteins. Our studies on the sequential fractionation of apolipoprotein B-containing lipoproteins have identified five major apolipoprotein-defined lipoprotein families including cholesterol-rich lipoprotein B and triglyceride-rich lipoproteins B:C, B:C:E, B:E and A-II:B:C:D:E. The evaluation of the results of Cholesterol Lowering Atherosclerosis Study has shown that some triglyceride-rich lipoproteins play an important role in the progression of atherosclerosis. The combined niacin-colestipol treatment resulted in a 40-50% decrease in the levels of cholesterol-rich lipoprotein B but had no effect on triglyceride-rich lipoproteins. Patients who had increased levels of latter lipoproteins, as demonstrated by decreased levels of apolipoprotein C-III in heparin-Mn++ supernates, showed progression of atherosclerotic lesions. On the other hand, in the Helsinki Heart Study, despite minimal reduction in the levels of LDL-cholesterol, patients with phenotypes IIB and IV had higher reduction rates in coronary end points than patients with phenotype IIA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Determination of potentially atherogenic triglyceride-rich lipoprotein particles]. 208 77

To elucidate the role of apolipoprotein E (apo E) in atherogenesis, we have investigated the localization of apo E in normal and atherosclerotic aortas as well as in other tissues of 32 post-mortem individuals. Using double immunofluorescence it has been found that normal intima of individuals older than 20 years and some adolescents contained immunoreactive material that reacted with poly- and monoclonal antibodies to apo E. A staining pattern of apo E differed from that of apolipoprotein B, the latter being seen in normal intima of each child older than 7 years. Apo E was present extracellularly in lipid streaks and atheromatous plaques, where its staining was particularly intensive around the necrotic zone of plaques. Some macrophages in the plaques of 4 aortas exhibited apo E-positive staining, while aortic endothelial and smooth muscle cells never contained apo E. Apo E-positive staining was not found in the majority of vessel cells, it was always, however, observed in other types of cells including hepatocytes. Kupffer cells, spleen macrophages and cerebral astrocytes. Our findings indicate that only some macrophages in human aorta may be responsible for the production of apo E that can participate in reverse cholesterol transport. At the same time, apo E accumulation in the aortic wall may promote the development of atherosclerosis.
Atherosclerosis 1990 Dec
PMID:Localization of apolipoprotein E in normal and atherosclerotic human aorta. 210 87

The correlations between lipid and lipoprotein measurements and other risk factors of coronary artery disease were evaluated in 101 men undergoing coronary angiography. Clinically significant disease was present in 75 patients, whereas 24 had no observable lesions and 2 had minimal lesions. Comparisons of individual lipid and lipoprotein levels were nearly all significantly different between patients with and patients without clinically significant disease; however, no single variable could predict the presence of disease among patients. Logistic regression analysis identified five factors: apolipoprotein A-I, apolipoprotein B, diabetes, age, and family history of heart disease, which account for most of the differences between the two patient groups. These results could have important implications for the evaluation and management of patients suspected of having coronary atherosclerosis.
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PMID:Correlates of atherosclerosis in coronary arteries of patients undergoing angiographic evaluation. 211 60

Apolipoprotein A-I, the major protein of high-density lipoproteins, and apolipoprotein B, the major protein of low-density lipoproteins can serve as important predictor of the risk of cardiovascular diseases. The lack of an internationally valid standardization is a serious impediment to a broad application of the apolipoprotein measurements in the laboratory diagnosis of atherosclerosis. A common effort is at the present made by the IFCC Committee on Apolipoproteins together with several commercial organizations to achieve a consensus on a practical standardization procedure for the measurement of apolipoprotein A-I and B. The aim is a) to calibrate all commercially available Apo A-I and Apo B test kits using frozen serum pools previously standardized against primary reference materials and b) to select the secondary serum reference preparations which will substitute the frozen serum pools and will be used for the control of the validity of the own calibration. The available results from a preliminary exercise prove with a variation less than 5% for Apo A-I and less than 8% for Apo B with patients' samples that the use of common reference materials leads to the harmonization of the results obtained with different test systems for measurement of apolipoprotein A-I and B.
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PMID:[Standardization of the immunochemical detection of apolipoprotein A-I and B]. 212 24

Lipoprotein(a) [Lp(a)] is a low-density lipoprotein (LDL)-like lipoprotein particle recently described as a risk factor for premature coronary heart disease, stroke, and atherosclerosis. Structurally, Lp(a) is similar to LDL in that it has comparable lipid composition and contains apolipoprotein B-100 (apo B-100). In addition, Lp(a) contains the glycoprotein apolipoprotein(a) [apo(a)], which is disulfide-linked to apo B-100. The recent awareness of a striking correlation between atherosclerosis and concentrations of Lp(a) in plasma prompted our development of an accurate quantitative assay for plasma Lp(a), a monoclonal-antibody-based enzyme-linked immunosorbent assay for Lp(a) that is shown to be sensitive, precise, and highly specific. The response to several isoforms of Lp(a) is linear, and as many as 80 samples can be quantified on one plate. This easily performed assay is suitable for use in the clinical laboratory and for screening large populations.
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PMID:A monoclonal-antibody-based enzyme-linked immunosorbent assay of lipoprotein(a). 213 83

Nine patients with type III hyperlipoproteinaemia and homozygosity for the apolipoprotein E2 isoform were treated with 15 g daily of MaxEPA, a fish oil preparation rich in eicosapentaenoic acid (2.7 g daily) and docosahexaenoic acid (1.8 g daily) for 16 weeks. Plasma lipoprotein and apolipoprotein concentrations were compared with those obtained during treatment with an olive oil preparation. MaxEPA treatment decreased plasma median total cholesterol, triglyceride and apolipoprotein B concentrations by 16, 53 and 19%, respectively. Plasma median very low density lipoprotein (VLDL)-cholesterol, triglyceride and apolipoprotein B concentrations were reduced by 45, 62 and 75% respectively, while the abnormal VLDL-cholesterol/triglyceride ratio remained unchanged. Individual reductions of VLDL concentrations varied considerably, for VLDL-cholesterol between 10 and 75%. In the majority of cases the abnormal late pre beta-bands on agarose electrophoresis, typical for type III hyperlipoproteinaemia normalized to pre beta-mobility on MaxEPA treatment. LDL-cholesterol and apolipoprotein B tended to increase after 8 weeks on MaxEPA but decreased again after 16 weeks. Median plasma high density lipoprotein cholesterol and apolipoprotein A-I did not change during MaxEPA treatment. It is concluded that MaxEPA have decreasing effects on plasma VLDL lipid and apolipoprotein concentrations in apolipoprotein E2 homozygous type III hyperlipoproteinaemia but that this effect is variable and unpredictable.
Atherosclerosis 1990 Feb
PMID:Effect of fish oil treatment on plasma lipoproteins in type III hyperlipoproteinaemia. 213 96

The effect of two oral contraceptives containing 30 micrograms ethinylestradiol + 75 micrograms gestodene (EE/GSD) or 30 micrograms ethinylestradiol + 150 micrograms desogestrel (EE/DG) upon serum lipids and lipoproteins were measured in 11 women each on days 1, 10, and 21 of the first, third, sixth, and twelfth treatment cycle and compared to the levels on days 1, 10, and 21 of the preceding control cycle. There was no change in total cholesterol (CH) and phospholipids (PL), while total triglycerides (TG) were significantly elevated only during treatment with EE/GSD. After 3 and 6 months of intake of both oral contraceptives, a transitory increase in the TG content of very low-density lipoprotein (VLDL) and low-density lipoprotein (LDL), and a decrease in LDL-PL was observed. After 12 months, VLDL-CH, VLDL-PL, and apolipoprotein B were significantly elevated, while VLDL-TG and all components of LDL were unchanged. Most of the components of high-density lipoprotein (HDL) were increased due to a rise in HDL3 and apolipoprotein A-II, while HDL2 and apolipoprotein A-I were not altered. There was no significant difference between the effects of the two preparations, although those of EE/GSD were mostly more pronounced. The time-dependent change in the effects of the oral contraceptives on various parameters of lipid metabolism demonstrates that the relevance of results of short-time studies may be questionable. There was also a significant alteration in some parameters between day 1 and 10 of the treatment cycles and a tendency to return to the pretreatment levels during the pill-free week, e.g., in total TG and in the PL component of VLDL, LDL and HDL. The increase in HDL, VLDL, and total TG reflects a slight preponderance of the effect of ethinylestradiol on lipid metabolism. The unchanged total CH and LDL-CH and the elevated HDL levels indicate that the risk of the development of atherosclerosis is in all probability not increased during treatment with both preparations.
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PMID:Changes in lipid metabolism during 12 months of treatment with two oral contraceptives containing 30 micrograms ethinylestradiol and 75 micrograms gestodene or 150 micrograms desogestrel. 213 73

In a randomized comparative study, changes in lipoprotein metabolism during the use of two low-dose oral contraceptives with similar doses of ethinyl estradiol but with different progestogenically active compounds were evaluated for their effective estrogen/androgen balance. Sixty-eight healthy women who did not take hormonally active drugs or were pregnant the previous 3 months took either 75 micrograms of gestodene + 30 micrograms of ethinyl estradiol or 150 micrograms of desogestrel + 30 micrograms ethinyl estradiol during 12 cycles. During the first three cycles serum levels of the following parameters increased: triglycerides, cholesterol in high-density lipoprotein, and apolipoproteins A1, A2, and B. Additional increase was observed in apolipoprotein B only after three and six cycles. The induced changes were not significantly different in the two groups, and the levels generally remained within normal limits. The changes seen with both pills reflect a mild estrogenic dominance. On the basis of current knowledge, moderately altered lipoprotein metabolism is not expected to impose an extra risk of atherosclerosis.
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PMID:Estrogenic effect of gestodene- or desogestrel-containing oral contraceptives on lipoprotein metabolism. 214 75

The effect of sex steroids on lipid metabolism depends on the type and dose of the compounds, the route of administration, and the duration of treatment. Therefore the composition of an oral contraceptive determines the resultant effect on lipids and lipoproteins. During 12 months of treatment, the effects of two oral contraceptives containing 30 micrograms of ethinyl estradiol and 150 micrograms of desogestrel (EE/DG) or 75 micrograms of gestodene (EE/GSD) on 19 serum parameters of lipid metabolism were followed in 11 women each. There was no change in total cholesterol and phospholipids. Total triglyceride levels were significantly elevated only by EE/GSD. After 3 and 6 months of intake of both preparations, a transitory increase in the triglyceride content of very low-density lipoprotein and low-density lipoprotein and a decrease in low-density lipoprotein-phospholipids was observed. After 12 months, very low-density lipoprotein cholesterol, very low-density lipoprotein phospholipids, and apolipoprotein B were significantly elevated, whereas very low-density lipoprotein triglycerides and all components of low-density lipoprotein were unchanged. Most of the components of high-density lipoprotein (HDL) were increased as a result of a rise in HDL3 and apolipoprotein A2, whereas HDL2 and apolipoprotein A1 were not altered. There was no significant difference between the effects of the two preparations, although those of EE/GSD were mostly more pronounced. The increase in high-density lipoprotein, very low-density lipoprotein, and total triglycerides reflects a slight preponderance of the effect of the estrogen component. Because low-density lipoprotein cholesterol and total cholesterol were not changed, treatment with both formulations is in all probability not associated with an elevated risk of atherosclerosis.
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PMID:Time-dependent alterations in lipid metabolism during treatment with low-dose oral contraceptives. 214 76


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