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)

To a group of 24 subjects with hypercholesterolaemia (hyperlipoproteinaemia type II) for a period of three months the non-absorbable resin Colestid was administered in order to reduce levels of atherogenic lipids and lipoproteins. The Colestid doses were graded from 5 g in the first month to 10-15 g during the third month. Reduction of cholesterol levels and the LDL fraction was significant already during the first month of treatment. The greatest reduction of LDL cholesterol was 25% and of total cholesterol 15%. A favourable effect was recorded also in HDL cholesterol which increased. The rise of triacylglycerols was not significant. Differences in the serum lipid response or their fractions did not depend on sex (15 women, 9 men), the clinical symptomatology (IHD) or family-history of atherosclerosis or concurrent administration of fibrates (Lipanthyl in 7 patients). In view of the small doses the symptomatology of side-effects was poor. Four patients, however, did not complete three months of treatment. With regard to the economical aspect of therapy and the favourable effect of small doses the authors draw attention to this experience which can be used as a basis also when using combinations with other preparations of antihypercholesterolemic therapy in those patients where an adequate reduction of cholesterol and its LDL fraction is not achieved.
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PMID:[Small doses of the resin Colestid in the treatment of hyperlipoproteinemia]. 200 12

The authors analysed the effectiveness of Lipanthyl treatment in 38 patients after stroke undergoing rehabilitation treatment. The effects of the drug were evaluated on the general condition, neurological and psychic status, progression of motor rehabilitation, and on lipid metabolism parameters. A statistically significant improvement was obtained in the subjective and psychic condition, and the results of motor rehabilitation were slightly better than in the compared groups of patients. Lipid metabolism was normalized only in part (cholesterol, chylomicrons). In the conclusions the authors state that it is useful to give this drug to patients with cerebral atherosclerosis only if disturbances of lipid metabolism coexist with this disease and are refractory to dietetic treatment.
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PMID:[Changes in blood lipids after stroke in patients treated with lipanthyl]. 687

Hyperleptinemia is considered to be one of predictors of early atherosklerosis complications. This stimulated us to investigate differences between leptinemia in persons with accelerated atherosclerosis and leptinemia in probands without atherosclerosis complications. The study also verified whether leptinemia and its relationship to other anthropometric and biochemical parameters can differ in hypolipemic-treated probands and hypolipemic-untreated individuals. We examined 89 probands with accelerated atherosclerosis. The controls were 20 persons without any signs of accelerated atherosclerosis. Probands with accelerated atherosclerosis had a slight hyperglycemia and were slightly obese, but they did not meet criteria of metabolic cardiovascular syndrome. No significant differences between both groups under study were found in terms of anthropometric and biochemical parameters (BMI, % body fat, glycemia, insulin, C-peptide, intact proinsulin, total proinsulin cholesterol, HDL, triglycerides, LDL, homeostatic model of insulin secretion and resistance). Leptin concentration was not different as well. Stratification into males and females showed that women had a significantly higher leptinemia and fat tissue mass. Other biochemical parameters were similar in both groups. We suppose that in individuals without signs of metabolic syndrome, leptinemia does not belong among predictors of accelerated atherosclerosis. The accelerated atherosclerosis persons were then divided into subgroups according to medication (28 probands--pravastatin Lipostat 20, 15 probands--phenofibrate Lipanthyl 200M, 9 probands--simvastatin Zocor 20, 47 probands--no hypolipemic medication). No significant differences between the groups were found in terms of the analysed anthropometric and biochemical parameters, except leptinemia. The pravastatin-medicated probands had a significantly lower leptinemia (significant at 99% significance level) which was evidently sex-related than other patients. The pravastatin-administered persons showed no correlation between leptinemia and body fat mass (in contrast to other groups where such a correlation was highly statistically significant). These findings can be explained by a still unclear effect of pravastatin on insulin metabolism and on other factors involved in leptin synthesis and elimination. Thus, a new therapeutic effect of pravastatin can be supposed. This may account for a highly favourable effect of pravastatin on reduced manifestations of atherosclerosis complications event at a low LDL cholesterol decrease (particularly in persons with metabolic cardiovascular syndrome).
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PMID:[Serum leptin, early atherosclerosis and hypolipidemia (a new, previously undescribed effect of pravastatin, a hypolipemic agent)]. 1042 91

Atherosclerosis is the major cause of heart attack and stroke in the western world. In this paper we present a computerized method for segmenting the athrerosclerotic carotid plaque from ultrasound images. The method uses the blood flow image first to detect the initial contour of the plaque, and then despeckle filtering and snakes to deform the initial contour for best fit of plaque boundaries. The accuracy and reproducibility of this method was tested using 35 longitudinal ultrasound images of carotid arteries and the results were compared with the manual delineations of an expert. The comparison showed that the computerized method gives satisfactory results with no manual correction needed in most of the cases. The true positive fraction, TPF, true negative fraction, TNF, false negative fraction, FNF and false positive fraction, FPF, were 86.44%, 84.03%, 8.5%, and 7% respectively.
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PMID:Atherosclerotic carotid plaque segmentation. 1727 56