Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is a definite need for replacement estrogen therapy in menopausal women exhibiting vasomotor symptoms or osteoporosis, particularly if the woman has had bilateral oophorectomy. There is a less clearly defined need in women complaining of emotional symptoms. Atrophic vaginitis and trigonitis is usually best treated with topical application of estrogen, which does not have systemic side effects if used weekly; more frequent use can lead to vascular absorption. Some of the problems associated with estrogen replacement are dose-related and can be eliminated by using smaller dosages. Uterine bleeding can usually be controlled by administering cyclically with progesterine. Hypertension, thrombosis, and adenocarcinoma are problems associated with administration of exogenous estrogens; use should be undertaken with great care in women exhibiting these conditions and patients should be followed closely to make sure such conditions are not developing. Other conditions which may worsen with estrogen therapy are diabetes mellitus, seizure disorders, migraine, multiple sclerosis, collagen diseases, cholelithiasis, and hyperlipidemia. None except hyperlipidemia is an absolute contraindication but risk/benefit ratios must be considered carefully in these cases.
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PMID:Estrogens for the menopause. Maximizing benefits, minimizing risks. 19 9

Rats were kept either on a standard laboratory diet or a high cholesterol, olive oil diet for periods ranging from 1 day to 22 weeks. The effect of the high cholesterol, olive oil diet on the concentrations of cholesterol, glycosaminoglycans (GAGs) and collagen in aortic intima-media, were studied and the developing hyperlipidemia was characterized. The concentration of cholesterol in rat aorta was increased after 22 weeks' high cholesterol, olive oil diet, while collagen concentration was not affected. On the contrary, the concentration of aortic sulphated GAGs was significantly increased already after one week's high cholesterol, olive oil diet. The diet increased the formation of a cholesterol-rich very low density lipoprotein (VLDL), decreased high density lipoprotein (HDL)-associated cholesterol and phospholipids, but had virtually no effect on low density lipoprotein (LDL)-lipids. The concentrations of VLDL-cholesterol and -phospholipids showed positive correlations with the concentration of aortic GAGs (r = 0.89 and 0.83, respectively, P less than 0.05 for both). Stronger (negative) correlations were found between aortic GAGs and HDL-cholesterol and -phospholipids (r = 0.94 for both, P less than 0.01) suggesting that HDL may have a role in the control of arterial sulphated GAG concentration.
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PMID:Rapid increase of glycosaminoglycans in the aorta of hypercholesterolemic rats; a negative correlation with plasma HDL concentration. 21 41

To determine whether the long-term feeding of dietary fats affect platelet functions in man, platelet aggregation (to thrombin ADP, collagen, epinephrine) and clotting activity of platelet-rich plasma (PRP), platelet-poor plasma and of washed platelets were studied in a mobile-laboratory in 44 healthy male farmers (40--45 years) from two French regions Var and Moselle, in relation to lipemia, glycemia, dietary nutriments, and platelet phospholipid composition. In the Moselle subjects, the platelet clotting activity of PRP and of washed platelets, the platelet aggregation to thrombin and ADP, were highly significantly (p less than 0.001) increased as compared to those of Var, but not the plasma cholesterol, which was identical in the two regions. In Moselle, the intake of total calories, total lipids and saturated fats was higher than in the Var. However, it was only with the saturated fat intake (mostly stearic acid) that the platelet clotting activity (p less than 0.01) and the platelet aggregation (p less than 0.001) were highly significantly correlated. The platelet clotting activity was also significantly (p less than 0.001) correlated with the fatty acid composition of the platelet phospholipid fractions phosphatidyl serine + phosphatidyl inositol.
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PMID:Platelet functions in relation to dietary fats in farmers from two regions of France. 42 66

Diabetes mellitus is associated with a high incidence of cardiovascular diseases not directly attributable to hyperlipidemia, smoking, or hypertension, but which in part may be explained by an enhanced tendency to thrombosis due to increased platelet activity. The aim of this study was to evaluate platelet function and compare the effectiveness of the antiplatelet drug aspirin on platelet aggregation in diabetic and nondiabetic subjects. Platelet aggregation and composition were examined in 20 male insulin-dependent diabetes mellitus (IDDM) patients and 20 nondiabetic control subjects matched for age and body mass index. All were normotensive with serum total cholesterol less than 6.5 mM. Although within the clinically acceptable normal range, blood pressure was significantly higher in diabetic patients (130/75 mmHg) than in control subjects (123/70 mmHg) (P less than 0.05). Serum thromboxane B2 and ex vivo aggregation of platelets in response to two doses of the agonists collagen and platelet-activating factor (PAF) were similar to nondiabetic subjects. However, after taking 100 mg/day aspirin for 5 days, platelet aggregation to collagen was reduced by 76% in control subjects compared to 56% in IDDM patients (P less than 0.001). Aspirin treatment also reduced the slope of the aggregation curve and increased the lag time (the period between the addition of collagen and the start of irreversible aggregation) significantly more in control than in diabetic platelets. This difference in platelet aggregation could not be attributed to differences in platelet serotonin or thromboxane A2 secretion, the latter being almost completely suppressed by aspirin in each group. Platelet aggregation to PAF was similar in both groups and was not affected by aspirin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential effect of aspirin on platelet aggregation in IDDM. 155 86

Three- to 15-month-old rabbits with Watanabe heritable hyperlipidemia (WHHL) were tested to determine if hematological abnormalities would accompany the known hyperlipidemia and deficiency of receptors for low-density lipoprotein; the findings were compared to those of New Zealand white (NZW) rabbits of the same ages. WHHL plasma cholesterol and triglyceride levels were always greater than or equal to 6x those of NZW, and both were lower in older than in younger WHHL rabbits. From age 7 to 18 months, WHHL platelet counts were higher than those of age-matched NZW; the average for all WHHL was 1.45x that for NZW (p = 0.001). Average WHHL mean platelet volume (MPV) was 0.94x that for NZW (p = 0.025), with a tendency for greater microcytosis to occur at more advanced ages; electron microscopy supported the small size of WHHL platelets. WHHL platelet mass per microliter of blood (platelet count x MPV) was 1.39x that of NZW (p = 0.001), with differences occurring after the age of 6 months. The average WHHL blood volume was 18.3% less than in NZW (33.5 vs 41.0 ml/kg body weight) (p = 0.00005), so platelet count and mass per kilogram of body weight were similar in the two strains. The predominant ploidy of mature megakaryocytes from each strain was 32N; megakaryocytes were smaller in WHHL than NZW due to a smaller size of 32N cells (p = 0.002). Total leukocyte counts were the same in WHHL and NZW rabbits, but eosinophils were 32% higher (p = 0.037) and lymphocytes 34% lower (p = 0.008) in WHHL. Hematocrits and reticulocytes did not differ. Platelet-free cholesterol was 1.2x, esterified cholesterol 11.3x, phospholipids 0.9x, triglyceride 2.4x, and free cholesterol/phospholipid molar ratio 1.29x corresponding values in NZW platelets. WHHL platelets released more serotonin in response to a small dose (5 micrograms/ml) of collagen than did NZW platelets. These findings suggest that: 1) megakaryocytopoiesis and leukopoiesis are affected by lipid metabolism and/or LDL receptors, and 2) platelet production may be regulated more by the total mass of platelets than by their concentration in the blood.
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PMID:Microcytic thrombocytosis, small megakaryocytes, platelet lipids and hyperreactivity to collagen, lymphocytopenia, eosinophilia, and low blood volume in genetically hyperlipidemic rabbits. 156 66

Platelet aggregations stimulated with different concentrations of collagen or ADP were reduced during postprandial hyperlipemia in normolipemic subjects. The concomitant formation of platelet AA metabolites (TXB2, 12-HHT, 12-HETE), however, was not significantly altered.
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PMID:Postprandial hyperlipemia and platelet eicosanoid metabolism. 208 67

Many general signs familiar to physicians can be found on the skin in cardiac patients. These include (a) cyanosis, central and peripheral, (b) erythremia, flushing and erythema, (c) digital clubbing and (d) alteration in texture. Specific cardiac conditions often have useful diagnostic cutaneous clues. Of these the association of coronary heart disease, hyperlipidemia and xanthomas is the most important. Rare syndromes such as the "leopard syndrome" often have distinctive skin signs. Multisystemic disorders may affect the heart and skin simultaneously or in sequence. They include collagen vascular diseases, amyloidosis, sarcoidosis and relapsing polychondritis. Finally iatrogenic disease arising from treatment of cardiac or cutaneous disease may induce changes in one or the other organ. The heart and the skin have much in common. These manifestations help elucidate the cause, evaluate the diagnosis, and follow the treatment and progress of these diseases.
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PMID:Cutaneous manifestations of cardiac diseases. 225 49

Arteries respond to long-term changes in flow rate by alterations in caliber that tend to restore wall shear stress to normal baseline levels. Changes in radius, pressure, or geometric configuration elicit changes in structure and composition of the media in keeping with the altered level and distribution of tensile stresses. Similar stabilizing adaptations occur in the presence of conditions that induce the formation of atherosclerotic plaques, but the ultimate effectiveness of these reactions is variable. Several recent experiments provide information on the possible effects of hyperlipidemia on the smooth muscle cell (SMC) response to normal or increased levels of mechanical stress: (a) Normolipemic serum increases collagen synthesis by SMCs grown on purified elastin membranes compared to synthesis in serum-free medium, but synthesis is not further enhanced by cyclic stretching of the cells. Collagen production increase is less marked in hyperlipemic serum, but cyclic stretching raises synthesis to a degree comparable to that noted for serum-free medium. (b) The increase in artery diameter in response to increased flow rate and the elaboration of media components in relation to the increase in diameter are not hampered by hyperlipidemia. (c) The compensatory enlargement of arteries in response to plaque formation is not prevented by hyperlipidemia even in the presence of hypertension. (d) The healing of a transmural necrotizing injury of the media is, however, retarded and incomplete in the presence of hyperlipidemia. These findings indicate that hyperlipidemia per se does not necessarily interfere with the SMC response to mechanical stimuli. The usual adaptive reactions remain intact.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Limited effects of hyperlipidemia on the arterial smooth muscle response to mechanical stress. 247 33

In this paper, we studied the effect of elastase on aminonucleoside (AN) nephrosis which is considered a model of focal glomerular sclerosis (FGS). Elastase is an enzyme which disintegrates elastin, discovered by Balo, and used in the treatment of arteriosclerosis and hyperlipidemia. It has also been known to improve metabolism of acid mucopolysaccharides, so, this study focused on metabolic improvement. Three groups of male Sprague-Dawley rats were studied and observed at regular intervals; 30, 60, 90 days. The ANE group (AN + elastase) was administered one shot of AN (10 mg/100 g B.W.) during the test interval, while elastase (5 mg/kg B.W.) was injected 5 days/week for the entire test interval. The AN group was administered one shot of AN only. The third group was a control (C). The following results were observed: (1) Focal segmental hyalinosis and sclerosis (FSHS); ANE group was weaker than AN group. (2) Other significant qualifying glomerular changes (vacuolar change and hyaline droplets of the epithelial cells, adhesion, and foam cells); ANE group was weaker than AN group. (3) Anion loss in GBM was shown by a lack of colloidal iron staining under light microscopy, and by a lack of PEI particles under electron microscopy; there was significantly less anion loss with ANE group, than with AN group. The findings suggest that elastase has an affect on the metabolism of acid mucopolysaccharide and collagen in sclerotic lesion, and may restrain the progress of amino-nucleoside nephrosis.
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PMID:[The effect of the elastase on aminonucleoside nephrosis]. 253 42

Using a complex stimulating mixture containing ADP, epinephrine and collagen, a significantly (p less than 0.002) enhanced platelet aggregability, expressed as platelet sensitivity factor (PSF) was noted in platelet rich plasma of patients with proteinuria (PSF = 472 +/- 125), as against normal weight normolipidemic control subjects (PSF = 32.76 +/- 2.67). A significantly negative correlation (r. -0.579; p less than 0.001) was found between serum albumin concentration and the logarithmic values of platelet sensitivity factor. Plasma von Willebrand factor activity expressed as a percentage of normal was also significantly (p less than 0.001) higher in proteinuric patients (287% +/- 25.8) than in control subjects (99% +/- 5.02), but this hemostatic variable did not correlate with the logarithm of platelet sensitivity factor. Platelet aggregability was higher in hyperlipidemic nephrotic patients than in proteinuric patients with normal serum lipids, while renal failure led to a decrease of platelet function. The raised plasma levels of von Willebrand factor noted in proteinuric patients were not influenced by either hyperlipidemia or by chronic renal failure. It is concluded that changes affecting platelet function in the nephrotic syndrome are produced by other mechanisms than these leading to an increase of endothelia-derived von Willebrand factor. Both changes may, however, contribute to the thrombotic tendency of nephrotic patients.
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PMID:Plasma von Willebrand factor antigen and activity and platelet aggregability in patients with proteinuria. 261 81


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